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ESP: PubMed Auto Bibliography 18 Apr 2021 at 01:39 Created:
Origin of Multicellular Eukaryotes
Created with PubMed® Query: (origin OR evolution) and (eukaryotes OR eukaryota) AND (multicelluarity OR multicellular) NOT pmcbook NOT ispreviousversion
Citations The Papers (from PubMed®)
RevDate: 2021-04-16
Identification of long regulatory elements in the genome of Plasmodium falciparum and other eukaryotes.
PLoS computational biology, 17(4):e1008909 pii:PCOMPBIOL-D-20-01622 [Epub ahead of print].
Long regulatory elements (LREs), such as CpG islands, polydA:dT tracts or AU-rich elements, are thought to play key roles in gene regulation but, as opposed to conventional binding sites of transcription factors, few methods have been proposed to formally and automatically characterize them. We present here a computational approach named DExTER (Domain Exploration To Explain gene Regulation) dedicated to the identification of candidate LREs (cLREs) and apply it to the analysis of the genomes of P. falciparum and other eukaryotes. Our analyses show that all tested genomes contain several cLREs that are somewhat conserved along evolution, and that gene expression can be predicted with surprising accuracy on the basis of these long regions only. Regulation by cLREs exhibits very different behaviours depending on species and conditions. In P. falciparum and other Apicomplexan organisms as well as in Dictyostelium discoideum, the process appears highly dynamic, with different cLREs involved at different phases of the life cycle. For multicellular organisms, the same cLREs are involved in all tissues, but a dynamic behavior is observed along embryonic development stages. In P. falciparum, whose genome is known to be strongly depleted of transcription factors, cLREs are predictive of expression with an accuracy above 70%, and our analyses show that they are associated with both transcriptional and post-transcriptional regulation signals. Moreover, we assessed the biological relevance of one LRE discovered by DExTER in P. falciparum using an in vivo reporter assay. The source code (python) of DExTER is available at https://gite.lirmm.fr/menichelli/DExTER.
Additional Links: PMID-33861755
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@article {pmid33861755,
year = {2021},
author = {Menichelli, C and Guitard, V and Martins, RM and Lèbre, S and Lopez-Rubio, JJ and Lecellier, CH and Bréhélin, L},
title = {Identification of long regulatory elements in the genome of Plasmodium falciparum and other eukaryotes.},
journal = {PLoS computational biology},
volume = {17},
number = {4},
pages = {e1008909},
doi = {10.1371/journal.pcbi.1008909},
pmid = {33861755},
issn = {1553-7358},
abstract = {Long regulatory elements (LREs), such as CpG islands, polydA:dT tracts or AU-rich elements, are thought to play key roles in gene regulation but, as opposed to conventional binding sites of transcription factors, few methods have been proposed to formally and automatically characterize them. We present here a computational approach named DExTER (Domain Exploration To Explain gene Regulation) dedicated to the identification of candidate LREs (cLREs) and apply it to the analysis of the genomes of P. falciparum and other eukaryotes. Our analyses show that all tested genomes contain several cLREs that are somewhat conserved along evolution, and that gene expression can be predicted with surprising accuracy on the basis of these long regions only. Regulation by cLREs exhibits very different behaviours depending on species and conditions. In P. falciparum and other Apicomplexan organisms as well as in Dictyostelium discoideum, the process appears highly dynamic, with different cLREs involved at different phases of the life cycle. For multicellular organisms, the same cLREs are involved in all tissues, but a dynamic behavior is observed along embryonic development stages. In P. falciparum, whose genome is known to be strongly depleted of transcription factors, cLREs are predictive of expression with an accuracy above 70%, and our analyses show that they are associated with both transcriptional and post-transcriptional regulation signals. Moreover, we assessed the biological relevance of one LRE discovered by DExTER in P. falciparum using an in vivo reporter assay. The source code (python) of DExTER is available at https://gite.lirmm.fr/menichelli/DExTER.},
}
RevDate: 2021-04-15
CmpDate: 2021-04-15
Artificial selection for host resistance to tumour growth and subsequent cancer cell adaptations: an evolutionary arms race.
British journal of cancer, 124(2):455-465.
BACKGROUND: Cancer progression is governed by evolutionary dynamics in both the tumour population and its host. Since cancers die with the host, each new population of cancer cells must reinvent strategies to overcome the host's heritable defences. In contrast, host species evolve defence strategies over generations if tumour development limits procreation.
METHODS: We investigate this "evolutionary arms race" through intentional breeding of immunodeficient SCID and immunocompetent Black/6 mice to evolve increased tumour suppression. Over 10 generations, we injected Lewis lung mouse carcinoma cells [LL/2-Luc-M38] and selectively bred the two individuals with the slowest tumour growth at day 11. Their male progeny were hosts in the subsequent round.
RESULTS: The evolved SCID mice suppressed tumour growth through biomechanical restriction from increased mesenchymal proliferation, and the evolved Black/6 mice suppressed tumour growth by increasing immune-mediated killing of cancer cells. However, transcriptomic changes of multicellular tissue organisation and function genes allowed LL/2-Luc-M38 cells to adapt through increased matrix remodelling in SCID mice, and reduced angiogenesis, increased energy utilisation and accelerated proliferation in Black/6 mice.
CONCLUSION: Host species can rapidly evolve both immunologic and non-immunologic tumour defences. However, cancer cell plasticity allows effective phenotypic and population-based counter strategies.
Additional Links: PMID-33024265
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@article {pmid33024265,
year = {2021},
author = {Ibrahim-Hashim, A and Luddy, K and Abrahams, D and Enriquez-Navas, P and Damgaci, S and Yao, J and Chen, T and Bui, MM and Gillies, RJ and O'Farrelly, C and Richards, CL and Brown, JS and Gatenby, RA},
title = {Artificial selection for host resistance to tumour growth and subsequent cancer cell adaptations: an evolutionary arms race.},
journal = {British journal of cancer},
volume = {124},
number = {2},
pages = {455-465},
pmid = {33024265},
issn = {1532-1827},
support = {P30 CA076292/CA/NCI NIH HHS/United States ; U54 CA143970/CA/NCI NIH HHS/United States ; R01 CA077575/CA/NCI NIH HHS/United States ; },
mesh = {Adaptation, Physiological/*physiology ; Animals ; *Biological Evolution ; *Carcinoma, Lewis Lung ; Cell Plasticity/*physiology ; Disease Resistance/*physiology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, SCID ; },
abstract = {BACKGROUND: Cancer progression is governed by evolutionary dynamics in both the tumour population and its host. Since cancers die with the host, each new population of cancer cells must reinvent strategies to overcome the host's heritable defences. In contrast, host species evolve defence strategies over generations if tumour development limits procreation.
METHODS: We investigate this "evolutionary arms race" through intentional breeding of immunodeficient SCID and immunocompetent Black/6 mice to evolve increased tumour suppression. Over 10 generations, we injected Lewis lung mouse carcinoma cells [LL/2-Luc-M38] and selectively bred the two individuals with the slowest tumour growth at day 11. Their male progeny were hosts in the subsequent round.
RESULTS: The evolved SCID mice suppressed tumour growth through biomechanical restriction from increased mesenchymal proliferation, and the evolved Black/6 mice suppressed tumour growth by increasing immune-mediated killing of cancer cells. However, transcriptomic changes of multicellular tissue organisation and function genes allowed LL/2-Luc-M38 cells to adapt through increased matrix remodelling in SCID mice, and reduced angiogenesis, increased energy utilisation and accelerated proliferation in Black/6 mice.
CONCLUSION: Host species can rapidly evolve both immunologic and non-immunologic tumour defences. However, cancer cell plasticity allows effective phenotypic and population-based counter strategies.},
}
MeSH Terms:
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Adaptation, Physiological/*physiology
Animals
*Biological Evolution
*Carcinoma, Lewis Lung
Cell Plasticity/*physiology
Disease Resistance/*physiology
Male
Mice
Mice, Inbred C57BL
Mice, SCID
RevDate: 2021-04-15
CmpDate: 2021-04-15
Gene Loss Predictably Drives Evolutionary Adaptation.
Molecular biology and evolution, 37(10):2989-3002.
Loss of gene function is common throughout evolution, even though it often leads to reduced fitness. In this study, we systematically evaluated how an organism adapts after deleting genes that are important for growth under oxidative stress. By evolving, sequencing, and phenotyping over 200 yeast lineages, we found that gene loss can enhance an organism's capacity to evolve and adapt. Although gene loss often led to an immediate decrease in fitness, many mutants rapidly acquired suppressor mutations that restored fitness. Depending on the strain's genotype, some ultimately even attained higher fitness levels than similarly adapted wild-type cells. Further, cells with deletions in different modules of the genetic network followed distinct and predictable mutational trajectories. Finally, losing highly connected genes increased evolvability by facilitating the emergence of a more diverse array of phenotypes after adaptation. Together, our findings show that loss of specific parts of a genetic network can facilitate adaptation by opening alternative evolutionary paths.
Additional Links: PMID-32658971
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@article {pmid32658971,
year = {2020},
author = {Helsen, J and Voordeckers, K and Vanderwaeren, L and Santermans, T and Tsontaki, M and Verstrepen, KJ and Jelier, R},
title = {Gene Loss Predictably Drives Evolutionary Adaptation.},
journal = {Molecular biology and evolution},
volume = {37},
number = {10},
pages = {2989-3002},
pmid = {32658971},
issn = {1537-1719},
mesh = {Adaptation, Biological/*genetics ; *Biological Evolution ; *Gene Deletion ; Gene Regulatory Networks ; *Genetic Fitness ; Oxidative Stress/genetics ; Saccharomyces cerevisiae ; },
abstract = {Loss of gene function is common throughout evolution, even though it often leads to reduced fitness. In this study, we systematically evaluated how an organism adapts after deleting genes that are important for growth under oxidative stress. By evolving, sequencing, and phenotyping over 200 yeast lineages, we found that gene loss can enhance an organism's capacity to evolve and adapt. Although gene loss often led to an immediate decrease in fitness, many mutants rapidly acquired suppressor mutations that restored fitness. Depending on the strain's genotype, some ultimately even attained higher fitness levels than similarly adapted wild-type cells. Further, cells with deletions in different modules of the genetic network followed distinct and predictable mutational trajectories. Finally, losing highly connected genes increased evolvability by facilitating the emergence of a more diverse array of phenotypes after adaptation. Together, our findings show that loss of specific parts of a genetic network can facilitate adaptation by opening alternative evolutionary paths.},
}
MeSH Terms:
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Adaptation, Biological/*genetics
*Biological Evolution
*Gene Deletion
Gene Regulatory Networks
*Genetic Fitness
Oxidative Stress/genetics
Saccharomyces cerevisiae
RevDate: 2021-04-15
CmpDate: 2021-04-15
The Evolution of Human Cancer Gene Duplications across Mammals.
Molecular biology and evolution, 37(10):2875-2886.
Cancer is caused by genetic alterations that affect cellular fitness, and multicellular organisms have evolved mechanisms to suppress cancer such as cell cycle checkpoints and apoptosis. These pathways may be enhanced by the addition of tumor suppressor gene paralogs or deletion of oncogenes. To provide insights to the evolution of cancer suppression across the mammalian radiation, we estimated copy numbers for 548 human tumor suppressor gene and oncogene homologs in 63 mammalian genome assemblies. The naked mole rat contained the most cancer gene copies, consistent with the extremely low rates of cancer found in this species. We found a positive correlation between a species' cancer gene copy number and its longevity, but not body size, contrary to predictions from Peto's Paradox. Extremely long-lived mammals also contained more copies of caretaker genes in their genomes, suggesting that the maintenance of genome integrity is an essential form of cancer prevention in long-lived species. We found the strongest association between longevity and copy numbers of genes that are both germline and somatic tumor suppressor genes, suggesting that selection has acted to suppress both hereditary and sporadic cancers. We also found a strong relationship between the number of tumor suppressor genes and the number of oncogenes in mammalian genomes, suggesting that complex regulatory networks mediate the balance between cell proliferation and checks on tumor progression. This study is the first to investigate cancer gene expansions across the mammalian radiation and provides a springboard for potential human therapies based on evolutionary medicine.
Additional Links: PMID-32421773
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@article {pmid32421773,
year = {2020},
author = {Tollis, M and Schneider-Utaka, AK and Maley, CC},
title = {The Evolution of Human Cancer Gene Duplications across Mammals.},
journal = {Molecular biology and evolution},
volume = {37},
number = {10},
pages = {2875-2886},
pmid = {32421773},
issn = {1537-1719},
support = {U54 CA217376/CA/NCI NIH HHS/United States ; R01 CA185138/CA/NCI NIH HHS/United States ; U2C CA233254/CA/NCI NIH HHS/United States ; R01 CA170595/CA/NCI NIH HHS/United States ; R01 CA140657/CA/NCI NIH HHS/United States ; P01 CA091955/CA/NCI NIH HHS/United States ; R01 CA149566/CA/NCI NIH HHS/United States ; },
mesh = {Animals ; *Evolution, Molecular ; Gene Dosage ; *Gene Duplication ; *Genes, Neoplasm ; Humans ; *Life History Traits ; Longevity ; Mammals/*genetics ; Mole Rats/genetics ; },
abstract = {Cancer is caused by genetic alterations that affect cellular fitness, and multicellular organisms have evolved mechanisms to suppress cancer such as cell cycle checkpoints and apoptosis. These pathways may be enhanced by the addition of tumor suppressor gene paralogs or deletion of oncogenes. To provide insights to the evolution of cancer suppression across the mammalian radiation, we estimated copy numbers for 548 human tumor suppressor gene and oncogene homologs in 63 mammalian genome assemblies. The naked mole rat contained the most cancer gene copies, consistent with the extremely low rates of cancer found in this species. We found a positive correlation between a species' cancer gene copy number and its longevity, but not body size, contrary to predictions from Peto's Paradox. Extremely long-lived mammals also contained more copies of caretaker genes in their genomes, suggesting that the maintenance of genome integrity is an essential form of cancer prevention in long-lived species. We found the strongest association between longevity and copy numbers of genes that are both germline and somatic tumor suppressor genes, suggesting that selection has acted to suppress both hereditary and sporadic cancers. We also found a strong relationship between the number of tumor suppressor genes and the number of oncogenes in mammalian genomes, suggesting that complex regulatory networks mediate the balance between cell proliferation and checks on tumor progression. This study is the first to investigate cancer gene expansions across the mammalian radiation and provides a springboard for potential human therapies based on evolutionary medicine.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Evolution, Molecular
Gene Dosage
*Gene Duplication
*Genes, Neoplasm
Humans
*Life History Traits
Longevity
Mammals/*genetics
Mole Rats/genetics
RevDate: 2021-04-14
CmpDate: 2021-04-14
Epigenetic Molecular Mechanisms in Insects.
Neotropical entomology, 49(5):615-642.
Insects are the largest animal group on Earth both in biomass and diversity. Their outstanding success has inspired genetics and developmental research, allowing the discovery of dynamic process explaining extreme phenotypic plasticity and canalization. Epigenetic molecular mechanisms (EMMs) are vital for several housekeeping functions in multicellular organisms, regulating developmental, ontogenetic trajectories and environmental adaptations. In Insecta, EMMs are involved in the development of extreme phenotypic divergences such as polyphenisms and eusocial castes. Here, we review the history of this research field and how the main EMMs found in insects help to understand their biological processes and diversity. EMMs in insects confer them rapid response capacity allowing insect either to change with plastic divergence or to keep constant when facing different stressors or stimuli. EMMs function both at intra as well as transgenerational scales, playing important roles in insect ecology and evolution. We discuss on how EMMs pervasive influences in Insecta require not only the control of gene expression but also the dynamic interplay of EMMs with further regulatory levels, including genetic, physiological, behavioral, and environmental among others, as was earlier proposed by the Probabilistic Epigenesis model and Developmental System Theory.
Additional Links: PMID-32514997
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@article {pmid32514997,
year = {2020},
author = {Villagra, C and Frías-Lasserre, D},
title = {Epigenetic Molecular Mechanisms in Insects.},
journal = {Neotropical entomology},
volume = {49},
number = {5},
pages = {615-642},
doi = {10.1007/s13744-020-00777-8},
pmid = {32514997},
issn = {1678-8052},
mesh = {*Adaptation, Physiological ; Animals ; *Epigenesis, Genetic ; Insecta/*genetics ; Life Cycle Stages ; Phenotype ; Social Behavior ; },
abstract = {Insects are the largest animal group on Earth both in biomass and diversity. Their outstanding success has inspired genetics and developmental research, allowing the discovery of dynamic process explaining extreme phenotypic plasticity and canalization. Epigenetic molecular mechanisms (EMMs) are vital for several housekeeping functions in multicellular organisms, regulating developmental, ontogenetic trajectories and environmental adaptations. In Insecta, EMMs are involved in the development of extreme phenotypic divergences such as polyphenisms and eusocial castes. Here, we review the history of this research field and how the main EMMs found in insects help to understand their biological processes and diversity. EMMs in insects confer them rapid response capacity allowing insect either to change with plastic divergence or to keep constant when facing different stressors or stimuli. EMMs function both at intra as well as transgenerational scales, playing important roles in insect ecology and evolution. We discuss on how EMMs pervasive influences in Insecta require not only the control of gene expression but also the dynamic interplay of EMMs with further regulatory levels, including genetic, physiological, behavioral, and environmental among others, as was earlier proposed by the Probabilistic Epigenesis model and Developmental System Theory.},
}
MeSH Terms:
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hide MeSH Terms
*Adaptation, Physiological
Animals
*Epigenesis, Genetic
Insecta/*genetics
Life Cycle Stages
Phenotype
Social Behavior
RevDate: 2021-04-12
CmpDate: 2021-04-12
Mitochondrial Signature in Human Monocytes and Resistance to Infection in C. elegans During Fumarate-Induced Innate Immune Training.
Frontiers in immunology, 11:1715.
Monocytes can develop immunological memory, a functional characteristic widely recognized as innate immune training, to distinguish it from memory in adaptive immune cells. Upon a secondary immune challenge, either homologous or heterologous, trained monocytes/macrophages exhibit a more robust production of pro-inflammatory cytokines, such as IL-1β, IL-6, and TNF-α, than untrained monocytes. Candida albicans, β-glucan, and BCG are all inducers of monocyte training and recent metabolic profiling analyses have revealed that training induction is dependent on glycolysis, glutaminolysis, and the cholesterol synthesis pathway, along with fumarate accumulation; interestingly, fumarate itself can induce training. Since fumarate is produced by the tricarboxylic acid (TCA) cycle within mitochondria, we asked whether extra-mitochondrial fumarate has an effect on mitochondrial function. Results showed that the addition of fumarate to monocytes induces mitochondrial Ca2+ uptake, fusion, and increased membrane potential (Δψm), while mitochondrial cristae became closer to each other, suggesting that immediate (from minutes to hours) mitochondrial activation plays a role in the induction phase of innate immune training of monocytes. To establish whether fumarate induces similar mitochondrial changes in vivo in a multicellular organism, effects of fumarate supplementation were tested in the nematode worm Caenorhabditis elegans. This induced mitochondrial fusion in both muscle and intestinal cells and also increased resistance to infection of the pharynx with E. coli. Together, these findings contribute to defining a mitochondrial signature associated with the induction of innate immune training by fumarate treatment, and to the understanding of whole organism infection resistance.
Additional Links: PMID-32849605
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@article {pmid32849605,
year = {2020},
author = {Pérez-Hernández, CA and Kern, CC and Butkeviciute, E and McCarthy, E and Dockrell, HM and Moreno-Altamirano, MMB and Aguilar-López, BA and Bhosale, G and Wang, H and Gems, D and Duchen, MR and Smith, SG and Sánchez-García, FJ},
title = {Mitochondrial Signature in Human Monocytes and Resistance to Infection in C. elegans During Fumarate-Induced Innate Immune Training.},
journal = {Frontiers in immunology},
volume = {11},
number = {},
pages = {1715},
pmid = {32849605},
issn = {1664-3224},
support = {MR/R005850/1/MRC_/Medical Research Council/United Kingdom ; /BB_/Biotechnology and Biological Sciences Research Council/United Kingdom ; 098565/Z/12/Z/WT_/Wellcome Trust/United Kingdom ; 215574/Z/19/Z/WT_/Wellcome Trust/United Kingdom ; },
mesh = {Animals ; Caenorhabditis elegans/*drug effects/immunology/metabolism/microbiology ; Calcium Signaling/drug effects ; Cells, Cultured ; Cytokines/metabolism ; Escherichia coli/immunology/*pathogenicity ; Escherichia coli Infections/immunology/metabolism/microbiology/*prevention & control ; Fumarates/*pharmacology ; Host-Pathogen Interactions ; Humans ; Immunity, Innate/*drug effects ; Immunologic Memory/*drug effects ; Membrane Potential, Mitochondrial/drug effects ; Mitochondria/*drug effects/immunology/metabolism ; Mitochondrial Dynamics/drug effects ; Monocytes/*drug effects/immunology/metabolism ; },
abstract = {Monocytes can develop immunological memory, a functional characteristic widely recognized as innate immune training, to distinguish it from memory in adaptive immune cells. Upon a secondary immune challenge, either homologous or heterologous, trained monocytes/macrophages exhibit a more robust production of pro-inflammatory cytokines, such as IL-1β, IL-6, and TNF-α, than untrained monocytes. Candida albicans, β-glucan, and BCG are all inducers of monocyte training and recent metabolic profiling analyses have revealed that training induction is dependent on glycolysis, glutaminolysis, and the cholesterol synthesis pathway, along with fumarate accumulation; interestingly, fumarate itself can induce training. Since fumarate is produced by the tricarboxylic acid (TCA) cycle within mitochondria, we asked whether extra-mitochondrial fumarate has an effect on mitochondrial function. Results showed that the addition of fumarate to monocytes induces mitochondrial Ca2+ uptake, fusion, and increased membrane potential (Δψm), while mitochondrial cristae became closer to each other, suggesting that immediate (from minutes to hours) mitochondrial activation plays a role in the induction phase of innate immune training of monocytes. To establish whether fumarate induces similar mitochondrial changes in vivo in a multicellular organism, effects of fumarate supplementation were tested in the nematode worm Caenorhabditis elegans. This induced mitochondrial fusion in both muscle and intestinal cells and also increased resistance to infection of the pharynx with E. coli. Together, these findings contribute to defining a mitochondrial signature associated with the induction of innate immune training by fumarate treatment, and to the understanding of whole organism infection resistance.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
Caenorhabditis elegans/*drug effects/immunology/metabolism/microbiology
Calcium Signaling/drug effects
Cells, Cultured
Cytokines/metabolism
Escherichia coli/immunology/*pathogenicity
Escherichia coli Infections/immunology/metabolism/microbiology/*prevention & control
Fumarates/*pharmacology
Host-Pathogen Interactions
Humans
Immunity, Innate/*drug effects
Immunologic Memory/*drug effects
Membrane Potential, Mitochondrial/drug effects
Mitochondria/*drug effects/immunology/metabolism
Mitochondrial Dynamics/drug effects
Monocytes/*drug effects/immunology/metabolism
RevDate: 2021-04-06
CmpDate: 2021-04-06
Multiple Roles for Cholinergic Signaling from the Perspective of Stem Cell Function.
International journal of molecular sciences, 22(2):.
Stem cells have extensive proliferative potential and the ability to differentiate into one or more mature cell types. The mechanisms by which stem cells accomplish self-renewal provide fundamental insight into the origin and design of multicellular organisms. These pathways allow the repair of damage and extend organismal life beyond that of component cells, and they probably preceded the evolution of complex metazoans. Understanding the true nature of stem cells can only come from discovering how they are regulated. The concept that stem cells are controlled by particular microenvironments, also known as niches, has been widely accepted. Technical advances now allow characterization of the zones that maintain and control stem cell activity in several organs, including the brain, skin, and gut. Cholinergic neurons release acetylcholine (ACh) that mediates chemical transmission via ACh receptors such as nicotinic and muscarinic receptors. Although the cholinergic system is composed of organized nerve cells, the system is also involved in mammalian non-neuronal cells, including stem cells, embryonic stem cells, epithelial cells, and endothelial cells. Thus, cholinergic signaling plays a pivotal role in controlling their behaviors. Studies regarding this signal are beginning to unify our understanding of stem cell regulation at the cellular and molecular levels, and they are expected to advance efforts to control stem cells therapeutically. The present article reviews recent findings about cholinergic signaling that is essential to control stem cell function in a cholinergic niche.
Additional Links: PMID-33440882
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@article {pmid33440882,
year = {2021},
author = {Takahashi, T},
title = {Multiple Roles for Cholinergic Signaling from the Perspective of Stem Cell Function.},
journal = {International journal of molecular sciences},
volume = {22},
number = {2},
pages = {},
pmid = {33440882},
issn = {1422-0067},
support = {JP17K07495 and JP20K06751//Japan Society for the Promotion of Science/ ; },
mesh = {Acetylcholine/*metabolism ; Age Factors ; Animals ; Biomarkers ; Brain/cytology/metabolism ; Cell Differentiation/genetics ; Homeostasis ; Humans ; Organ Specificity ; Receptors, Cholinergic/*metabolism ; *Signal Transduction ; Stem Cells/cytology/*metabolism ; },
abstract = {Stem cells have extensive proliferative potential and the ability to differentiate into one or more mature cell types. The mechanisms by which stem cells accomplish self-renewal provide fundamental insight into the origin and design of multicellular organisms. These pathways allow the repair of damage and extend organismal life beyond that of component cells, and they probably preceded the evolution of complex metazoans. Understanding the true nature of stem cells can only come from discovering how they are regulated. The concept that stem cells are controlled by particular microenvironments, also known as niches, has been widely accepted. Technical advances now allow characterization of the zones that maintain and control stem cell activity in several organs, including the brain, skin, and gut. Cholinergic neurons release acetylcholine (ACh) that mediates chemical transmission via ACh receptors such as nicotinic and muscarinic receptors. Although the cholinergic system is composed of organized nerve cells, the system is also involved in mammalian non-neuronal cells, including stem cells, embryonic stem cells, epithelial cells, and endothelial cells. Thus, cholinergic signaling plays a pivotal role in controlling their behaviors. Studies regarding this signal are beginning to unify our understanding of stem cell regulation at the cellular and molecular levels, and they are expected to advance efforts to control stem cells therapeutically. The present article reviews recent findings about cholinergic signaling that is essential to control stem cell function in a cholinergic niche.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Acetylcholine/*metabolism
Age Factors
Animals
Biomarkers
Brain/cytology/metabolism
Cell Differentiation/genetics
Homeostasis
Humans
Organ Specificity
Receptors, Cholinergic/*metabolism
*Signal Transduction
Stem Cells/cytology/*metabolism
RevDate: 2021-04-02
CmpDate: 2021-04-02
Unmatched Level of Molecular Convergence among Deeply Divergent Complex Multicellular Fungi.
Molecular biology and evolution, 37(8):2228-2240.
Convergent evolution is pervasive in nature, but it is poorly understood how various constraints and natural selection limit the diversity of evolvable phenotypes. Here, we analyze the transcriptome across fruiting body development to understand the independent evolution of complex multicellularity in the two largest clades of fungi-the Agarico- and Pezizomycotina. Despite >650 My of divergence between these clades, we find that very similar sets of genes have convergently been co-opted for complex multicellularity, followed by expansions of their gene families by duplications. Over 82% of shared multicellularity-related gene families were expanding in both clades, indicating a high prevalence of convergence also at the gene family level. This convergence is coupled with a rich inferred repertoire of multicellularity-related genes in the most recent common ancestor of the Agarico- and Pezizomycotina, consistent with the hypothesis that the coding capacity of ancestral fungal genomes might have promoted the repeated evolution of complex multicellularity. We interpret this repertoire as an indication of evolutionary predisposition of fungal ancestors for evolving complex multicellular fruiting bodies. Our work suggests that evolutionary convergence may happen not only when organisms are closely related or are under similar selection pressures, but also when ancestral genomic repertoires render certain evolutionary trajectories more likely than others, even across large phylogenetic distances.
Additional Links: PMID-32191325
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@article {pmid32191325,
year = {2020},
author = {Merényi, Z and Prasanna, AN and Wang, Z and Kovács, K and Hegedüs, B and Bálint, B and Papp, B and Townsend, JP and Nagy, LG},
title = {Unmatched Level of Molecular Convergence among Deeply Divergent Complex Multicellular Fungi.},
journal = {Molecular biology and evolution},
volume = {37},
number = {8},
pages = {2228-2240},
pmid = {32191325},
issn = {1537-1719},
mesh = {Ascomycota/*genetics ; Basidiomycota/*genetics ; *Biological Evolution ; Fruiting Bodies, Fungal/*genetics ; Gene Expression Regulation, Developmental ; Multigene Family ; },
abstract = {Convergent evolution is pervasive in nature, but it is poorly understood how various constraints and natural selection limit the diversity of evolvable phenotypes. Here, we analyze the transcriptome across fruiting body development to understand the independent evolution of complex multicellularity in the two largest clades of fungi-the Agarico- and Pezizomycotina. Despite >650 My of divergence between these clades, we find that very similar sets of genes have convergently been co-opted for complex multicellularity, followed by expansions of their gene families by duplications. Over 82% of shared multicellularity-related gene families were expanding in both clades, indicating a high prevalence of convergence also at the gene family level. This convergence is coupled with a rich inferred repertoire of multicellularity-related genes in the most recent common ancestor of the Agarico- and Pezizomycotina, consistent with the hypothesis that the coding capacity of ancestral fungal genomes might have promoted the repeated evolution of complex multicellularity. We interpret this repertoire as an indication of evolutionary predisposition of fungal ancestors for evolving complex multicellular fruiting bodies. Our work suggests that evolutionary convergence may happen not only when organisms are closely related or are under similar selection pressures, but also when ancestral genomic repertoires render certain evolutionary trajectories more likely than others, even across large phylogenetic distances.},
}
MeSH Terms:
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Ascomycota/*genetics
Basidiomycota/*genetics
*Biological Evolution
Fruiting Bodies, Fungal/*genetics
Gene Expression Regulation, Developmental
Multigene Family
RevDate: 2021-03-29
Phylogenetic reconstruction and evolution of the Rab GTPase gene family in Amoebozoa.
Small GTPases [Epub ahead of print].
Rab GTPase is a paralog-rich gene family that controls the maintenance of the eukaryotic cell compartmentalization system. Diverse eukaryotes have varying numbers of Rab paralogs. Currently, little is known about the evolutionary pattern of Rab GTPase in most major eukaryotic 'supergroups'. Here, we present a comprehensive phylogenetic reconstruction of the Rab GTPase gene family in the eukaryotic 'supergroup' Amoebozoa, a diverse lineage represented by unicellular and multicellular organisms. We demonstrate that Amoebozoa conserved 20 of the 23 ancestral Rab GTPases predicted to be present in the last eukaryotic common ancestor and massively expanded several 'novel' in-paralogs. Due to these 'novel' in-paralogs, the Rab family composition dramatically varies between the members of Amoebozoa; as a consequence, 'supergroup'-based studies may significantly change our current understanding of the evolution and diversity of this gene family. The high diversity of the Rab GTPase gene family in Amoebozoa makes this 'supergroup' a key lineage to study and advance our knowledge of the evolution of Rab in Eukaryotes.
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@article {pmid33779495,
year = {2021},
author = {Porfírio-Sousa, AL and Tice, AK and Brown, MW and J G Lahr, D},
title = {Phylogenetic reconstruction and evolution of the Rab GTPase gene family in Amoebozoa.},
journal = {Small GTPases},
volume = {},
number = {},
pages = {1-14},
doi = {10.1080/21541248.2021.1903794},
pmid = {33779495},
issn = {2154-1256},
abstract = {Rab GTPase is a paralog-rich gene family that controls the maintenance of the eukaryotic cell compartmentalization system. Diverse eukaryotes have varying numbers of Rab paralogs. Currently, little is known about the evolutionary pattern of Rab GTPase in most major eukaryotic 'supergroups'. Here, we present a comprehensive phylogenetic reconstruction of the Rab GTPase gene family in the eukaryotic 'supergroup' Amoebozoa, a diverse lineage represented by unicellular and multicellular organisms. We demonstrate that Amoebozoa conserved 20 of the 23 ancestral Rab GTPases predicted to be present in the last eukaryotic common ancestor and massively expanded several 'novel' in-paralogs. Due to these 'novel' in-paralogs, the Rab family composition dramatically varies between the members of Amoebozoa; as a consequence, 'supergroup'-based studies may significantly change our current understanding of the evolution and diversity of this gene family. The high diversity of the Rab GTPase gene family in Amoebozoa makes this 'supergroup' a key lineage to study and advance our knowledge of the evolution of Rab in Eukaryotes.},
}
RevDate: 2021-03-26
CmpDate: 2021-03-26
Cooperative Interaction of Janthinobacterium sp. SLB01 and Flavobacterium sp. SLB02 in the Diseased Sponge Lubomirskiabaicalensis.
International journal of molecular sciences, 21(21):.
Endemic freshwater sponges (demosponges, Lubomirskiidae) dominate in Lake Baikal, Central Siberia, Russia. These sponges are multicellular filter-feeding animals that represent a complex consortium of many species of eukaryotes and prokaryotes. In recent years, mass disease and death of Lubomirskia baicalensis has been a significant problem in Lake Baikal. The etiology and ecology of these events remain unknown. Bacteria from the families Flavobacteriaceae and Oxalobacteraceae dominate the microbiomes of diseased sponges. Both species are opportunistic pathogens common in freshwater ecosystems. The aim of our study was to analyze the genomes of strains Janthinobacterium sp. SLB01 and Flavobacterium sp. SLB02, isolated from diseased sponges to identify the reasons for their joint dominance. Janthinobacterium sp. SLB01 attacks other cells using a type VI secretion system and suppresses gram-positive bacteria with violacein, and regulates its own activity via quorum sensing. It produces floc and strong biofilm by exopolysaccharide biosynthesis and PEP-CTERM/XrtA protein expression. Flavobacterium sp. SLB02 utilizes the fragments of cell walls produced by polysaccharides. These two strains have a marked difference in carbohydrate acquisition. We described a possible means of joint occupation of the ecological niche in the freshwater sponge microbial community. This study expands the understanding of the symbiotic relationship of microorganisms with freshwater Baikal sponges.
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@article {pmid33143227,
year = {2020},
author = {Petrushin, I and Belikov, S and Chernogor, L},
title = {Cooperative Interaction of Janthinobacterium sp. SLB01 and Flavobacterium sp. SLB02 in the Diseased Sponge Lubomirskiabaicalensis.},
journal = {International journal of molecular sciences},
volume = {21},
number = {21},
pages = {},
pmid = {33143227},
issn = {1422-0067},
support = {19-14-00088//Russian Science Foundation/ ; 0345-2019-0002 (AAAA-A16-116122110066-1)//Siberian Branch, Russian Academy of Sciences/ ; },
mesh = {Animals ; Cooperative Behavior ; *Ecosystem ; Flavobacterium/*physiology ; Lakes ; Oxalobacteraceae/*physiology ; Phylogeny ; Porifera/*metabolism/*microbiology ; *Symbiosis ; },
abstract = {Endemic freshwater sponges (demosponges, Lubomirskiidae) dominate in Lake Baikal, Central Siberia, Russia. These sponges are multicellular filter-feeding animals that represent a complex consortium of many species of eukaryotes and prokaryotes. In recent years, mass disease and death of Lubomirskia baicalensis has been a significant problem in Lake Baikal. The etiology and ecology of these events remain unknown. Bacteria from the families Flavobacteriaceae and Oxalobacteraceae dominate the microbiomes of diseased sponges. Both species are opportunistic pathogens common in freshwater ecosystems. The aim of our study was to analyze the genomes of strains Janthinobacterium sp. SLB01 and Flavobacterium sp. SLB02, isolated from diseased sponges to identify the reasons for their joint dominance. Janthinobacterium sp. SLB01 attacks other cells using a type VI secretion system and suppresses gram-positive bacteria with violacein, and regulates its own activity via quorum sensing. It produces floc and strong biofilm by exopolysaccharide biosynthesis and PEP-CTERM/XrtA protein expression. Flavobacterium sp. SLB02 utilizes the fragments of cell walls produced by polysaccharides. These two strains have a marked difference in carbohydrate acquisition. We described a possible means of joint occupation of the ecological niche in the freshwater sponge microbial community. This study expands the understanding of the symbiotic relationship of microorganisms with freshwater Baikal sponges.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
Cooperative Behavior
*Ecosystem
Flavobacterium/*physiology
Lakes
Oxalobacteraceae/*physiology
Phylogeny
Porifera/*metabolism/*microbiology
*Symbiosis
RevDate: 2021-03-26
CmpDate: 2021-03-26
Clinicopathological Analysis of Acquired Melanocytic Nevi and a Preliminary Study on the Possible Origin of Nevus Cells.
The American Journal of dermatopathology, 42(6):414-422.
BACKGROUND: The pathogenesis of acquired melanocytic nevi (AMN) is still unclear, and the origin of nevus cells has not been clarified.
OBJECTIVE: To analyze the clinical features and pathological types of AMN and identify the possible origin of nevus cells.
METHODS: A retrospective study of 2929 cases of AMN was conducted, and 96 specimens of intradermal and junctional nevi were selected. Immunohistochemical assays were performed to detect the expression of basement membrane component receptor DDR-1 and the molecular markers on epidermal melanocytes, dermal stem cells (DSCs), and hair follicle stem cells.
RESULTS: Junctional nevi and compound nevi were prone to occur on glabrous skin, such as the palms, soles, and vulva, and on the extremities in children, whereas intradermal nevi tended to develop on the trunk, head, and face of adults. The immunohistochemical data revealed that both junctional nevi and intradermal nevi expressed the epidermal melanocyte surface markers E-cadherin, DDR-1, and integrin α6 and the DSC molecular markers NGFRp-75 and nestin. CD34 was expressed only in junctional nevi, whereas K19 was not expressed in any type of melanocytic nevi. There was no significant difference in molecular expression at different sites or in different ages of onset. Nestin expression was markedly stronger in the intradermal nevi than in the junctional nevi, but there was no difference between the superficial and deep nevus cell nests of intradermal nevi.
CONCLUSION: AMN may have a multicellular origin that commonly follows the mode of Abtropfung. Furthermore, DSCs may partly or independently participate in the formation of nevus cells.
Additional Links: PMID-31880593
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@article {pmid31880593,
year = {2020},
author = {Wang, DG and Huang, FR and Chen, W and Zhou, Y and Wang, CY and Zhu, F and Shao, BJ and Luo, D},
title = {Clinicopathological Analysis of Acquired Melanocytic Nevi and a Preliminary Study on the Possible Origin of Nevus Cells.},
journal = {The American Journal of dermatopathology},
volume = {42},
number = {6},
pages = {414-422},
doi = {10.1097/DAD.0000000000001599},
pmid = {31880593},
issn = {1533-0311},
mesh = {Adolescent ; Adult ; Aged ; Aged, 80 and over ; Biomarkers/analysis ; Child ; Child, Preschool ; Female ; Humans ; Male ; Middle Aged ; Nevus, Pigmented/*pathology ; Retrospective Studies ; Skin Neoplasms/*pathology ; Stem Cells/*pathology ; Young Adult ; },
abstract = {BACKGROUND: The pathogenesis of acquired melanocytic nevi (AMN) is still unclear, and the origin of nevus cells has not been clarified.
OBJECTIVE: To analyze the clinical features and pathological types of AMN and identify the possible origin of nevus cells.
METHODS: A retrospective study of 2929 cases of AMN was conducted, and 96 specimens of intradermal and junctional nevi were selected. Immunohistochemical assays were performed to detect the expression of basement membrane component receptor DDR-1 and the molecular markers on epidermal melanocytes, dermal stem cells (DSCs), and hair follicle stem cells.
RESULTS: Junctional nevi and compound nevi were prone to occur on glabrous skin, such as the palms, soles, and vulva, and on the extremities in children, whereas intradermal nevi tended to develop on the trunk, head, and face of adults. The immunohistochemical data revealed that both junctional nevi and intradermal nevi expressed the epidermal melanocyte surface markers E-cadherin, DDR-1, and integrin α6 and the DSC molecular markers NGFRp-75 and nestin. CD34 was expressed only in junctional nevi, whereas K19 was not expressed in any type of melanocytic nevi. There was no significant difference in molecular expression at different sites or in different ages of onset. Nestin expression was markedly stronger in the intradermal nevi than in the junctional nevi, but there was no difference between the superficial and deep nevus cell nests of intradermal nevi.
CONCLUSION: AMN may have a multicellular origin that commonly follows the mode of Abtropfung. Furthermore, DSCs may partly or independently participate in the formation of nevus cells.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Adolescent
Adult
Aged
Aged, 80 and over
Biomarkers/analysis
Child
Child, Preschool
Female
Humans
Male
Middle Aged
Nevus, Pigmented/*pathology
Retrospective Studies
Skin Neoplasms/*pathology
Stem Cells/*pathology
Young Adult
RevDate: 2021-03-25
Cross Kingdom Immunity: The Role of Immune Receptors and Downstream Signaling in Animal and Plant Cell Death.
Frontiers in immunology, 11:612452.
Both plants and animals are endowed with sophisticated innate immune systems to combat microbial attack. In these multicellular eukaryotes, innate immunity implies the presence of cell surface receptors and intracellular receptors able to detect danger signal referred as damage-associated molecular patterns (DAMPs) and pathogen-associated molecular patterns (PAMPs). Membrane-associated pattern recognition receptors (PRRs), such as Toll-like receptors (TLRs), C-type lectin receptors (CLRs), receptor-like kinases (RLKs), and receptor-like proteins (RLPs) are employed by these organisms for sensing different invasion patterns before triggering antimicrobial defenses that can be associated with a form of regulated cell death. Intracellularly, animals nucleotide-binding and oligomerization domain (NOD)-like receptors or plants nucleotide-binding domain (NBD)-containing leucine rich repeats (NLRs) immune receptors likely detect effectors injected into the host cell by the pathogen to hijack the immune signaling cascade. Interestingly, during the co-evolution between the hosts and their invaders, key cross-kingdom cell death-signaling macromolecular NLR-complexes have been selected, such as the inflammasome in mammals and the recently discovered resistosome in plants. In both cases, a regulated cell death located at the site of infection constitutes a very effective mean for blocking the pathogen spread and protecting the whole organism from invasion. This review aims to describe the immune mechanisms in animals and plants, mainly focusing on cell death signaling pathways, in order to highlight recent advances that could be used on one side or the other to identify the missing signaling elements between the perception of the invasion pattern by immune receptors, the induction of defenses or the transmission of danger signals to other cells. Although knowledge of plant immunity is less advanced, these organisms have certain advantages allowing easier identification of signaling events, regulators and executors of cell death, which could then be exploited directly for crop protection purposes or by analogy for medical research.
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@article {pmid33763054,
year = {2020},
author = {Roudaire, T and Héloir, MC and Wendehenne, D and Zadoroznyj, A and Dubrez, L and Poinssot, B},
title = {Cross Kingdom Immunity: The Role of Immune Receptors and Downstream Signaling in Animal and Plant Cell Death.},
journal = {Frontiers in immunology},
volume = {11},
number = {},
pages = {612452},
doi = {10.3389/fimmu.2020.612452},
pmid = {33763054},
issn = {1664-3224},
abstract = {Both plants and animals are endowed with sophisticated innate immune systems to combat microbial attack. In these multicellular eukaryotes, innate immunity implies the presence of cell surface receptors and intracellular receptors able to detect danger signal referred as damage-associated molecular patterns (DAMPs) and pathogen-associated molecular patterns (PAMPs). Membrane-associated pattern recognition receptors (PRRs), such as Toll-like receptors (TLRs), C-type lectin receptors (CLRs), receptor-like kinases (RLKs), and receptor-like proteins (RLPs) are employed by these organisms for sensing different invasion patterns before triggering antimicrobial defenses that can be associated with a form of regulated cell death. Intracellularly, animals nucleotide-binding and oligomerization domain (NOD)-like receptors or plants nucleotide-binding domain (NBD)-containing leucine rich repeats (NLRs) immune receptors likely detect effectors injected into the host cell by the pathogen to hijack the immune signaling cascade. Interestingly, during the co-evolution between the hosts and their invaders, key cross-kingdom cell death-signaling macromolecular NLR-complexes have been selected, such as the inflammasome in mammals and the recently discovered resistosome in plants. In both cases, a regulated cell death located at the site of infection constitutes a very effective mean for blocking the pathogen spread and protecting the whole organism from invasion. This review aims to describe the immune mechanisms in animals and plants, mainly focusing on cell death signaling pathways, in order to highlight recent advances that could be used on one side or the other to identify the missing signaling elements between the perception of the invasion pattern by immune receptors, the induction of defenses or the transmission of danger signals to other cells. Although knowledge of plant immunity is less advanced, these organisms have certain advantages allowing easier identification of signaling events, regulators and executors of cell death, which could then be exploited directly for crop protection purposes or by analogy for medical research.},
}
RevDate: 2021-03-25
CmpDate: 2021-03-25
Cell Communications among Microorganisms, Plants, and Animals: Origin, Evolution, and Interplays.
International journal of molecular sciences, 21(21):.
Cellular communications play pivotal roles in multi-cellular species, but they do so also in uni-cellular species. Moreover, cells communicate with each other not only within the same individual, but also with cells in other individuals belonging to the same or other species. These communications occur between two unicellular species, two multicellular species, or between unicellular and multicellular species. The molecular mechanisms involved exhibit diversity and specificity, but they share common basic features, which allow common pathways of communication between different species, often phylogenetically very distant. These interactions are possible by the high degree of conservation of the basic molecular mechanisms of interaction of many ligand-receptor pairs in evolutionary remote species. These inter-species cellular communications played crucial roles during Evolution and must have been positively selected, particularly when collectively beneficial in hostile environments. It is likely that communications between cells did not arise after their emergence, but were part of the very nature of the first cells. Synchronization of populations of non-living protocells through chemical communications may have been a mandatory step towards their emergence as populations of living cells and explain the large commonality of cell communication mechanisms among microorganisms, plants, and animals.
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@article {pmid33126770,
year = {2020},
author = {Combarnous, Y and Nguyen, TMD},
title = {Cell Communications among Microorganisms, Plants, and Animals: Origin, Evolution, and Interplays.},
journal = {International journal of molecular sciences},
volume = {21},
number = {21},
pages = {},
pmid = {33126770},
issn = {1422-0067},
mesh = {Animals ; Bacteria/*metabolism ; *Biological Evolution ; *Cell Communication ; Fungi/*metabolism ; Phylogeny ; Plants/*metabolism ; Viruses/*metabolism ; },
abstract = {Cellular communications play pivotal roles in multi-cellular species, but they do so also in uni-cellular species. Moreover, cells communicate with each other not only within the same individual, but also with cells in other individuals belonging to the same or other species. These communications occur between two unicellular species, two multicellular species, or between unicellular and multicellular species. The molecular mechanisms involved exhibit diversity and specificity, but they share common basic features, which allow common pathways of communication between different species, often phylogenetically very distant. These interactions are possible by the high degree of conservation of the basic molecular mechanisms of interaction of many ligand-receptor pairs in evolutionary remote species. These inter-species cellular communications played crucial roles during Evolution and must have been positively selected, particularly when collectively beneficial in hostile environments. It is likely that communications between cells did not arise after their emergence, but were part of the very nature of the first cells. Synchronization of populations of non-living protocells through chemical communications may have been a mandatory step towards their emergence as populations of living cells and explain the large commonality of cell communication mechanisms among microorganisms, plants, and animals.},
}
MeSH Terms:
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Animals
Bacteria/*metabolism
*Biological Evolution
*Cell Communication
Fungi/*metabolism
Phylogeny
Plants/*metabolism
Viruses/*metabolism
RevDate: 2021-03-23
CmpDate: 2021-03-23
Distributed physiology and the molecular basis of social life in eusocial insects.
Hormones and behavior, 122:104757.
The traditional focus of physiological and functional genomic research is on molecular processes that play out within a single multicellular organism. In the colonial (eusocial) insects such as ants, bees, and termites, molecular and behavioral responses of interacting nestmates are tightly linked, and key physiological processes are regulated at the scale of the colony. Such colony-level physiological processes regulate nestmate physiology in a distributed fashion, through various social communication mechanisms. As a result of physiological decentralization over evolutionary time, organismal mechanisms, for example related to pheromone detection, hormone signaling, and neural signaling pathways, are deployed in novel contexts to influence nestmate and colony traits. Here we explore how functional genomic, physiological, and behavioral studies can benefit from considering the traits of eusocial insects in this light. We highlight functional genomic work exploring how nestmate-level and colony-level traits arise and are influenced by interactions among physiologically-specialized nestmates of various developmental stages. We also consider similarities and differences between nestmate-level (organismal) and colony-level (superorganismal) physiological processes, and make specific hypotheses regarding the physiology of eusocial taxa. Integrating theoretical models of distributed systems with empirical functional genomics approaches will be useful in addressing fundamental questions related to the evolution of eusociality and collective behavior in natural systems.
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@article {pmid32305342,
year = {2020},
author = {Friedman, DA and Johnson, BR and Linksvayer, TA},
title = {Distributed physiology and the molecular basis of social life in eusocial insects.},
journal = {Hormones and behavior},
volume = {122},
number = {},
pages = {104757},
doi = {10.1016/j.yhbeh.2020.104757},
pmid = {32305342},
issn = {1095-6867},
mesh = {Animals ; Ants/genetics/physiology ; Bees/genetics/physiology ; Behavior, Animal/*physiology ; Biological Evolution ; Cooperative Behavior ; Genome, Insect/*physiology ; Insecta/*genetics/*physiology ; Isoptera/genetics/physiology ; Nesting Behavior/physiology ; Phenotype ; *Social Behavior ; },
abstract = {The traditional focus of physiological and functional genomic research is on molecular processes that play out within a single multicellular organism. In the colonial (eusocial) insects such as ants, bees, and termites, molecular and behavioral responses of interacting nestmates are tightly linked, and key physiological processes are regulated at the scale of the colony. Such colony-level physiological processes regulate nestmate physiology in a distributed fashion, through various social communication mechanisms. As a result of physiological decentralization over evolutionary time, organismal mechanisms, for example related to pheromone detection, hormone signaling, and neural signaling pathways, are deployed in novel contexts to influence nestmate and colony traits. Here we explore how functional genomic, physiological, and behavioral studies can benefit from considering the traits of eusocial insects in this light. We highlight functional genomic work exploring how nestmate-level and colony-level traits arise and are influenced by interactions among physiologically-specialized nestmates of various developmental stages. We also consider similarities and differences between nestmate-level (organismal) and colony-level (superorganismal) physiological processes, and make specific hypotheses regarding the physiology of eusocial taxa. Integrating theoretical models of distributed systems with empirical functional genomics approaches will be useful in addressing fundamental questions related to the evolution of eusociality and collective behavior in natural systems.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
Ants/genetics/physiology
Bees/genetics/physiology
Behavior, Animal/*physiology
Biological Evolution
Cooperative Behavior
Genome, Insect/*physiology
Insecta/*genetics/*physiology
Isoptera/genetics/physiology
Nesting Behavior/physiology
Phenotype
*Social Behavior
RevDate: 2021-03-22
Evolution of Reproductive Division of Labor - Lessons Learned From the Social Amoeba Dictyostelium discoideum During Its Multicellular Development.
Frontiers in cell and developmental biology, 9:599525.
The origin of multicellular life from unicellular beings is an epochal step in the evolution of eukaryotes. There are several factors influencing cell fate choices during differentiation and morphogenesis of an organism. Genetic make-up of two cells that unite and fertilize is the key factor to signal the formation of various cell-types in due course of development. Although ploidy of the cell-types determines the genetics of an individual, the role of ploidy in cell fate decisions remains unclear. Dictyostelium serves as a versatile model to study the emergence of multicellular life from unicellular life forms. In this work, we investigate the role played by ploidy status of a cell on cell fate commitments during Dictyostelium development. To answer this question, we created Dictyostelium cells of different ploidy: haploid parents and derived isogenic diploids, allowing them to undergo development. The diploid strains used in this study were generated using parasexual genetics. The ploidy status of the haploids and diploids were confirmed by microscopy, flow cytometry, and karyotyping. Prior to reconstitution, we labeled the cells by two methods. First, intragenic expression of red fluorescent protein (RFP) and second, staining the amoebae with a vital, fluorescent dye carboxyfluorescein succinimidyl ester (CFSE). RFP labeled haploid cells allowed us to track the haploids in the chimeric aggregates, slugs, and fruiting bodies. The CFSE labeling method allowed us to track both the haploids and the diploids in the chimeric developmental structures. Our findings illustrate that the haploids demonstrate sturdy cell fate commitment starting from the aggregation stage. The haploids remain crowded at the aggregation centers of the haploid-diploid chimeric aggregates. At the slug stage haploids are predominantly occupying the slug posterior, and are visible in the spore population in the fruiting bodies. Our findings show that cell fate decisions during D. discoideum development are highly influenced by the ploidy status of a cell, adding a new aspect to already known factors Here, we report that ploidy status of a cell could also play a crucial role in regulating the cell fate commitments.
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@article {pmid33748102,
year = {2021},
author = {Dhakshinamoorthy, R and Singh, SP},
title = {Evolution of Reproductive Division of Labor - Lessons Learned From the Social Amoeba Dictyostelium discoideum During Its Multicellular Development.},
journal = {Frontiers in cell and developmental biology},
volume = {9},
number = {},
pages = {599525},
doi = {10.3389/fcell.2021.599525},
pmid = {33748102},
issn = {2296-634X},
abstract = {The origin of multicellular life from unicellular beings is an epochal step in the evolution of eukaryotes. There are several factors influencing cell fate choices during differentiation and morphogenesis of an organism. Genetic make-up of two cells that unite and fertilize is the key factor to signal the formation of various cell-types in due course of development. Although ploidy of the cell-types determines the genetics of an individual, the role of ploidy in cell fate decisions remains unclear. Dictyostelium serves as a versatile model to study the emergence of multicellular life from unicellular life forms. In this work, we investigate the role played by ploidy status of a cell on cell fate commitments during Dictyostelium development. To answer this question, we created Dictyostelium cells of different ploidy: haploid parents and derived isogenic diploids, allowing them to undergo development. The diploid strains used in this study were generated using parasexual genetics. The ploidy status of the haploids and diploids were confirmed by microscopy, flow cytometry, and karyotyping. Prior to reconstitution, we labeled the cells by two methods. First, intragenic expression of red fluorescent protein (RFP) and second, staining the amoebae with a vital, fluorescent dye carboxyfluorescein succinimidyl ester (CFSE). RFP labeled haploid cells allowed us to track the haploids in the chimeric aggregates, slugs, and fruiting bodies. The CFSE labeling method allowed us to track both the haploids and the diploids in the chimeric developmental structures. Our findings illustrate that the haploids demonstrate sturdy cell fate commitment starting from the aggregation stage. The haploids remain crowded at the aggregation centers of the haploid-diploid chimeric aggregates. At the slug stage haploids are predominantly occupying the slug posterior, and are visible in the spore population in the fruiting bodies. Our findings show that cell fate decisions during D. discoideum development are highly influenced by the ploidy status of a cell, adding a new aspect to already known factors Here, we report that ploidy status of a cell could also play a crucial role in regulating the cell fate commitments.},
}
RevDate: 2021-03-18
CmpDate: 2021-03-18
Aspects of Multicellularity in Saccharomyces cerevisiae Yeast: A Review of Evolutionary and Physiological Mechanisms.
Genes, 11(6):.
The evolutionary transition from single-celled to multicellular growth is a classic and intriguing problem in biology. Saccharomyces cerevisiae is a useful model to study questions regarding cell aggregation, heterogeneity and cooperation. In this review, we discuss scenarios of group formation and how this promotes facultative multicellularity in S. cerevisiae. We first describe proximate mechanisms leading to aggregation. These mechanisms include staying together and coming together, and can lead to group heterogeneity. Heterogeneity is promoted by nutrient limitation, structured environments and aging. We then characterize the evolutionary benefits and costs of facultative multicellularity in yeast. We summarize current knowledge and focus on the newest state-of-the-art discoveries that will fuel future research programmes aiming to understand facultative microbial multicellularity.
Additional Links: PMID-32599749
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@article {pmid32599749,
year = {2020},
author = {Opalek, M and Wloch-Salamon, D},
title = {Aspects of Multicellularity in Saccharomyces cerevisiae Yeast: A Review of Evolutionary and Physiological Mechanisms.},
journal = {Genes},
volume = {11},
number = {6},
pages = {},
pmid = {32599749},
issn = {2073-4425},
mesh = {*Biological Evolution ; Phenotype ; Saccharomyces cerevisiae/*genetics ; },
abstract = {The evolutionary transition from single-celled to multicellular growth is a classic and intriguing problem in biology. Saccharomyces cerevisiae is a useful model to study questions regarding cell aggregation, heterogeneity and cooperation. In this review, we discuss scenarios of group formation and how this promotes facultative multicellularity in S. cerevisiae. We first describe proximate mechanisms leading to aggregation. These mechanisms include staying together and coming together, and can lead to group heterogeneity. Heterogeneity is promoted by nutrient limitation, structured environments and aging. We then characterize the evolutionary benefits and costs of facultative multicellularity in yeast. We summarize current knowledge and focus on the newest state-of-the-art discoveries that will fuel future research programmes aiming to understand facultative microbial multicellularity.},
}
MeSH Terms:
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*Biological Evolution
Phenotype
Saccharomyces cerevisiae/*genetics
RevDate: 2021-03-18
CmpDate: 2021-03-18
Enhancers Facilitate the Birth of De Novo Genes and Gene Integration into Regulatory Networks.
Molecular biology and evolution, 37(4):1165-1178.
Regulatory networks control the spatiotemporal gene expression patterns that give rise to and define the individual cell types of multicellular organisms. In eumetazoa, distal regulatory elements called enhancers play a key role in determining the structure of such networks, particularly the wiring diagram of "who regulates whom." Mutations that affect enhancer activity can therefore rewire regulatory networks, potentially causing adaptive changes in gene expression. Here, we use whole-tissue and single-cell transcriptomic and chromatin accessibility data from mouse to show that enhancers play an additional role in the evolution of regulatory networks: They facilitate network growth by creating transcriptionally active regions of open chromatin that are conducive to de novo gene evolution. Specifically, our comparative transcriptomic analysis with three other mammalian species shows that young, mouse-specific intergenic open reading frames are preferentially located near enhancers, whereas older open reading frames are not. Mouse-specific intergenic open reading frames that are proximal to enhancers are more highly and stably transcribed than those that are not proximal to enhancers or promoters, and they are transcribed in a limited diversity of cellular contexts. Furthermore, we report several instances of mouse-specific intergenic open reading frames proximal to promoters showing evidence of being repurposed enhancers. We also show that open reading frames gradually acquire interactions with enhancers over macroevolutionary timescales, helping integrate genes-those that have arisen de novo or by other means-into existing regulatory networks. Taken together, our results highlight a dual role of enhancers in expanding and rewiring gene regulatory networks.
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@article {pmid31845961,
year = {2020},
author = {Majic, P and Payne, JL},
title = {Enhancers Facilitate the Birth of De Novo Genes and Gene Integration into Regulatory Networks.},
journal = {Molecular biology and evolution},
volume = {37},
number = {4},
pages = {1165-1178},
pmid = {31845961},
issn = {1537-1719},
mesh = {Animals ; DNA, Intergenic ; *Enhancer Elements, Genetic ; *Evolution, Molecular ; *Gene Regulatory Networks ; Mice ; Open Reading Frames ; Promoter Regions, Genetic ; Transcription, Genetic ; },
abstract = {Regulatory networks control the spatiotemporal gene expression patterns that give rise to and define the individual cell types of multicellular organisms. In eumetazoa, distal regulatory elements called enhancers play a key role in determining the structure of such networks, particularly the wiring diagram of "who regulates whom." Mutations that affect enhancer activity can therefore rewire regulatory networks, potentially causing adaptive changes in gene expression. Here, we use whole-tissue and single-cell transcriptomic and chromatin accessibility data from mouse to show that enhancers play an additional role in the evolution of regulatory networks: They facilitate network growth by creating transcriptionally active regions of open chromatin that are conducive to de novo gene evolution. Specifically, our comparative transcriptomic analysis with three other mammalian species shows that young, mouse-specific intergenic open reading frames are preferentially located near enhancers, whereas older open reading frames are not. Mouse-specific intergenic open reading frames that are proximal to enhancers are more highly and stably transcribed than those that are not proximal to enhancers or promoters, and they are transcribed in a limited diversity of cellular contexts. Furthermore, we report several instances of mouse-specific intergenic open reading frames proximal to promoters showing evidence of being repurposed enhancers. We also show that open reading frames gradually acquire interactions with enhancers over macroevolutionary timescales, helping integrate genes-those that have arisen de novo or by other means-into existing regulatory networks. Taken together, our results highlight a dual role of enhancers in expanding and rewiring gene regulatory networks.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
DNA, Intergenic
*Enhancer Elements, Genetic
*Evolution, Molecular
*Gene Regulatory Networks
Mice
Open Reading Frames
Promoter Regions, Genetic
Transcription, Genetic
RevDate: 2021-03-15
CmpDate: 2021-03-15
Genome editing enables reverse genetics of multicellular development in the choanoflagellate Salpingoeca rosetta.
eLife, 9:.
In a previous study, we established a forward genetic screen to identify genes required for multicellular development in the choanoflagellate, Salpingoeca rosetta (Levin et al., 2014). Yet, the paucity of reverse genetic tools for choanoflagellates has hampered direct tests of gene function and impeded the establishment of choanoflagellates as a model for reconstructing the origin of their closest living relatives, the animals. Here we establish CRISPR/Cas9-mediated genome editing in S. rosetta by engineering a selectable marker to enrich for edited cells. We then use genome editing to disrupt the coding sequence of a S. rosetta C-type lectin gene, rosetteless, and thereby demonstrate its necessity for multicellular rosette development. This work advances S. rosetta as a model system in which to investigate how genes identified from genetic screens and genomic surveys function in choanoflagellates and evolved as critical regulators of animal biology.
Additional Links: PMID-32496191
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Citation:
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@article {pmid32496191,
year = {2020},
author = {Booth, DS and King, N},
title = {Genome editing enables reverse genetics of multicellular development in the choanoflagellate Salpingoeca rosetta.},
journal = {eLife},
volume = {9},
number = {},
pages = {},
pmid = {32496191},
issn = {2050-084X},
support = {/HHMI/Howard Hughes Medical Institute/United States ; },
mesh = {CRISPR-Cas Systems ; Choanoflagellata/*genetics/*growth & development ; Gene Editing ; Genome, Protozoan ; Lectins, C-Type/genetics ; Protozoan Proteins/genetics ; Reverse Genetics/*methods ; },
abstract = {In a previous study, we established a forward genetic screen to identify genes required for multicellular development in the choanoflagellate, Salpingoeca rosetta (Levin et al., 2014). Yet, the paucity of reverse genetic tools for choanoflagellates has hampered direct tests of gene function and impeded the establishment of choanoflagellates as a model for reconstructing the origin of their closest living relatives, the animals. Here we establish CRISPR/Cas9-mediated genome editing in S. rosetta by engineering a selectable marker to enrich for edited cells. We then use genome editing to disrupt the coding sequence of a S. rosetta C-type lectin gene, rosetteless, and thereby demonstrate its necessity for multicellular rosette development. This work advances S. rosetta as a model system in which to investigate how genes identified from genetic screens and genomic surveys function in choanoflagellates and evolved as critical regulators of animal biology.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
CRISPR-Cas Systems
Choanoflagellata/*genetics/*growth & development
Gene Editing
Genome, Protozoan
Lectins, C-Type/genetics
Protozoan Proteins/genetics
Reverse Genetics/*methods
RevDate: 2021-03-11
CmpDate: 2021-03-11
The Oncogenic PRL Protein Causes Acid Addiction of Cells by Stimulating Lysosomal Exocytosis.
Developmental cell, 55(4):387-397.e8.
Extracellular pH is usually maintained around 7.4 in multicellular organisms, and cells are optimized to proliferate under this condition. Here, we find cells can adapt to a more acidic pH of 6.5 and become addicted to this acidic microenvironment by expressing phosphatase of regenerating liver (PRL), a driver of cancer malignancy. Genome-scale CRISPR-Cas9 knockout screening and subsequent analyses revealed that PRL promotes H+ extrusion and acid addiction by stimulating lysosomal exocytosis. Further experiments using cultured cells and Caenorhabditis elegans clarified the molecular link between PRL and lysosomal exocytosis across species, involving activation of lysosomal Ca2+ channel TRPML by ROS. Indeed, disruption of TRPML in cancer cells abolished PRL-stimulated lysosomal exocytosis, acid addiction, and metastasis. Thus, PRL is the molecular switch turning cells addicted to an acidic condition, which should benefit cancer cells to thrive in an acidic tumor microenvironment.
Additional Links: PMID-32918875
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PubMed:
Citation:
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@article {pmid32918875,
year = {2020},
author = {Funato, Y and Yoshida, A and Hirata, Y and Hashizume, O and Yamazaki, D and Miki, H},
title = {The Oncogenic PRL Protein Causes Acid Addiction of Cells by Stimulating Lysosomal Exocytosis.},
journal = {Developmental cell},
volume = {55},
number = {4},
pages = {387-397.e8},
doi = {10.1016/j.devcel.2020.08.009},
pmid = {32918875},
issn = {1878-1551},
mesh = {Acids/*metabolism ; Animals ; CRISPR-Cas Systems/genetics ; Caenorhabditis elegans/metabolism ; Conserved Sequence ; Dogs ; Evolution, Molecular ; *Exocytosis ; HEK293 Cells ; Humans ; Immediate-Early Proteins/*metabolism ; Intracellular Membranes/metabolism ; Lysosomes/*metabolism ; Madin Darby Canine Kidney Cells ; Mice, Inbred C57BL ; Neoplasm Metastasis ; Neoplasm Proteins/*metabolism ; Protein Tyrosine Phosphatases/*metabolism ; },
abstract = {Extracellular pH is usually maintained around 7.4 in multicellular organisms, and cells are optimized to proliferate under this condition. Here, we find cells can adapt to a more acidic pH of 6.5 and become addicted to this acidic microenvironment by expressing phosphatase of regenerating liver (PRL), a driver of cancer malignancy. Genome-scale CRISPR-Cas9 knockout screening and subsequent analyses revealed that PRL promotes H+ extrusion and acid addiction by stimulating lysosomal exocytosis. Further experiments using cultured cells and Caenorhabditis elegans clarified the molecular link between PRL and lysosomal exocytosis across species, involving activation of lysosomal Ca2+ channel TRPML by ROS. Indeed, disruption of TRPML in cancer cells abolished PRL-stimulated lysosomal exocytosis, acid addiction, and metastasis. Thus, PRL is the molecular switch turning cells addicted to an acidic condition, which should benefit cancer cells to thrive in an acidic tumor microenvironment.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Acids/*metabolism
Animals
CRISPR-Cas Systems/genetics
Caenorhabditis elegans/metabolism
Conserved Sequence
Dogs
Evolution, Molecular
*Exocytosis
HEK293 Cells
Humans
Immediate-Early Proteins/*metabolism
Intracellular Membranes/metabolism
Lysosomes/*metabolism
Madin Darby Canine Kidney Cells
Mice, Inbred C57BL
Neoplasm Metastasis
Neoplasm Proteins/*metabolism
Protein Tyrosine Phosphatases/*metabolism
RevDate: 2021-03-10
CmpDate: 2021-03-10
Glandular trichomes of Robinia viscosa Vent. var. hartwigii (Koehne) Ashe (Faboideae, Fabaceae)-morphology, histochemistry and ultrastructure.
Planta, 252(6):102.
MAIN CONCLUSION: Permanent glandular trichomes of Robinia viscosa var. hartwigii produce viscous secretion containing several secondary metabolites, as lipids, mucilage, flavonoids, proteins and alkaloids. Robinia viscosa var. hartwigii (Hartweg's locust) is an ornamental tree with high apicultural value. It can be planted in urban greenery and in degraded areas. The shoots, leaves, and inflorescences of this plant are equipped with numerous persistent glandular trichomes producing sticky secretion. The distribution, origin, development, morphology, anatomy, and ultrastructure of glandular trichomes of Hartweg's locust flowers as well as the localisation and composition of their secretory products were investigated for the first time. To this end, light, scanning, and transmission electron microscopy combined with histochemical and fluorescence techniques were used. The massive glandular trichomes differing in the distribution, length, and stage of development were built of a multicellular and multiseriate stalk and a multicellular head. The secretory cells in the stalk and head had large nuclei with nucleoli, numerous chloroplasts with thylakoids and starch grains, mitochondria, endoplasmic reticulum profiles, Golgi apparatus, vesicles, and multivesicular bodies. Many vacuoles contained phenolic compounds dissolved or forming various condensed deposits. The secretion components were transported through symplast elements, and the granulocrine and eccrine modes of nectar secretion were observed. The secretion was accumulated in the subcuticular space at the trichome apex and released through a pore in the cuticle. Histochemical and fluorescence assays showed that the trichomes and secretion contained lipophilic and polyphenol compounds, polysaccharides, proteins, and alkaloids. We suggest that these metabolites may serve an important function in protection of plants against biotic stress conditions and may also be a source of phytopharmaceuticals in the future.
Additional Links: PMID-33180181
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Citation:
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@article {pmid33180181,
year = {2020},
author = {Konarska, A and Łotocka, B},
title = {Glandular trichomes of Robinia viscosa Vent. var. hartwigii (Koehne) Ashe (Faboideae, Fabaceae)-morphology, histochemistry and ultrastructure.},
journal = {Planta},
volume = {252},
number = {6},
pages = {102},
pmid = {33180181},
issn = {1432-2048},
mesh = {Flowers ; *Histocytochemistry ; Microscopy, Electron ; Plant Leaves ; *Robinia/chemistry/ultrastructure ; *Trichomes/chemistry/ultrastructure ; },
abstract = {MAIN CONCLUSION: Permanent glandular trichomes of Robinia viscosa var. hartwigii produce viscous secretion containing several secondary metabolites, as lipids, mucilage, flavonoids, proteins and alkaloids. Robinia viscosa var. hartwigii (Hartweg's locust) is an ornamental tree with high apicultural value. It can be planted in urban greenery and in degraded areas. The shoots, leaves, and inflorescences of this plant are equipped with numerous persistent glandular trichomes producing sticky secretion. The distribution, origin, development, morphology, anatomy, and ultrastructure of glandular trichomes of Hartweg's locust flowers as well as the localisation and composition of their secretory products were investigated for the first time. To this end, light, scanning, and transmission electron microscopy combined with histochemical and fluorescence techniques were used. The massive glandular trichomes differing in the distribution, length, and stage of development were built of a multicellular and multiseriate stalk and a multicellular head. The secretory cells in the stalk and head had large nuclei with nucleoli, numerous chloroplasts with thylakoids and starch grains, mitochondria, endoplasmic reticulum profiles, Golgi apparatus, vesicles, and multivesicular bodies. Many vacuoles contained phenolic compounds dissolved or forming various condensed deposits. The secretion components were transported through symplast elements, and the granulocrine and eccrine modes of nectar secretion were observed. The secretion was accumulated in the subcuticular space at the trichome apex and released through a pore in the cuticle. Histochemical and fluorescence assays showed that the trichomes and secretion contained lipophilic and polyphenol compounds, polysaccharides, proteins, and alkaloids. We suggest that these metabolites may serve an important function in protection of plants against biotic stress conditions and may also be a source of phytopharmaceuticals in the future.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Flowers
*Histocytochemistry
Microscopy, Electron
Plant Leaves
*Robinia/chemistry/ultrastructure
*Trichomes/chemistry/ultrastructure
RevDate: 2021-03-09
CmpDate: 2021-03-09
Ancient Evolutionary Origin of Intrinsically Disordered Cancer Risk Regions.
Biomolecules, 10(8):.
Cancer is a heterogeneous genetic disease that alters the proper functioning of proteins involved in key regulatory processes such as cell cycle, DNA repair, survival, or apoptosis. Mutations often accumulate in hot-spots regions, highlighting critical functional modules within these proteins that need to be altered, amplified, or abolished for tumor formation. Recent evidence suggests that these mutational hotspots can correspond not only to globular domains, but also to intrinsically disordered regions (IDRs), which play a significant role in a subset of cancer types. IDRs have distinct functional properties that originate from their inherent flexibility. Generally, they correspond to more recent evolutionary inventions and show larger sequence variations across species. In this work, we analyzed the evolutionary origin of disordered regions that are specifically targeted in cancer. Surprisingly, the majority of these disordered cancer risk regions showed remarkable conservation with ancient evolutionary origin, stemming from the earliest multicellular animals or even beyond. Nevertheless, we encountered several examples where the mutated region emerged at a later stage compared with the origin of the gene family. We also showed the cancer risk regions become quickly fixated after their emergence, but evolution continues to tinker with their genes with novel regulatory elements introduced even at the level of humans. Our concise analysis provides a much clearer picture of the emergence of key regulatory elements in proteins and highlights the importance of taking into account the modular organisation of proteins for the analyses of evolutionary origin.
Additional Links: PMID-32731489
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@article {pmid32731489,
year = {2020},
author = {Pajkos, M and Zeke, A and Dosztányi, Z},
title = {Ancient Evolutionary Origin of Intrinsically Disordered Cancer Risk Regions.},
journal = {Biomolecules},
volume = {10},
number = {8},
pages = {},
pmid = {32731489},
issn = {2218-273X},
support = {FIEK16-1-2016-0005//FIEK Grant of the National Research, Development and Innovation Office/International ; ED-18-1-2019-003//ELTE Thematic Excellence Programme supported by the Hungarian Ministry for Innovation and Technology./International ; },
mesh = {Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Evolution, Molecular ; Gene Duplication ; Humans ; Intrinsically Disordered Proteins/chemistry/*genetics ; Mutation ; Neoplasms/*genetics ; Protein Conformation ; Protein Domains ; },
abstract = {Cancer is a heterogeneous genetic disease that alters the proper functioning of proteins involved in key regulatory processes such as cell cycle, DNA repair, survival, or apoptosis. Mutations often accumulate in hot-spots regions, highlighting critical functional modules within these proteins that need to be altered, amplified, or abolished for tumor formation. Recent evidence suggests that these mutational hotspots can correspond not only to globular domains, but also to intrinsically disordered regions (IDRs), which play a significant role in a subset of cancer types. IDRs have distinct functional properties that originate from their inherent flexibility. Generally, they correspond to more recent evolutionary inventions and show larger sequence variations across species. In this work, we analyzed the evolutionary origin of disordered regions that are specifically targeted in cancer. Surprisingly, the majority of these disordered cancer risk regions showed remarkable conservation with ancient evolutionary origin, stemming from the earliest multicellular animals or even beyond. Nevertheless, we encountered several examples where the mutated region emerged at a later stage compared with the origin of the gene family. We also showed the cancer risk regions become quickly fixated after their emergence, but evolution continues to tinker with their genes with novel regulatory elements introduced even at the level of humans. Our concise analysis provides a much clearer picture of the emergence of key regulatory elements in proteins and highlights the importance of taking into account the modular organisation of proteins for the analyses of evolutionary origin.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Amino Acid Motifs
Amino Acid Sequence
Animals
Evolution, Molecular
Gene Duplication
Humans
Intrinsically Disordered Proteins/chemistry/*genetics
Mutation
Neoplasms/*genetics
Protein Conformation
Protein Domains
RevDate: 2021-03-05
CmpDate: 2021-03-05
Identification of NLR-associated Amyloid Signaling Motifs in Bacterial Genomes.
Journal of molecular biology, 432(23):6005-6027.
In filamentous fungi, amyloid signaling sequences allow Nod-like receptors (NLRs) to activate downstream cell-death inducing proteins with HeLo and HeLo-like (HELL) domains and amyloid RHIM and RHIM-related motifs control immune defense pathways in mammals and flies. Herein, we show bioinformatically that analogous amyloid signaling motifs exist in bacteria. These short motifs are found at the N terminus of NLRs and at the C terminus of proteins with a domain we term BELL. The corresponding NLR and BELL proteins are encoded by adjacent genes. We identify 10 families of such bacterial amyloid signaling sequences (BASS), one of which (BASS3) is homologous to RHIM and a fungal amyloid motif termed PP. BASS motifs occur nearly exclusively in bacteria forming multicellular structures (mainly in Actinobacteria and Cyanobacteria). We analyze experimentally a subset of seven of these motifs (from the most common BASS1 family and the RHIM-related BASS3 family) and find that these sequences form fibrils in vitro. Using a fungal in vivo model, we show that all tested BASS-motifs form prions and that the NLR-side motifs seed prion-formation of the corresponding BELL-side motif. We find that BASS3 motifs show partial prion cross-seeding with mammalian RHIM and fungal PP-motifs and that proline mutations on key positions of the BASS3 core motif, conserved in RHIM and PP-motifs, abolish prion formation. This work expands the paradigm of prion amyloid signaling to multicellular prokaryotes and suggests a long-term evolutionary conservation of these motifs from bacteria, to fungi and animals.
Additional Links: PMID-33058872
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PubMed:
Citation:
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@article {pmid33058872,
year = {2020},
author = {Dyrka, W and Coustou, V and Daskalov, A and Lends, A and Bardin, T and Berbon, M and Kauffmann, B and Blancard, C and Salin, B and Loquet, A and Saupe, SJ},
title = {Identification of NLR-associated Amyloid Signaling Motifs in Bacterial Genomes.},
journal = {Journal of molecular biology},
volume = {432},
number = {23},
pages = {6005-6027},
doi = {10.1016/j.jmb.2020.10.004},
pmid = {33058872},
issn = {1089-8638},
mesh = {Amino Acid Motifs/genetics ; Amino Acid Sequence/genetics ; Amyloid/*genetics ; Amyloidogenic Proteins/genetics ; Animals ; Cyanobacteria/genetics ; Drosophila/genetics ; *Evolution, Molecular ; Fungi/genetics ; Genome, Bacterial/genetics ; Immunity, Innate/*genetics ; NLR Proteins/*genetics ; Prions/genetics ; Signal Transduction/genetics ; },
abstract = {In filamentous fungi, amyloid signaling sequences allow Nod-like receptors (NLRs) to activate downstream cell-death inducing proteins with HeLo and HeLo-like (HELL) domains and amyloid RHIM and RHIM-related motifs control immune defense pathways in mammals and flies. Herein, we show bioinformatically that analogous amyloid signaling motifs exist in bacteria. These short motifs are found at the N terminus of NLRs and at the C terminus of proteins with a domain we term BELL. The corresponding NLR and BELL proteins are encoded by adjacent genes. We identify 10 families of such bacterial amyloid signaling sequences (BASS), one of which (BASS3) is homologous to RHIM and a fungal amyloid motif termed PP. BASS motifs occur nearly exclusively in bacteria forming multicellular structures (mainly in Actinobacteria and Cyanobacteria). We analyze experimentally a subset of seven of these motifs (from the most common BASS1 family and the RHIM-related BASS3 family) and find that these sequences form fibrils in vitro. Using a fungal in vivo model, we show that all tested BASS-motifs form prions and that the NLR-side motifs seed prion-formation of the corresponding BELL-side motif. We find that BASS3 motifs show partial prion cross-seeding with mammalian RHIM and fungal PP-motifs and that proline mutations on key positions of the BASS3 core motif, conserved in RHIM and PP-motifs, abolish prion formation. This work expands the paradigm of prion amyloid signaling to multicellular prokaryotes and suggests a long-term evolutionary conservation of these motifs from bacteria, to fungi and animals.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Amino Acid Motifs/genetics
Amino Acid Sequence/genetics
Amyloid/*genetics
Amyloidogenic Proteins/genetics
Animals
Cyanobacteria/genetics
Drosophila/genetics
*Evolution, Molecular
Fungi/genetics
Genome, Bacterial/genetics
Immunity, Innate/*genetics
NLR Proteins/*genetics
Prions/genetics
Signal Transduction/genetics
RevDate: 2021-03-03
Predominantly inverse modulation of gene expression in genomically unbalanced disomic haploid maize.
The Plant cell pii:6126470 [Epub ahead of print].
The phenotypic consequences of the addition or subtraction of part of a chromosome is more severe than changing the dosage of the whole genome. By crossing diploid trisomies to a haploid inducer, we identified 17 distal segmental haploid disomies that cover ∼80% of the maize genome. Disomic haploids provide a level of genomic imbalance that is not ordinarily achievable in multicellular eukaryotes, allowing the impact to be stronger and more easily studied. Transcriptome size estimates revealed that a few disomies inversely modulate most of the transcriptome. Based on RNA sequencing, the expression levels of genes located on the varied chromosome arms (cis) in disomies ranged from being proportional to chromosomal dosage (dosage effect) to showing dosage compensation with no expression change with dosage. For genes not located on the varied chromosome arm (trans), an obvious trans-acting effect can be observed, with the majority showing a decreased modulation (inverse effect). The extent of dosage compensation of varied cis genes correlates with the extent of trans inverse effects across the 17 genomic regions studied. The results also have implications for the role of stoichiometry in gene expression, the control of quantitative traits, and the evolution of dosage-sensitive genes.
Additional Links: PMID-33656551
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PubMed:
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@article {pmid33656551,
year = {2021},
author = {Yang, H and Shi, X and Chen, C and Hou, J and Ji, T and Cheng, J and Birchler, JA},
title = {Predominantly inverse modulation of gene expression in genomically unbalanced disomic haploid maize.},
journal = {The Plant cell},
volume = {},
number = {},
pages = {},
doi = {10.1093/plcell/koab029},
pmid = {33656551},
issn = {1532-298X},
abstract = {The phenotypic consequences of the addition or subtraction of part of a chromosome is more severe than changing the dosage of the whole genome. By crossing diploid trisomies to a haploid inducer, we identified 17 distal segmental haploid disomies that cover ∼80% of the maize genome. Disomic haploids provide a level of genomic imbalance that is not ordinarily achievable in multicellular eukaryotes, allowing the impact to be stronger and more easily studied. Transcriptome size estimates revealed that a few disomies inversely modulate most of the transcriptome. Based on RNA sequencing, the expression levels of genes located on the varied chromosome arms (cis) in disomies ranged from being proportional to chromosomal dosage (dosage effect) to showing dosage compensation with no expression change with dosage. For genes not located on the varied chromosome arm (trans), an obvious trans-acting effect can be observed, with the majority showing a decreased modulation (inverse effect). The extent of dosage compensation of varied cis genes correlates with the extent of trans inverse effects across the 17 genomic regions studied. The results also have implications for the role of stoichiometry in gene expression, the control of quantitative traits, and the evolution of dosage-sensitive genes.},
}
RevDate: 2021-03-02
CmpDate: 2021-03-02
Phyllotaxis from a Single Apical Cell.
Trends in plant science, 26(2):124-131.
Phyllotaxis, the geometry of leaf arrangement around stems, determines plant architecture. Molecular interactions coordinating the formation of phyllotactic patterns have mainly been studied in multicellular shoot apical meristems of flowering plants. Phyllotaxis evolved independently in the major land plant lineages. In mosses, it arises from a single apical cell, raising the question of how asymmetric divisions of a single-celled meristem create phyllotactic patterns and whether associated genetic processes are shared across lineages. We present an overview of the mechanisms governing shoot apical cell specification and activity in the model moss, Physcomitrium patens, and argue that similar molecular regulatory modules have been deployed repeatedly across evolution to operate at different scales and drive apical function in convergent shoot forms.
Additional Links: PMID-33097400
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@article {pmid33097400,
year = {2021},
author = {Véron, E and Vernoux, T and Coudert, Y},
title = {Phyllotaxis from a Single Apical Cell.},
journal = {Trends in plant science},
volume = {26},
number = {2},
pages = {124-131},
doi = {10.1016/j.tplants.2020.09.014},
pmid = {33097400},
issn = {1878-4372},
mesh = {*Bryopsida ; *Meristem/genetics ; Plant Leaves ; Plant Shoots ; },
abstract = {Phyllotaxis, the geometry of leaf arrangement around stems, determines plant architecture. Molecular interactions coordinating the formation of phyllotactic patterns have mainly been studied in multicellular shoot apical meristems of flowering plants. Phyllotaxis evolved independently in the major land plant lineages. In mosses, it arises from a single apical cell, raising the question of how asymmetric divisions of a single-celled meristem create phyllotactic patterns and whether associated genetic processes are shared across lineages. We present an overview of the mechanisms governing shoot apical cell specification and activity in the model moss, Physcomitrium patens, and argue that similar molecular regulatory modules have been deployed repeatedly across evolution to operate at different scales and drive apical function in convergent shoot forms.},
}
MeSH Terms:
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*Bryopsida
*Meristem/genetics
Plant Leaves
Plant Shoots
RevDate: 2021-03-02
CmpDate: 2021-03-02
Bacterial and Protozoan Lipoxygenases Could be Involved in Cell-to-Cell Signaling and Immune Response Suppression.
Biochemistry. Biokhimiia, 85(9):1048-1071.
Lipoxygenases are found in animals, plants, and fungi, where they are involved in a wide range of cell-to-cell signaling processes. The presence of lipoxygenases in a number of bacteria and protozoa has been also established, but their biological significance remains poorly understood. Several hypothetical functions of lipoxygenases in bacteria and protozoa have been suggested without experimental validation. The objective of our study was evaluating the functions of bacterial and protozoan lipoxygenases by evolutionary and taxonomic analysis using bioinformatics tools. Lipoxygenase sequences were identified and examined using BLAST, followed by analysis of constructed phylogenetic trees and networks. Our results support the theory on the involvement of lipoxygenases in the formation of multicellular structures by microorganisms and their possible evolutionary significance in the emergence of multicellularity. Furthermore, we observed association of lipoxygenases with the suppression of host immune response by parasitic and symbiotic bacteria including dangerous opportunistic pathogens.
Additional Links: PMID-33050851
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PubMed:
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@article {pmid33050851,
year = {2020},
author = {Kurakin, GF and Samoukina, AM and Potapova, NA},
title = {Bacterial and Protozoan Lipoxygenases Could be Involved in Cell-to-Cell Signaling and Immune Response Suppression.},
journal = {Biochemistry. Biokhimiia},
volume = {85},
number = {9},
pages = {1048-1071},
doi = {10.1134/S0006297920090059},
pmid = {33050851},
issn = {1608-3040},
mesh = {Animals ; Bacteria/*enzymology ; *Biological Evolution ; *Cell Communication ; Humans ; Immunity/*immunology ; Lipoxygenases/*metabolism ; Protozoan Proteins/*metabolism ; },
abstract = {Lipoxygenases are found in animals, plants, and fungi, where they are involved in a wide range of cell-to-cell signaling processes. The presence of lipoxygenases in a number of bacteria and protozoa has been also established, but their biological significance remains poorly understood. Several hypothetical functions of lipoxygenases in bacteria and protozoa have been suggested without experimental validation. The objective of our study was evaluating the functions of bacterial and protozoan lipoxygenases by evolutionary and taxonomic analysis using bioinformatics tools. Lipoxygenase sequences were identified and examined using BLAST, followed by analysis of constructed phylogenetic trees and networks. Our results support the theory on the involvement of lipoxygenases in the formation of multicellular structures by microorganisms and their possible evolutionary significance in the emergence of multicellularity. Furthermore, we observed association of lipoxygenases with the suppression of host immune response by parasitic and symbiotic bacteria including dangerous opportunistic pathogens.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
Bacteria/*enzymology
*Biological Evolution
*Cell Communication
Humans
Immunity/*immunology
Lipoxygenases/*metabolism
Protozoan Proteins/*metabolism
RevDate: 2021-02-26
Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition).
Autophagy [Epub ahead of print].
In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field.
Additional Links: PMID-33634751
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PubMed:
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@article {pmid33634751,
year = {2021},
author = {Klionsky, DJ and Abdel-Aziz, AK and Abdelfatah, S and Abdellatif, M and Abdoli, A and Abel, S and Abeliovich, H and Abildgaard, MH and Abudu, YP and Acevedo-Arozena, A and Adamopoulos, IE and Adeli, K and Adolph, TE and Adornetto, A and Aflaki, E and Agam, G and Agarwal, A and Aggarwal, BB and Agnello, M and Agostinis, P and Agrewala, JN and Agrotis, A and Aguilar, PV and Ahmad, ST and Ahmed, ZM and Ahumada-Castro, U and Aits, S and Aizawa, S and Akkoc, Y and Akoumianaki, T and Akpinar, HA and Al-Abd, AM and Al-Akra, L and Al-Gharaibeh, A and Alaoui-Jamali, MA and Alberti, S and Alcocer-Gómez, E and Alessandri, C and Ali, M and Alim Al-Bari, MA and Aliwaini, S and Alizadeh, J and Almacellas, E and Almasan, A and Alonso, A and Alonso, GD and Altan-Bonnet, N and Altieri, DC and Álvarez, ÉMC and Alves, S and Alves da Costa, C and Alzaharna, MM and Amadio, M and Amantini, C and Amaral, C and Ambrosio, S and Amer, AO and Ammanathan, V and An, Z and Andersen, SU and Andrabi, SA and Andrade-Silva, M and Andres, AM and Angelini, S and Ann, D and Anozie, UC and Ansari, MY and Antas, P and Antebi, A and Antón, Z and Anwar, T and Apetoh, L and Apostolova, N and Araki, T and Araki, Y and Arasaki, K and Araújo, WL and Araya, J and Arden, C and Arévalo, MA and Arguelles, S and Arias, E and Arikkath, J and Arimoto, H and Ariosa, AR and Armstrong-James, D and Arnauné-Pelloquin, L and Aroca, A and Arroyo, DS and Arsov, I and Artero, R and Asaro, DML and Aschner, M and Ashrafizadeh, M and Ashur-Fabian, O and Atanasov, AG and Au, AK and Auberger, P and Auner, HW and Aurelian, L and Autelli, R and Avagliano, L and Ávalos, Y and Aveic, S and Aveleira, CA and Avin-Wittenberg, T and Aydin, Y and Ayton, S and Ayyadevara, S and Azzopardi, M and Baba, M and Backer, JM and Backues, SK and Bae, DH and Bae, ON and Bae, SH and Baehrecke, EH and Baek, A and Baek, SH and Baek, SH and Bagetta, G and Bagniewska-Zadworna, A and Bai, H and Bai, J and Bai, X and Bai, Y and Bairagi, N and Baksi, S and Balbi, T and Baldari, CT and Balduini, W and Ballabio, A and Ballester, M and Balazadeh, S and Balzan, R and Bandopadhyay, R and Banerjee, S and Banerjee, S and Bánréti, Á and Bao, Y and Baptista, MS and Baracca, A and Barbati, C and Bargiela, A and Barilà, D and Barlow, PG and Barmada, SJ and Barreiro, E and Barreto, GE and Bartek, J and Bartel, B and Bartolome, A and Barve, GR and Basagoudanavar, SH and Bassham, DC and Bast, RC and Basu, A and Batoko, H and Batten, I and Baulieu, EE and Baumgarner, BL and Bayry, J and Beale, R and Beau, I and Beaumatin, F and Bechara, LRG and Beck, GR and Beers, MF and Begun, J and Behrends, C and Behrens, GMN and Bei, R and Bejarano, E and Bel, S and Behl, C and Belaid, A and Belgareh-Touzé, N and Bellarosa, C and Belleudi, F and Belló Pérez, M and Bello-Morales, R and Beltran, JSO and Beltran, S and Benbrook, DM and Bendorius, M and Benitez, BA and Benito-Cuesta, I and Bensalem, J and Berchtold, MW and Berezowska, S and Bergamaschi, D and Bergami, M and Bergmann, A and Berliocchi, L and Berlioz-Torrent, C and Bernard, A and Berthoux, L and Besirli, CG and Besteiro, S and Betin, VM and Beyaert, R and Bezbradica, JS and Bhaskar, K and Bhatia-Kissova, I and Bhattacharya, R and Bhattacharya, S and Bhattacharyya, S and Bhuiyan, MS and Bhutia, SK and Bi, L and Bi, X and Biden, TJ and Bijian, K and Billes, VA and Binart, N and Bincoletto, C and Birgisdottir, AB and Bjorkoy, G and Blanco, G and Blas-Garcia, A and Blasiak, J and Blomgran, R and Blomgren, K and Blum, JS and Boada-Romero, E and Boban, M and Boesze-Battaglia, K and Boeuf, P and Boland, B and Bomont, P and Bonaldo, P and Bonam, SR and Bonfili, L and Bonifacino, JS and Boone, BA and Bootman, MD and Bordi, M and Borner, C and Bornhauser, BC and Borthakur, G and Bosch, J and Bose, S and Botana, LM and Botas, J and Boulanger, CM and Boulton, ME and Bourdenx, M and Bourgeois, B and Bourke, NM and Bousquet, G and Boya, P and Bozhkov, PV and Bozi, LHM and Bozkurt, TO and Brackney, DE and Brandts, CH and Braun, RJ and Braus, GH and Bravo-Sagua, R and Bravo-San Pedro, JM and Brest, P and Bringer, MA and Briones-Herrera, A and Broaddus, VC and Brodersen, P and Brodsky, JL and Brody, SL and Bronson, PG and Bronstein, JM and Brown, CN and Brown, RE and Brum, PC and Brumell, JH and Brunetti-Pierri, N and Bruno, D and Bryson-Richardson, RJ and Bucci, C and Buchrieser, C and Bueno, M and Buitrago-Molina, LE and Buraschi, S and Buch, S and Buchan, JR and Buckingham, EM and Budak, H and Budini, M and Bultynck, G and Burada, F and Burgoyne, JR and Burón, MI and Bustos, V and Büttner, S and Butturini, E and Byrd, A and Cabas, I and Cabrera-Benitez, S and Cadwell, K and Cai, J and Cai, L and Cai, Q and Cairó, M and Calbet, JA and Caldwell, GA and Caldwell, KA and Call, JA and Calvani, R and Calvo, AC and Calvo-Rubio Barrera, M and Camara, NO and Camonis, JH and Camougrand, N and Campanella, M and Campbell, EM and Campbell-Valois, FX and Campello, S and Campesi, I and Campos, JC and Camuzard, O and Cancino, J and Candido de Almeida, D and Canesi, L and Caniggia, I and Canonico, B and Cantí, C and Cao, B and Caraglia, M and Caramés, B and Carchman, EH and Cardenal-Muñoz, E and Cardenas, C and Cardenas, L and Cardoso, SM and Carew, JS and Carle, GF and Carleton, G and Carloni, S and Carmona-Gutierrez, D and Carneiro, LA and Carnevali, O and Carosi, JM and Carra, S and Carrier, A and Carrier, L and Carroll, B and Carter, AB and Carvalho, AN and Casanova, M and Casas, C and Casas, J and Cassioli, C and Castillo, EF and Castillo, K and Castillo-Lluva, S and Castoldi, F and Castori, M and Castro, AF and Castro-Caldas, M and Castro-Hernandez, J and Castro-Obregon, S and Catz, SD and Cavadas, C and Cavaliere, F and Cavallini, G and Cavinato, M and Cayuela, ML and Cebollada Rica, P and Cecarini, V and Cecconi, F and Cechowska-Pasko, M and Cenci, S and Ceperuelo-Mallafré, V and Cerqueira, JJ and Cerutti, JM and Cervia, D and Cetintas, VB and Cetrullo, S and Chae, HJ and Chagin, AS and Chai, CY and Chakrabarti, G and Chakrabarti, O and Chakraborty, T and Chakraborty, T and Chami, M and Chamilos, G and Chan, DW and Chan, EYW and Chan, ED and Chan, HYE and Chan, HH and Chan, H and Chan, MTV and Chan, YS and Chandra, PK and Chang, CP and Chang, C and Chang, HC and Chang, K and Chao, J and Chapman, T and Charlet-Berguerand, N and Chatterjee, S and Chaube, SK and Chaudhary, A and Chauhan, S and Chaum, E and Checler, F and Cheetham, ME and Chen, CS and Chen, GC and Chen, JF and Chen, LL and Chen, L and Chen, L and Chen, M and Chen, MK and Chen, N and Chen, Q and Chen, RH and Chen, S and Chen, W and Chen, W and Chen, XM and Chen, XW and Chen, X and Chen, Y and Chen, YG and Chen, Y and Chen, Y and Chen, YJ and Chen, YQ and Chen, ZS and Chen, Z and Chen, ZH and Chen, ZJ and Chen, Z and Cheng, H and Cheng, J and Cheng, SY and Cheng, W and Cheng, X and Cheng, XT and Cheng, Y and Cheng, Z and Chen, Z and Cheong, H and Cheong, JK and Chernyak, BV and Cherry, S and Cheung, CFR and Cheung, CHA and Cheung, KH and Chevet, E and Chi, RJ and Chiang, AKS and Chiaradonna, F and Chiarelli, R and Chiariello, M and Chica, N and Chiocca, S and Chiong, M and Chiou, SH and Chiramel, AI and Chiurchiù, V and Cho, DH and Choe, SK and Choi, AMK and Choi, ME and Choudhury, KR and Chow, NS and Chu, CT and Chua, JP and Chua, JJE and Chung, H and Chung, KP and Chung, S and Chung, SH and Chung, YL and Cianfanelli, V and Ciechomska, IA and Cifuentes, M and Cinque, L and Cirak, S and Cirone, M and Clague, MJ and Clarke, R and Clementi, E and Coccia, EM and Codogno, P and Cohen, E and Cohen, MM and Colasanti, T and Colasuonno, F and Colbert, RA and Colell, A and Čolić, M and Coll, NS and Collins, MO and Colombo, MI and Colón-Ramos, DA and Combaret, L and Comincini, S and Cominetti, MR and Consiglio, A and Conte, A and Conti, F and Contu, VR and Cookson, MR and Coombs, KM and Coppens, I and Corasaniti, MT and Corkery, DP and Cordes, N and Cortese, K and Costa, MDC and Costantino, S and Costelli, P and Coto-Montes, A and Crack, PJ and Crespo, JL and Criollo, A and Crippa, V and Cristofani, R and Csizmadia, T and Cuadrado, A and Cui, B and Cui, J and Cui, Y and Cui, Y and Culetto, E and Cumino, AC and Cybulsky, AV and Czaja, MJ and Czuczwar, SJ and D'Adamo, S and D'Amelio, M and D'Arcangelo, D and D'Lugos, AC and D'Orazi, G and da Silva, JA and Dafsari, HS and Dagda, RK and Dagdas, Y and Daglia, M and Dai, X and Dai, Y and Dai, Y and Dal Col, J and Dalhaimer, P and Dalla Valle, L and Dallenga, T and Dalmasso, G and Damme, M and Dando, I and Dantuma, NP and Darling, AL and Das, H and Dasarathy, S and Dasari, SK and Dash, S and Daumke, O and Dauphinee, AN and Davies, JS and Dávila, VA and Davis, RJ and Davis, T and Dayalan Naidu, S and De Amicis, F and De Bosscher, K and De Felice, F and De Franceschi, L and De Leonibus, C and de Mattos Barbosa, MG and De Meyer, GRY and De Milito, A and De Nunzio, C and De Palma, C and De Santi, M and De Virgilio, C and De Zio, D and Debnath, J and DeBosch, BJ and Decuypere, JP and Deehan, MA and Deflorian, G and DeGregori, J and Dehay, B and Del Rio, G and Delaney, JR and Delbridge, LMD and Delorme-Axford, E and Delpino, MV and Demarchi, F and Dembitz, V and Demers, ND and Deng, H and Deng, Z and Dengjel, J and Dent, P and Denton, D and DePamphilis, ML and Der, CJ and Deretic, V and Descoteaux, A and Devis, L and Devkota, S and Devuyst, O and Dewson, G and Dharmasivam, M and Dhiman, R and di Bernardo, D and Di Cristina, M and Di Domenico, F and Di Fazio, P and Di Fonzo, A and Di Guardo, G and Di Guglielmo, GM and Di Leo, L and Di Malta, C and Di Nardo, A and Di Rienzo, M and Di Sano, F and Diallinas, G and Diao, J and Diaz-Araya, G and Díaz-Laviada, I and Dickinson, JM and Diederich, M and Dieudé, M and Dikic, I and Ding, S and Ding, WX and Dini, L and Dinić, J and Dinic, M and Dinkova-Kostova, AT and Dionne, MS and Distler, JHW and Diwan, A and Dixon, IMC and Djavaheri-Mergny, M and Dobrinski, I and Dobrovinskaya, O and Dobrowolski, R and Dobson, RCJ and Đokić, J and Dokmeci Emre, S and Donadelli, M and Dong, B and Dong, X and Dong, Z and Dorn Ii, GW and Dotsch, V and Dou, H and Dou, J and Dowaidar, M and Dridi, S and Drucker, L and Du, A and Du, C and Du, G and Du, HN and Du, LL and du Toit, A and Duan, SB and Duan, X and Duarte, SP and Dubrovska, A and Dunlop, EA and Dupont, N and Durán, RV and Dwarakanath, BS and Dyshlovoy, SA and Ebrahimi-Fakhari, D and Eckhart, L and Edelstein, CL and Efferth, T and Eftekharpour, E and Eichinger, L and Eid, N and Eisenberg, T and Eissa, NT and Eissa, S and Ejarque, M and El Andaloussi, A and El-Hage, N and El-Naggar, S and Eleuteri, AM and El-Shafey, ES and Elgendy, M and Eliopoulos, AG and Elizalde, MM and Elks, PM and Elsasser, HP and Elsherbiny, ES and Emerling, BM and Emre, NCT and Eng, CH and Engedal, N and Engelbrecht, AM and Engelsen, AST and Enserink, JM and Escalante, R and Esclatine, A and Escobar-Henriques, M and Eskelinen, EL and Espert, L and Eusebio, MO and Fabrias, G and Fabrizi, C and Facchiano, A and Facchiano, F and Fadeel, B and Fader, C and Faesen, AC and Fairlie, WD and Falcó, A and Falkenburger, BH and Fan, D and Fan, J and Fan, Y and Fang, EF and Fang, Y and Fang, Y and Fanto, M and Farfel-Becker, T and Faure, M and Fazeli, G and Fedele, AO and Feldman, AM and Feng, D and Feng, J and Feng, L and Feng, Y and Feng, Y and Feng, W and Fenz Araujo, T and Ferguson, TA and Fernández, ÁF and Fernandez-Checa, JC and Fernández-Veledo, S and Fernie, AR and Ferrante, AW and Ferraresi, A and Ferrari, MF and Ferreira, JCB and Ferro-Novick, S and Figueras, A and Filadi, R and Filigheddu, N and Filippi-Chiela, E and Filomeni, G and Fimia, GM and Fineschi, V and Finetti, F and Finkbeiner, S and Fisher, EA and Fisher, PB and Flamigni, F and Fliesler, SJ and Flo, TH and Florance, I and Florey, O and Florio, T and Fodor, E and Follo, C and Fon, EA and Forlino, A and Fornai, F and Fortini, P and Fracassi, A and Fraldi, A and Franco, B and Franco, R and Franconi, F and Frankel, LB and Friedman, SL and Fröhlich, LF and Frühbeck, G and Fuentes, JM and Fujiki, Y and Fujita, N and Fujiwara, Y and Fukuda, M and Fulda, S and Furic, L and Furuya, N and Fusco, C and Gack, MU and Gaffke, L and Galadari, S and Galasso, A and Galindo, MF and Gallolu Kankanamalage, S and Galluzzi, L and Galy, V and Gammoh, N and Gan, B and Ganley, IG and Gao, F and Gao, H and Gao, M and Gao, P and Gao, SJ and Gao, W and Gao, X and Garcera, A and Garcia, MN and Garcia, VE and García-Del Portillo, F and Garcia-Escudero, V and Garcia-Garcia, A and Garcia-Macia, M and García-Moreno, D and Garcia-Ruiz, C and García-Sanz, P and Garg, AD and Gargini, R and Garofalo, T and Garry, RF and Gassen, NC and Gatica, D and Ge, L and Ge, W and Geiss-Friedlander, R and Gelfi, C and Genschik, P and Gentle, IE and Gerbino, V and Gerhardt, C and Germain, K and Germain, M and Gewirtz, DA and Ghasemipour Afshar, E and Ghavami, S and Ghigo, A and Ghosh, M and Giamas, G and Giampietri, C and Giatromanolaki, A and Gibson, GE and Gibson, SB and Ginet, V and Giniger, E and Giorgi, C and Girao, H and Girardin, SE and Giridharan, M and Giuliano, S and Giulivi, C and Giuriato, S and Giustiniani, J and Gluschko, A and Goder, V and Goginashvili, A and Golab, J and Goldstone, DC and Golebiewska, A and Gomes, LR and Gomez, R and Gómez-Sánchez, R and Gomez-Puerto, MC and Gomez-Sintes, R and Gong, Q and Goni, FM and González-Gallego, J and Gonzalez-Hernandez, T and Gonzalez-Polo, RA and Gonzalez-Reyes, JA and González-Rodríguez, P and Goping, IS and Gorbatyuk, MS and Gorbunov, NV and Görgülü, K and Gorojod, RM and Gorski, SM and Goruppi, S and Gotor, C and Gottlieb, RA and Gozes, I and Gozuacik, D and Graef, M and Gräler, MH and Granatiero, V and Grasso, D and Gray, JP and Green, DR and Greenhough, A and Gregory, SL and Griffin, EF and Grinstaff, MW and Gros, F and Grose, C and Gross, AS and Gruber, F and Grumati, P and Grune, T and Gu, X and Guan, JL and Guardia, CM and Guda, K and Guerra, F and Guerri, C and Guha, P and Guillén, C and Gujar, S and Gukovskaya, A and Gukovsky, I and Gunst, J and Günther, A and Guntur, AR and Guo, C and Guo, C and Guo, H and Guo, LW and Guo, M and Gupta, P and Gupta, SK and Gupta, S and Gupta, VB and Gupta, V and Gustafsson, AB and Gutterman, DD and H B, R and Haapasalo, A and Haber, JE and Hać, A and Hadano, S and Hafrén, AJ and Haidar, M and Hall, BS and Halldén, G and Hamacher-Brady, A and Hamann, A and Hamasaki, M and Han, W and Hansen, M and Hanson, PI and Hao, Z and Harada, M and Harhaji-Trajkovic, L and Hariharan, N and Haroon, N and Harris, J and Hasegawa, T and Hasima Nagoor, N and Haspel, JA and Haucke, V and Hawkins, WD and Hay, BA and Haynes, CM and Hayrabedyan, SB and Hays, TS and He, C and He, Q and He, RR and He, YW and He, YY and Heakal, Y and Heberle, AM and Hejtmancik, JF and Helgason, GV and Henkel, V and Herb, M and Hergovich, A and Herman-Antosiewicz, A and Hernández, A and Hernandez, C and Hernandez-Diaz, S and Hernandez-Gea, V and Herpin, A and Herreros, J and Hervás, JH and Hesselson, D and Hetz, C and Heussler, VT and Higuchi, Y and Hilfiker, S and Hill, JA and Hlavacek, WS and Ho, EA and Ho, IHT and Ho, PW and Ho, SL and Ho, WY and Hobbs, GA and Hochstrasser, M and Hoet, PHM and Hofius, D and Hofman, P and Höhn, A and Holmberg, CI and Hombrebueno, JR and Yi-Ren Hong, CH and Hooper, LV and Hoppe, T and Horos, R and Hoshida, Y and Hsin, IL and Hsu, HY and Hu, B and Hu, D and Hu, LF and Hu, MC and Hu, R and Hu, W and Hu, YC and Hu, ZW and Hua, F and Hua, J and Hua, Y and Huan, C and Huang, C and Huang, C and Huang, C and Huang, C and Huang, H and Huang, K and Huang, MLH and Huang, R and Huang, S and Huang, T and Huang, X and Huang, YJ and Huber, TB and Hubert, V and Hubner, CA and Hughes, SM and Hughes, WE and Humbert, M and Hummer, G and Hurley, JH and Hussain, S and Hussain, S and Hussey, PJ and Hutabarat, M and Hwang, HY and Hwang, S and Ieni, A and Ikeda, F and Imagawa, Y and Imai, Y and Imbriano, C and Imoto, M and Inman, DM and Inoki, K and Iovanna, J and Iozzo, RV and Ippolito, G and Irazoqui, JE and Iribarren, P and Ishaq, M and Ishikawa, M and Ishimwe, N and Isidoro, C and Ismail, N and Issazadeh-Navikas, S and Itakura, E and Ito, D and Ivankovic, D and Ivanova, S and Iyer, AKV and Izquierdo, JM and Izumi, M and Jäättelä, M and Jabir, MS and Jackson, WT and Jacobo-Herrera, N and Jacomin, AC and Jacquin, E and Jadiya, P and Jaeschke, H and Jagannath, C and Jakobi, AJ and Jakobsson, J and Janji, B and Jansen-Dürr, P and Jansson, PJ and Jantsch, J and Januszewski, S and Jassey, A and Jean, S and Jeltsch-David, H and Jendelova, P and Jenny, A and Jensen, TE and Jessen, N and Jewell, JL and Ji, J and Jia, L and Jia, R and Jiang, L and Jiang, Q and Jiang, R and Jiang, T and Jiang, X and Jiang, Y and Jimenez-Sanchez, M and Jin, EJ and Jin, F and Jin, H and Jin, L and Jin, L and Jin, M and Jin, S and Jo, EK and Joffre, C and Johansen, T and Johnson, GVW and Johnston, SA and Jokitalo, E and Jolly, MK and Joosten, LAB and Jordan, J and Joseph, B and Ju, D and Ju, JS and Ju, J and Juárez, E and Judith, D and Juhász, G and Jun, Y and Jung, CH and Jung, SC and Jung, YK and Jungbluth, H and Jungverdorben, J and Just, S and Kaarniranta, K and Kaasik, A and Kabuta, T and Kaganovich, D and Kahana, A and Kain, R and Kajimura, S and Kalamvoki, M and Kalia, M and Kalinowski, DS and Kaludercic, N and Kalvari, I and Kaminska, J and Kaminskyy, VO and Kanamori, H and Kanasaki, K and Kang, C and Kang, R and Kang, SS and Kaniyappan, S and Kanki, T and Kanneganti, TD and Kanthasamy, AG and Kanthasamy, A and Kantorow, M and Kapuy, O and Karamouzis, MV and Karim, MR and Karmakar, P and Katare, RG and Kato, M and Kaufmann, SHE and Kauppinen, A and Kaushal, GP and Kaushik, S and Kawasaki, K and Kazan, K and Ke, PY and Keating, DJ and Keber, U and Kehrl, JH and Keller, KE and Keller, CW and Kemper, JK and Kenific, CM and Kepp, O and Kermorgant, S and Kern, A and Ketteler, R and Keulers, TG and Khalfin, B and Khalil, H and Khambu, B and Khan, SY and Khandelwal, VKM and Khandia, R and Kho, W and Khobrekar, NV and Khuansuwan, S and Khundadze, M and Killackey, SA and Kim, D and Kim, DR and Kim, DH and Kim, DE and Kim, EY and Kim, EK and Kim, HR and Kim, HS and Hyung-Ryong Kim, and Kim, JH and Kim, JK and Kim, JH and Kim, J and Kim, JH and Kim, KI and Kim, PK and Kim, SJ and Kimball, SR and Kimchi, A and Kimmelman, AC and Kimura, T and King, MA and Kinghorn, KJ and Kinsey, CG and Kirkin, V and Kirshenbaum, LA and Kiselev, SL and Kishi, S and Kitamoto, K and Kitaoka, Y and Kitazato, K and Kitsis, RN and Kittler, JT and Kjaerulff, O and Klein, PS and Klopstock, T and Klucken, J and Knævelsrud, H and Knorr, RL and Ko, BCB and Ko, F and Ko, JL and Kobayashi, H and Kobayashi, S and Koch, I and Koch, JC and Koenig, U and Kögel, D and Koh, YH and Koike, M and Kohlwein, SD and Kocaturk, NM and Komatsu, M and König, J and Kono, T and Kopp, BT and Korcsmaros, T and Korkmaz, G and Korolchuk, VI and Korsnes, MS and Koskela, A and Kota, J and Kotake, Y and Kotler, ML and Kou, Y and Koukourakis, MI and Koustas, E and Kovacs, AL and Kovács, T and Koya, D and Kozako, T and Kraft, C and Krainc, D and Krämer, H and Krasnodembskaya, AD and Kretz-Remy, C and Kroemer, G and Ktistakis, NT and Kuchitsu, K and Kuenen, S and Kuerschner, L and Kukar, T and Kumar, A and Kumar, A and Kumar, D and Kumar, D and Kumar, S and Kume, S and Kumsta, C and Kundu, CN and Kundu, M and Kunnumakkara, AB and Kurgan, L and Kutateladze, TG and Kutlu, O and Kwak, S and Kwon, HJ and Kwon, TK and Kwon, YT and Kyrmizi, I and La Spada, A and Labonté, P and Ladoire, S and Laface, I and Lafont, F and Lagace, DC and Lahiri, V and Lai, Z and Laird, AS and Lakkaraju, A and Lamark, T and Lan, SH and Landajuela, A and Lane, DJR and Lane, JD and Lang, CH and Lange, C and Langel, Ü and Langer, R and Lapaquette, P and Laporte, J and LaRusso, NF and Lastres-Becker, I and Lau, WCY and Laurie, GW and Lavandero, S and Law, BYK and Law, HK and Layfield, R and Le, W and Le Stunff, H and Leary, AY and Lebrun, JJ and Leck, LYW and Leduc-Gaudet, JP and Lee, C and Lee, CP and Lee, DH and Lee, EB and Lee, EF and Lee, GM and Lee, HJ and Lee, HK and Lee, JM and Lee, JS and Lee, JA and Lee, JY and Lee, JH and Lee, M and Lee, MG and Lee, MJ and Lee, MS and Lee, SY and Lee, SJ and Lee, SY and Lee, SB and Lee, WH and Lee, YR and Lee, YH and Lee, Y and Lefebvre, C and Legouis, R and Lei, YL and Lei, Y and Leikin, S and Leitinger, G and Lemus, L and Leng, S and Lenoir, O and Lenz, G and Lenz, HJ and Lenzi, P and León, Y and Leopoldino, AM and Leschczyk, C and Leskelä, S and Letellier, E and Leung, CT and Leung, PS and Leventhal, JS and Levine, B and Lewis, PA and Ley, K and Li, B and Li, DQ and Li, J and Li, J and Li, J and Li, K and Li, L and Li, M and Li, M and Li, M and Li, M and Li, M and Li, PL and Li, MQ and Li, Q and Li, S and Li, T and Li, W and Li, W and Li, X and Li, YP and Li, Y and Li, Z and Li, Z and Li, Z and Lian, J and Liang, C and Liang, Q and Liang, W and Liang, Y and Liang, Y and Liao, G and Liao, L and Liao, M and Liao, YF and Librizzi, M and Lie, PPY and Lilly, MA and Lim, HJ and Lima, TRR and Limana, F and Lin, C and Lin, CW and Lin, DS and Lin, FC and Lin, JD and Lin, KM and Lin, KH and Lin, LT and Lin, PH and Lin, Q and Lin, S and Lin, SJ and Lin, W and Lin, X and Lin, YX and Lin, YS and Linden, R and Lindner, P and Ling, SC and Lingor, P and Linnemann, AK and Liou, YC and Lipinski, MM and Lipovšek, S and Lira, VA and Lisiak, N and Liton, PB and Liu, C and Liu, CH and Liu, CF and Liu, CH and Liu, F and Liu, H and Liu, HS and Liu, HF and Liu, H and Liu, J and Liu, J and Liu, J and Liu, L and Liu, L and Liu, M and Liu, Q and Liu, W and Liu, W and Liu, XH and Liu, X and Liu, X and Liu, X and Liu, X and Liu, Y and Liu, Y and Liu, Y and Liu, Y and Liu, Y and 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MacKeigan, JP and Macleod, KF and Maday, S and Madeo, F and Madesh, M and Madl, T and Madrigal-Matute, J and Maeda, A and Maejima, Y and Magarinos, M and Mahavadi, P and Maiani, E and Maiese, K and Maiti, P and Maiuri, MC and Majello, B and Major, MB and Makareeva, E and Malik, F and Mallilankaraman, K and Malorni, W and Maloyan, A and Mammadova, N and Man, GCW and Manai, F and Mancias, JD and Mandelkow, EM and Mandell, MA and Manfredi, AA and Manjili, MH and Manjithaya, R and Manque, P and Manshian, BB and Manzano, R and Manzoni, C and Mao, K and Marchese, C and Marchetti, S and Marconi, AM and Marcucci, F and Mardente, S and Mareninova, OA and Margeta, M and Mari, M and Marinelli, S and Marinelli, O and Mariño, G and Mariotto, S and Marshall, RS and Marten, MR and Martens, S and Martin, APJ and Martin, KR and Martin, S and Martin, S and Martín-Segura, A and Martín-Acebes, MA and Martin-Burriel, I and Martin-Rincon, M and Martin-Sanz, P and Martina, JA and Martinet, W and Martinez, A 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G and Ray, SK and Razani, B and Rebecca, V and Reggiori, F and Régnier-Vigouroux, A and Reichert, AS and Reigada, D and Reiling, JH and Rein, T and Reipert, S and Rekha, RS and Ren, H and Ren, J and Ren, W and Renault, T and Renga, G and Reue, K and Rewitz, K and Ribeiro de Andrade Ramos, B and Riazuddin, SA and Ribeiro-Rodrigues, TM and Ricci, JE and Ricci, R and Riccio, V and Richardson, DR and Rikihisa, Y and Risbud, MV and Risueño, RM and Ritis, K and Rizza, S and Rizzuto, R and Roberts, HC and Roberts, LD and Robinson, KJ and Roccheri, MC and Rocchi, S and Rodney, GG and Rodrigues, T and Rodrigues Silva, VR and Rodriguez, A and Rodriguez-Barrueco, R and Rodriguez-Henche, N and Rodriguez-Rocha, H and Roelofs, J and Rogers, RS and Rogov, VV and Rojo, AI and Rolka, K and Romanello, V and Romani, L and Romano, A and Romano, PS and Romeo-Guitart, D and Romero, LC and Romero, M and Roney, JC and Rongo, C and Roperto, S and Rosenfeldt, MT and Rosenstiel, P and Rosenwald, AG and Roth, KA and Roth, L and Roth, S and Rouschop, KMA and Roussel, BD and Roux, S and Rovere-Querini, P and Roy, A and Rozieres, A and Ruano, D and Rubinsztein, DC and Rubtsova, MP and Ruckdeschel, K and Ruckenstuhl, C and Rudolf, E and Rudolf, R and Ruggieri, A and Ruparelia, AA and Rusmini, P and Russell, RR and Russo, GL and Russo, M and Russo, R and Ryabaya, OO and Ryan, KM and Ryu, KY and Sabater-Arcis, M and Sachdev, U and Sacher, M and Sachse, C and Sadhu, A and Sadoshima, J and Safren, N and Saftig, P and Sagona, AP and Sahay, G and Sahebkar, A and Sahin, M and Sahin, O and Sahni, S and Saito, N and Saito, S and Saito, T and Sakai, R and Sakai, Y and Sakamaki, JI and Saksela, K and Salazar, G and Salazar-Degracia, A and Salekdeh, GH and Saluja, AK and Sampaio-Marques, B and Sanchez, MC and Sanchez-Alcazar, JA and Sanchez-Vera, V and Sancho-Shimizu, V and Sanderson, JT and Sandri, M and Santaguida, S and Santambrogio, L and Santana, MM and Santoni, G and Sanz, A and Sanz, P and Saran, S and 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and Vaccari, T and Vaccaro, MI and Vahsen, BF and Vakifahmetoglu-Norberg, H and Valdor, R and Valente, MJ and Valko, A and Vallee, RB and Valverde, AM and Van den Berghe, G and van der Veen, S and Van Kaer, L and van Loosdregt, J and van Wijk, SJL and Vandenberghe, W and Vanhorebeek, I and Vannier-Santos, MA and Vannini, N and Vanrell, MC and Vantaggiato, C and Varano, G and Varela-Nieto, I and Varga, M and Vasconcelos, MH and Vats, S and Vavvas, DG and Vega-Naredo, I and Vega-Rubin-de-Celis, S and Velasco, G and Velázquez, AP and Vellai, T and Vellenga, E and Velotti, F and Verdier, M and Verginis, P and Vergne, I and Verkade, P and Verma, M and Verstreken, P and Vervliet, T and Vervoorts, J and Vessoni, AT and Victor, VM and Vidal, M and Vidoni, C and Vieira, OV and Vierstra, RD and Viganó, S and Vihinen, H and Vijayan, V and Vila, M and Vilar, M and Villalba, JM and Villalobo, A and Villarejo-Zori, B and Villarroya, F and Villarroya, J and Vincent, O and Vindis, C and Viret, C and Viscomi, MT and Visnjic, D and Vitale, I and Vocadlo, DJ and Voitsekhovskaja, OV and Volonté, C and Volta, M and Vomero, M and Von Haefen, C and Vooijs, MA and Voos, W and Vucicevic, L and Wade-Martins, R and Waguri, S and Waite, KA and Wakatsuki, S and Walker, DW and Walker, MJ and Walker, SA and Walter, J and Wandosell, FG and Wang, B and Wang, CY and Wang, C and Wang, C and Wang, C and Wang, CY and Wang, D and Wang, F and Wang, F and Wang, F and Wang, G and Wang, H and Wang, H and Wang, H and Wang, HG and Wang, J and Wang, J and Wang, J and Wang, J and Wang, K and Wang, L and Wang, L and Wang, MH and Wang, M and Wang, N and Wang, P and Wang, P and Wang, P and Wang, P and Wang, QJ and Wang, Q and Wang, QK and Wang, QA and Wang, WT and Wang, W and Wang, X and Wang, X and Wang, Y and Wang, Y and Wang, Y and Wang, YY and Wang, Y and Wang, Y and Wang, Y and Wang, Y and Wang, Z and Wang, Z and Wang, Z and Warnes, G and Warnsmann, V and Watada, H and Watanabe, E and Watchon, M and Wawrzyńska, A and Weaver, TE and Wegrzyn, G and Wehman, AM and Wei, H and Wei, L and Wei, T and Wei, Y and Weiergräber, OH and Weihl, CC and Weindl, G and Weiskirchen, R and Wells, A and Wen, RH and Wen, X and Werner, A and Weykopf, B and Wheatley, SP and Whitton, JL and Whitworth, AJ and Wiktorska, K and Wildenberg, ME and Wileman, T and Wilkinson, S and Willbold, D and Williams, B and Williams, RSB and Williams, RL and Williamson, PR and Wilson, RA and Winner, B and Winsor, NJ and Witkin, SS and Wodrich, H and Woehlbier, U and Wollert, T and Wong, E and Wong, JH and Wong, RW and Wong, VKW and Wong, WW and Wu, AG and Wu, C and Wu, J and Wu, J and Wu, KK and Wu, M and Wu, SY and Wu, S and Wu, SY and Wu, S and Wu, WKK and Wu, X and Wu, X and Wu, YW and Wu, Y and Xavier, RJ and Xia, H and Xia, L and Xia, Z and Xiang, G and Xiang, J and Xiang, M and Xiang, W and Xiao, B and Xiao, G and Xiao, H and Xiao, HT and Xiao, J and Xiao, L and Xiao, S and Xiao, Y and Xie, B and Xie, CM and Xie, M and Xie, Y and Xie, Z and Xie, Z and Xilouri, M and Xu, C and Xu, E and Xu, H and Xu, J and Xu, J and Xu, L and Xu, WW and Xu, X and Xue, Y and Yakhine-Diop, SMS and Yamaguchi, M and Yamaguchi, O and Yamamoto, A and Yamashina, S and Yan, S and Yan, SJ and Yan, Z and Yanagi, Y and Yang, C and Yang, DS and Yang, H and Yang, HT and Yang, H and Yang, JM and Yang, J and Yang, J and Yang, L and Yang, L and Yang, M and Yang, PM and Yang, Q and Yang, S and Yang, S and Yang, SF and Yang, W and Yang, WY and Yang, X and Yang, X and Yang, Y and Yang, Y and Yao, H and Yao, S and Yao, X and Yao, YG and Yao, YM and Yasui, T and Yazdankhah, M and Yen, PM and Yi, C and Yin, XM and Yin, Y and Yin, Z and Yin, Z and Ying, M and Ying, Z and Yip, CK and Yiu, SPT and Yoo, YH and Yoshida, K and Yoshii, SR and Yoshimori, T and Yousefi, B and Yu, B and Yu, H and Yu, J and Yu, J and Yu, L and Yu, ML and Yu, SW and Yu, VC and Yu, WH and Yu, Z and Yu, Z and Yuan, J and Yuan, LQ and Yuan, S and Yuan, SF and Yuan, Y and Yuan, Z and Yue, J and Yue, Z and Yun, J and Yung, RL and Zacks, DN and Zaffagnini, G and Zambelli, VO and Zanella, I and Zang, QS and Zanivan, S and Zappavigna, S and Zaragoza, P and Zarbalis, KS and Zarebkohan, A and Zarrouk, A and Zeitlin, SO and Zeng, J and Zeng, JD and Žerovnik, E and Zhan, L and Zhang, B and Zhang, DD and Zhang, H and Zhang, H and Zhang, H and Zhang, H and Zhang, H and Zhang, H and Zhang, H and Zhang, HL and Zhang, J and Zhang, J and Zhang, JP and Zhang, KYB and Zhang, LW and Zhang, L and Zhang, L and Zhang, L and Zhang, L and Zhang, M and Zhang, P and Zhang, S and Zhang, W and Zhang, X and Zhang, XW and Zhang, X and Zhang, X and Zhang, X and Zhang, X and Zhang, XD and Zhang, Y and Zhang, Y and Zhang, Y and Zhang, YD and Zhang, Y and Zhang, YY and Zhang, Y and Zhang, Z and Zhang, Z and Zhang, Z and Zhang, Z and Zhang, Z and Zhang, Z and Zhao, H and Zhao, L and Zhao, S and Zhao, T and Zhao, XF and Zhao, Y and Zhao, Y and Zhao, Y and Zhao, Y and Zheng, G and Zheng, K and Zheng, L and Zheng, S and Zheng, XL and Zheng, Y and Zheng, ZG and Zhivotovsky, B and Zhong, Q and Zhou, A and Zhou, B and Zhou, C and Zhou, G and Zhou, H and Zhou, H and Zhou, H and Zhou, J and Zhou, J and Zhou, J and Zhou, J and Zhou, K and Zhou, R and Zhou, XJ and Zhou, Y and Zhou, Y and Zhou, Y and Zhou, ZY and Zhou, Z and Zhu, B and Zhu, C and Zhu, GQ and Zhu, H and Zhu, H and Zhu, H and Zhu, WG and Zhu, Y and Zhu, Y and Zhuang, H and Zhuang, X and Zientara-Rytter, K and Zimmermann, CM and Ziviani, E and Zoladek, T and Zong, WX and Zorov, DB and Zorzano, A and Zou, W and Zou, Z and Zou, Z and Zuryn, S and Zwerschke, W and Brand-Saberi, B and Dong, XC and Kenchappa, CS and Li, Z and Lin, Y and Oshima, S and Rong, Y and Sluimer, JC and Stallings, CL and Tong, CK},
title = {Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition).},
journal = {Autophagy},
volume = {},
number = {},
pages = {1-382},
doi = {10.1080/15548627.2020.1797280},
pmid = {33634751},
issn = {1554-8635},
abstract = {In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field.},
}
RevDate: 2021-02-23
CmpDate: 2021-02-23
Reverse-genetics studies of lncRNAs-what we have learnt and paths forward.
Genome biology, 21(1):93.
Long non-coding RNAs (lncRNAs) represent a major fraction of the transcriptome in multicellular organisms. Although a handful of well-studied lncRNAs are broadly recognized as biologically meaningful, the fraction of such transcripts out of the entire collection of lncRNAs remains a subject of vigorous debate. Here we review the evidence for and against biological functionalities of lncRNAs and attempt to arrive at potential modes of lncRNA functionality that would reconcile the contradictory conclusions. Finally, we discuss different strategies of phenotypic analyses that could be used to investigate such modes of lncRNA functionality.
Additional Links: PMID-32290841
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@article {pmid32290841,
year = {2020},
author = {Gao, F and Cai, Y and Kapranov, P and Xu, D},
title = {Reverse-genetics studies of lncRNAs-what we have learnt and paths forward.},
journal = {Genome biology},
volume = {21},
number = {1},
pages = {93},
pmid = {32290841},
issn = {1474-760X},
mesh = {Animals ; Evolution, Molecular ; Phenotype ; RNA, Long Noncoding/*physiology ; Reverse Genetics ; Vertebrates/genetics ; },
abstract = {Long non-coding RNAs (lncRNAs) represent a major fraction of the transcriptome in multicellular organisms. Although a handful of well-studied lncRNAs are broadly recognized as biologically meaningful, the fraction of such transcripts out of the entire collection of lncRNAs remains a subject of vigorous debate. Here we review the evidence for and against biological functionalities of lncRNAs and attempt to arrive at potential modes of lncRNA functionality that would reconcile the contradictory conclusions. Finally, we discuss different strategies of phenotypic analyses that could be used to investigate such modes of lncRNA functionality.},
}
MeSH Terms:
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Animals
Evolution, Molecular
Phenotype
RNA, Long Noncoding/*physiology
Reverse Genetics
Vertebrates/genetics
RevDate: 2021-02-19
CmpDate: 2021-02-19
Somatic deficiency causes reproductive parasitism in a fungus.
Nature communications, 12(1):783.
Some multicellular organisms can fuse because mergers potentially provide mutual benefits. However, experimental evolution in the fungus Neurospora crassa has demonstrated that free fusion of mycelia favours cheater lineages, but the mechanism and evolutionary dynamics of this exploitation are unknown. Here we show, paradoxically, that all convergently evolved cheater lineages have similar fusion deficiencies. These mutants are unable to initiate fusion but retain access to wild-type mycelia that fuse with them. This asymmetry reduces cheater-mutant contributions to somatic substrate-bound hyphal networks, but increases representation of their nuclei in the aerial reproductive hyphae. Cheaters only benefit when relatively rare and likely impose genetic load reminiscent of germline senescence. We show that the consequences of somatic fusion can be unequally distributed among fusion partners, with the passive non-fusing partner profiting more. We discuss how our findings may relate to the extensive variation in fusion frequency of fungi found in nature.
Additional Links: PMID-33542245
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Citation:
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@article {pmid33542245,
year = {2021},
author = {Grum-Grzhimaylo, AA and Bastiaans, E and van den Heuvel, J and Berenguer Millanes, C and Debets, AJM and Aanen, DK},
title = {Somatic deficiency causes reproductive parasitism in a fungus.},
journal = {Nature communications},
volume = {12},
number = {1},
pages = {783},
pmid = {33542245},
issn = {2041-1723},
mesh = {Cell Fusion ; DNA Mutational Analysis ; *Evolution, Molecular ; Fungal Proteins/*genetics/metabolism ; Gene Knockout Techniques ; Genes, Fungal/genetics ; Hyphae/*physiology ; Mutation ; Neurospora crassa/*physiology ; },
abstract = {Some multicellular organisms can fuse because mergers potentially provide mutual benefits. However, experimental evolution in the fungus Neurospora crassa has demonstrated that free fusion of mycelia favours cheater lineages, but the mechanism and evolutionary dynamics of this exploitation are unknown. Here we show, paradoxically, that all convergently evolved cheater lineages have similar fusion deficiencies. These mutants are unable to initiate fusion but retain access to wild-type mycelia that fuse with them. This asymmetry reduces cheater-mutant contributions to somatic substrate-bound hyphal networks, but increases representation of their nuclei in the aerial reproductive hyphae. Cheaters only benefit when relatively rare and likely impose genetic load reminiscent of germline senescence. We show that the consequences of somatic fusion can be unequally distributed among fusion partners, with the passive non-fusing partner profiting more. We discuss how our findings may relate to the extensive variation in fusion frequency of fungi found in nature.},
}
MeSH Terms:
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hide MeSH Terms
Cell Fusion
DNA Mutational Analysis
*Evolution, Molecular
Fungal Proteins/*genetics/metabolism
Gene Knockout Techniques
Genes, Fungal/genetics
Hyphae/*physiology
Mutation
Neurospora crassa/*physiology
RevDate: 2021-02-16
CmpDate: 2021-02-16
Unusual Occurrence of Two Bona-Fide CCA-Adding Enzymes in Dictyostelium discoideum.
International journal of molecular sciences, 21(15):.
Dictyostelium discoideum, the model organism for the evolutionary supergroup of Amoebozoa, is a social amoeba that, upon starvation, undergoes transition from a unicellular to a multicellular organism. In its genome, we identified two genes encoding for tRNA nucleotidyltransferases. Such pairs of tRNA nucleotidyltransferases usually represent collaborating partial activities catalyzing CC- and A-addition to the tRNA 3'-end, respectively. In D. discoideum, however, both enzymes exhibit identical activities, representing bona-fide CCA-adding enzymes. Detailed characterization of the corresponding activities revealed that both enzymes seem to be essential and are regulated inversely during different developmental stages of D. discoideum. Intriguingly, this is the first description of two functionally equivalent CCA-adding enzymes using the same set of tRNAs and showing a similar distribution within the cell. This situation seems to be a common feature in Dictyostelia, as other members of this phylum carry similar pairs of tRNA nucleotidyltransferase genes in their genome.
Additional Links: PMID-32717856
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Citation:
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@article {pmid32717856,
year = {2020},
author = {Erber, L and Hoffmann, A and Fallmann, J and Hagedorn, M and Hammann, C and Stadler, PF and Betat, H and Prohaska, S and Mörl, M},
title = {Unusual Occurrence of Two Bona-Fide CCA-Adding Enzymes in Dictyostelium discoideum.},
journal = {International journal of molecular sciences},
volume = {21},
number = {15},
pages = {},
pmid = {32717856},
issn = {1422-0067},
support = {MO 634/8-2; PR 1288/6-2//Deutsche Forschungsgemeinschaft/ ; },
mesh = {*Dictyostelium/enzymology/genetics ; *Genome, Protozoan ; *Protozoan Proteins/genetics/metabolism ; *RNA Nucleotidyltransferases/genetics/metabolism ; RNA, Protozoan/genetics/metabolism ; RNA, Transfer/genetics/metabolism ; },
abstract = {Dictyostelium discoideum, the model organism for the evolutionary supergroup of Amoebozoa, is a social amoeba that, upon starvation, undergoes transition from a unicellular to a multicellular organism. In its genome, we identified two genes encoding for tRNA nucleotidyltransferases. Such pairs of tRNA nucleotidyltransferases usually represent collaborating partial activities catalyzing CC- and A-addition to the tRNA 3'-end, respectively. In D. discoideum, however, both enzymes exhibit identical activities, representing bona-fide CCA-adding enzymes. Detailed characterization of the corresponding activities revealed that both enzymes seem to be essential and are regulated inversely during different developmental stages of D. discoideum. Intriguingly, this is the first description of two functionally equivalent CCA-adding enzymes using the same set of tRNAs and showing a similar distribution within the cell. This situation seems to be a common feature in Dictyostelia, as other members of this phylum carry similar pairs of tRNA nucleotidyltransferase genes in their genome.},
}
MeSH Terms:
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hide MeSH Terms
*Dictyostelium/enzymology/genetics
*Genome, Protozoan
*Protozoan Proteins/genetics/metabolism
*RNA Nucleotidyltransferases/genetics/metabolism
RNA, Protozoan/genetics/metabolism
RNA, Transfer/genetics/metabolism
RevDate: 2021-02-16
CmpDate: 2021-02-16
New data on spermatogenic cyst formation and cellular composition of the testis in a marine gastropod, Littorina saxatilis.
International journal of molecular sciences, 21(11):.
Knowledge of the testis structure is important for gastropod taxonomy and phylogeny, particularly for the comparative analysis of sympatric Littorina species. Observing fresh tissue and squashing fixed tissue with gradually increasing pressure, we have recently described a peculiar type of cystic spermatogenesis, rare in mollusks. It has not been documented in most mollusks until now. The testis of adult males consists of numerous lobules filled with multicellular cysts containing germline cells at different stages of differentiation. Each cyst is formed by one cyst cell of somatic origin. Here, we provide evidence for the existence of two ways of cyst formation in Littorina saxatilis. One of them begins with a goniablast cyst formation; it somewhat resembles cyst formation in Drosophila testes. The second way begins with capture of a free spermatogonium by the polyploid cyst cell which is capable to move along the gonad tissues. This way of cyst formation has not been described previously. Our data expand the understanding of the diversity of spermatogenesis types in invertebrates.
Additional Links: PMID-32471172
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@article {pmid32471172,
year = {2020},
author = {Demin, SI and Bogolyubov, DS and Granovitch, AI and Mikhailova, NA},
title = {New data on spermatogenic cyst formation and cellular composition of the testis in a marine gastropod, Littorina saxatilis.},
journal = {International journal of molecular sciences},
volume = {21},
number = {11},
pages = {},
pmid = {32471172},
issn = {1422-0067},
support = {АААА-А17-117122790092-9//Russian Academy of Sciences/ ; 19-14-00321//Russian Science Support Foundation/ ; 0.40.491.2017//St. Petersburg State University/ ; },
mesh = {Animals ; Gastropoda/*cytology ; Male ; Spermatogonia/ultrastructure ; Testis/*cytology ; },
abstract = {Knowledge of the testis structure is important for gastropod taxonomy and phylogeny, particularly for the comparative analysis of sympatric Littorina species. Observing fresh tissue and squashing fixed tissue with gradually increasing pressure, we have recently described a peculiar type of cystic spermatogenesis, rare in mollusks. It has not been documented in most mollusks until now. The testis of adult males consists of numerous lobules filled with multicellular cysts containing germline cells at different stages of differentiation. Each cyst is formed by one cyst cell of somatic origin. Here, we provide evidence for the existence of two ways of cyst formation in Littorina saxatilis. One of them begins with a goniablast cyst formation; it somewhat resembles cyst formation in Drosophila testes. The second way begins with capture of a free spermatogonium by the polyploid cyst cell which is capable to move along the gonad tissues. This way of cyst formation has not been described previously. Our data expand the understanding of the diversity of spermatogenesis types in invertebrates.},
}
MeSH Terms:
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Animals
Gastropoda/*cytology
Male
Spermatogonia/ultrastructure
Testis/*cytology
RevDate: 2021-02-11
CmpDate: 2021-02-11
Parapodial glandular organs in Owenia borealis (Annelida: Oweniidae) and their possible relationship with nephridia.
Journal of experimental zoology. Part B, Molecular and developmental evolution, 334(2):88-99.
Oweniidae is a basal group of recent annelids and nowadays it attracts the attention of researchers of many biological fields. Surprisingly, details of their anatomy, like the adult excretory system, remain obscure. Researchers recently suggested that the paired organs of tubeworms in the family Oweniidae are related to nephridia. In the current study of Owenia borealis adults, we determined that these structures are parapodial glandular organs (PGOs) and are located in the first two segments of adults. The PGOs are complex subepidermal multicellular glands that contain secretory cells, that is, goblet cells, which are differentiated by the type of the producing tube matter. The goblet cells are surrounded by muscles that are used to extrude material stored in the PGO's lumen into the external environment. The anterior pair of PGOs have very well-developed rough endoplasmatic reticulum in the proximal cells, spacious Golgi complexes, numerous nail-shaped microvilli, and apocrine secretory processes in the goblet cells of the distal parts. The posterior pair of PGOs only consists of cells, which probably produce proteinaceous fibrils. We discuss the homology of goblet cells with specific nail-shaped microvilli that produce β-chitin within annelids. We also discuss the possibility that PGOs and nephridia have a common origin. This study provides new information on the ultrastructure of cells that secrete the organic material used to form the tubes inhabited by tube-dwelling annelids.
Additional Links: PMID-32003151
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PubMed:
Citation:
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@article {pmid32003151,
year = {2020},
author = {Rimskaya-Korsakova, N and Dyachuk, V and Temereva, E},
title = {Parapodial glandular organs in Owenia borealis (Annelida: Oweniidae) and their possible relationship with nephridia.},
journal = {Journal of experimental zoology. Part B, Molecular and developmental evolution},
volume = {334},
number = {2},
pages = {88-99},
doi = {10.1002/jez.b.22928},
pmid = {32003151},
issn = {1552-5015},
mesh = {Animals ; Annelida/*anatomy & histology/physiology ; Microscopy, Electron, Transmission ; Urinary Tract/anatomy & histology/ultrastructure ; },
abstract = {Oweniidae is a basal group of recent annelids and nowadays it attracts the attention of researchers of many biological fields. Surprisingly, details of their anatomy, like the adult excretory system, remain obscure. Researchers recently suggested that the paired organs of tubeworms in the family Oweniidae are related to nephridia. In the current study of Owenia borealis adults, we determined that these structures are parapodial glandular organs (PGOs) and are located in the first two segments of adults. The PGOs are complex subepidermal multicellular glands that contain secretory cells, that is, goblet cells, which are differentiated by the type of the producing tube matter. The goblet cells are surrounded by muscles that are used to extrude material stored in the PGO's lumen into the external environment. The anterior pair of PGOs have very well-developed rough endoplasmatic reticulum in the proximal cells, spacious Golgi complexes, numerous nail-shaped microvilli, and apocrine secretory processes in the goblet cells of the distal parts. The posterior pair of PGOs only consists of cells, which probably produce proteinaceous fibrils. We discuss the homology of goblet cells with specific nail-shaped microvilli that produce β-chitin within annelids. We also discuss the possibility that PGOs and nephridia have a common origin. This study provides new information on the ultrastructure of cells that secrete the organic material used to form the tubes inhabited by tube-dwelling annelids.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
Annelida/*anatomy & histology/physiology
Microscopy, Electron, Transmission
Urinary Tract/anatomy & histology/ultrastructure
RevDate: 2021-02-09
CmpDate: 2021-02-09
Phylodynamics for cell biologists.
Science (New York, N.Y.), 371(6526):.
Multicellular organisms are composed of cells connected by ancestry and descent from progenitor cells. The dynamics of cell birth, death, and inheritance within an organism give rise to the fundamental processes of development, differentiation, and cancer. Technical advances in molecular biology now allow us to study cellular composition, ancestry, and evolution at the resolution of individual cells within an organism or tissue. Here, we take a phylogenetic and phylodynamic approach to single-cell biology. We explain how "tree thinking" is important to the interpretation of the growing body of cell-level data and how ecological null models can benefit statistical hypothesis testing. Experimental progress in cell biology should be accompanied by theoretical developments if we are to exploit fully the dynamical information in single-cell data.
Additional Links: PMID-33446527
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PubMed:
Citation:
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@article {pmid33446527,
year = {2021},
author = {Stadler, T and Pybus, OG and Stumpf, MPH},
title = {Phylodynamics for cell biologists.},
journal = {Science (New York, N.Y.)},
volume = {371},
number = {6526},
pages = {},
doi = {10.1126/science.aah6266},
pmid = {33446527},
issn = {1095-9203},
mesh = {Animals ; Caenorhabditis elegans/cytology/growth & development ; Cell Biology/trends ; *Cell Lineage ; Humans ; *Phylogeny ; *Single-Cell Analysis ; Stem Cells/cytology/physiology ; },
abstract = {Multicellular organisms are composed of cells connected by ancestry and descent from progenitor cells. The dynamics of cell birth, death, and inheritance within an organism give rise to the fundamental processes of development, differentiation, and cancer. Technical advances in molecular biology now allow us to study cellular composition, ancestry, and evolution at the resolution of individual cells within an organism or tissue. Here, we take a phylogenetic and phylodynamic approach to single-cell biology. We explain how "tree thinking" is important to the interpretation of the growing body of cell-level data and how ecological null models can benefit statistical hypothesis testing. Experimental progress in cell biology should be accompanied by theoretical developments if we are to exploit fully the dynamical information in single-cell data.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
Caenorhabditis elegans/cytology/growth & development
Cell Biology/trends
*Cell Lineage
Humans
*Phylogeny
*Single-Cell Analysis
Stem Cells/cytology/physiology
RevDate: 2021-02-04
Metabolic Stress and Immunity: Nutrient-Sensing Kinases and Tryptophan Metabolism.
Advances in experimental medicine and biology, 1275:395-405.
The tryptophan catabolizing enzyme indoleamine 2,3-dioxygenase (IDO-1) has gained major attention due the immunoregulatory nature of this pathway. Both depletion of tryptophan concentrations as well as the accumulation of downstream metabolites are relevant for the mediation of the manifold consequences of increased tryptophan metabolism. Increased tryptophan catabolism is indicative for several chronic inflammatory disorders such as infections, autoimmune diseases or cancer. Low tryptophan availability is likely to be involved in the manifestation of a variety of comorbidities such as anemia, cachexia, depression and neurocognitive disturbances.Several nutrient sensing kinases are implicated in the downstream effects of dysregulated tryptophan metabolism. These include mechanisms that were conserved during evolution but have gained special features in multicellular eukaryotes, such as pathways regulated by eukaryotic translation initiation factor 2 (eIF-2)-alpha kinase (GCN2, also named general control nonderepressible 2 kinase), 5'-adenosine monophosphate (AMP)-activated protein kinase (AMPK) and target of rapamycin (TOR).The interplay between IDO-1 and above-mentioned pathway seems to be highly context dependent. A better understanding of the crosstalk is necessary to support the search for druggable targets for the treatment of inflammatory and autoimmune disorders.
Additional Links: PMID-33539025
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Citation:
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@article {pmid33539025,
year = {2021},
author = {Gostner, JM and Fuchs, D and Kurz, K},
title = {Metabolic Stress and Immunity: Nutrient-Sensing Kinases and Tryptophan Metabolism.},
journal = {Advances in experimental medicine and biology},
volume = {1275},
number = {},
pages = {395-405},
pmid = {33539025},
issn = {0065-2598},
abstract = {The tryptophan catabolizing enzyme indoleamine 2,3-dioxygenase (IDO-1) has gained major attention due the immunoregulatory nature of this pathway. Both depletion of tryptophan concentrations as well as the accumulation of downstream metabolites are relevant for the mediation of the manifold consequences of increased tryptophan metabolism. Increased tryptophan catabolism is indicative for several chronic inflammatory disorders such as infections, autoimmune diseases or cancer. Low tryptophan availability is likely to be involved in the manifestation of a variety of comorbidities such as anemia, cachexia, depression and neurocognitive disturbances.Several nutrient sensing kinases are implicated in the downstream effects of dysregulated tryptophan metabolism. These include mechanisms that were conserved during evolution but have gained special features in multicellular eukaryotes, such as pathways regulated by eukaryotic translation initiation factor 2 (eIF-2)-alpha kinase (GCN2, also named general control nonderepressible 2 kinase), 5'-adenosine monophosphate (AMP)-activated protein kinase (AMPK) and target of rapamycin (TOR).The interplay between IDO-1 and above-mentioned pathway seems to be highly context dependent. A better understanding of the crosstalk is necessary to support the search for druggable targets for the treatment of inflammatory and autoimmune disorders.},
}
RevDate: 2021-02-04
CmpDate: 2021-02-04
Brain MRI Findings in Coenurosis: A Helminth Infection.
Journal of neuroimaging : official journal of the American Society of Neuroimaging, 30(3):359-369.
BACKGROUND AND PURPOSE: Parasitic neuroinfections in humans have etiological agents spanning a broad spectrum from unicellular (protozoan) to multicellular helminthic (metazoan) organisms. Cerebral coenurosis is a rare cestodal helminthic infection caused by Taenia multiceps. The neuroimaging features of this entity were reviewed to discern an imaging phenotype.
METHODS: Retrospective analysis was performed on 6 cases of cerebral coenurosis, whose diagnoses were confirmed by histopathology. The clinical, imaging, and histopathological features were recorded for analysis.
RESULTS: Clinical expressions included focal neurological deficit due to mass effect (n = 4), intraventricular obstruction with features of raised intracranial tension (n = 1), headache (n = 3), seizures (n = 3), and incidental lesions (n = 1). One patient presented with recurrence 1 year after surgical excision. Neuroimaging revealed cystic thin-walled lesions with clustered eccentric internal nodules corresponding to the plenitude of protoscolices of the tapeworm. Three of the lesions showed a multilocular cystic morphology. Spectroscopic metabolite signature of alanine and succinate commensurate with the parasitic etiology was remarkable in the lesions. Enhancement and edema inversely correlated with the signal suppression on fluid-attenuated inversion recovery (FLAIR) imaging. The lesions had a predominantly juxtacortical distribution.
CONCLUSIONS: In an appropriate clinical setting, a cystic lesion with clustered eccentric internal nodular foci ought to raise the suspicion of this rare infection. Magnetic resonance spectroscopic signature of succinate and alanine, if present, further strengthens the likelihood of coenurosis. Signal characteristics, wall enhancement, and perilesional edema may vary, possibly determined by the stage in the evolution of the parasite.
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@article {pmid32072723,
year = {2020},
author = {Kulanthaivelu, K and Bhat, MD and Prasad, C and Srinivas, D and Mhatre, R and Nandeesh, BN},
title = {Brain MRI Findings in Coenurosis: A Helminth Infection.},
journal = {Journal of neuroimaging : official journal of the American Society of Neuroimaging},
volume = {30},
number = {3},
pages = {359-369},
doi = {10.1111/jon.12696},
pmid = {32072723},
issn = {1552-6569},
mesh = {Adult ; Aged ; Brain/*diagnostic imaging ; Female ; Humans ; Magnetic Resonance Imaging/methods ; Magnetic Resonance Spectroscopy ; Male ; Middle Aged ; Neoplasm Recurrence, Local ; Neurocysticercosis/complications/*diagnostic imaging ; Neuroimaging ; Retrospective Studies ; Seizures/*diagnostic imaging/etiology ; },
abstract = {BACKGROUND AND PURPOSE: Parasitic neuroinfections in humans have etiological agents spanning a broad spectrum from unicellular (protozoan) to multicellular helminthic (metazoan) organisms. Cerebral coenurosis is a rare cestodal helminthic infection caused by Taenia multiceps. The neuroimaging features of this entity were reviewed to discern an imaging phenotype.
METHODS: Retrospective analysis was performed on 6 cases of cerebral coenurosis, whose diagnoses were confirmed by histopathology. The clinical, imaging, and histopathological features were recorded for analysis.
RESULTS: Clinical expressions included focal neurological deficit due to mass effect (n = 4), intraventricular obstruction with features of raised intracranial tension (n = 1), headache (n = 3), seizures (n = 3), and incidental lesions (n = 1). One patient presented with recurrence 1 year after surgical excision. Neuroimaging revealed cystic thin-walled lesions with clustered eccentric internal nodules corresponding to the plenitude of protoscolices of the tapeworm. Three of the lesions showed a multilocular cystic morphology. Spectroscopic metabolite signature of alanine and succinate commensurate with the parasitic etiology was remarkable in the lesions. Enhancement and edema inversely correlated with the signal suppression on fluid-attenuated inversion recovery (FLAIR) imaging. The lesions had a predominantly juxtacortical distribution.
CONCLUSIONS: In an appropriate clinical setting, a cystic lesion with clustered eccentric internal nodular foci ought to raise the suspicion of this rare infection. Magnetic resonance spectroscopic signature of succinate and alanine, if present, further strengthens the likelihood of coenurosis. Signal characteristics, wall enhancement, and perilesional edema may vary, possibly determined by the stage in the evolution of the parasite.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Adult
Aged
Brain/*diagnostic imaging
Female
Humans
Magnetic Resonance Imaging/methods
Magnetic Resonance Spectroscopy
Male
Middle Aged
Neoplasm Recurrence, Local
Neurocysticercosis/complications/*diagnostic imaging
Neuroimaging
Retrospective Studies
Seizures/*diagnostic imaging/etiology
RevDate: 2021-02-03
CmpDate: 2021-02-03
Diversity of activator of G-protein signaling (AGS)-family proteins and their impact on asymmetric cell division across taxa.
Developmental biology, 465(2):89-99.
Asymmetric cell division (ACD) is a cellular process that forms two different cell types through a cell division and is thus critical for the development of all multicellular organisms. Not all but many of the ACD processes are mediated by proper orientation of the mitotic spindle, which segregates the fate determinants asymmetrically into daughter cells. In many cell types, the evolutionarily conserved protein complex of Gαi/AGS-family protein/NuMA-like protein appears to play critical roles in orienting the spindle and/or generating the polarized cortical forces to regulate ACD. Studies in various organisms reveal that this conserved protein complex is slightly modified in each phylum or even within species. In particular, AGS-family proteins appear to be modified with a variable number of motifs in their functional domains across taxa. This apparently creates different molecular interactions and mechanisms of ACD in each developmental program, ultimately contributing to developmental diversity across species. In this review, we discuss how a conserved ACD machinery has been modified in each phylum over the course of evolution with a major focus on the molecular evolution of AGS-family proteins and its impact on ACD regulation.
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@article {pmid32687894,
year = {2020},
author = {Wavreil, FDM and Yajima, M},
title = {Diversity of activator of G-protein signaling (AGS)-family proteins and their impact on asymmetric cell division across taxa.},
journal = {Developmental biology},
volume = {465},
number = {2},
pages = {89-99},
pmid = {32687894},
issn = {1095-564X},
support = {R01 GM126043/GM/NIGMS NIH HHS/United States ; },
mesh = {Animals ; Asymmetric Cell Division/*physiology ; Cell Cycle Proteins/genetics/*metabolism ; Humans ; *Multigene Family ; Signal Transduction/*physiology ; Species Specificity ; Spindle Apparatus/genetics/*metabolism ; },
abstract = {Asymmetric cell division (ACD) is a cellular process that forms two different cell types through a cell division and is thus critical for the development of all multicellular organisms. Not all but many of the ACD processes are mediated by proper orientation of the mitotic spindle, which segregates the fate determinants asymmetrically into daughter cells. In many cell types, the evolutionarily conserved protein complex of Gαi/AGS-family protein/NuMA-like protein appears to play critical roles in orienting the spindle and/or generating the polarized cortical forces to regulate ACD. Studies in various organisms reveal that this conserved protein complex is slightly modified in each phylum or even within species. In particular, AGS-family proteins appear to be modified with a variable number of motifs in their functional domains across taxa. This apparently creates different molecular interactions and mechanisms of ACD in each developmental program, ultimately contributing to developmental diversity across species. In this review, we discuss how a conserved ACD machinery has been modified in each phylum over the course of evolution with a major focus on the molecular evolution of AGS-family proteins and its impact on ACD regulation.},
}
MeSH Terms:
show MeSH Terms
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Animals
Asymmetric Cell Division/*physiology
Cell Cycle Proteins/genetics/*metabolism
Humans
*Multigene Family
Signal Transduction/*physiology
Species Specificity
Spindle Apparatus/genetics/*metabolism
RevDate: 2021-02-01
Taphonomic experiments imply a possible link between the evolution of multicellularity and the fossilization potential of soft-bodied organisms.
Ecology and evolution, 11(2):1037-1056 pii:ECE37120.
The reliability of evolutionary reconstructions based on the fossil record critically depends on our knowledge of the factors affecting the fossilization of soft-bodied organisms. Despite considerable research effort, these factors are still poorly understood. In order to elucidate the main prerequisites for the preservation of soft-bodied organisms, we conducted long-term (1-5 years) taphonomic experiments with the model crustacean Artemia salina buried in five different sediments. The subsequent analysis of the carcasses and sediments revealed that, in our experimental settings, better preservation was associated with the fast deposition of aluminum and silicon on organic tissues. Other elements such as calcium, magnesium, and iron, which can also accumulate quickly on the carcasses, appear to be much less efficient in preventing decay. Next, we asked if the carcasses of uni- and multicellular organisms differ in their ability to accumulate aluminum ions on their surface. The experiments with the flagellate Euglena gracilis and the sponge Spongilla lacustris showed that aluminum ions are more readily deposited onto a multicellular body. This was further confirmed by the experiments with uni- and multicellular stages of the social ameba Dictyostelium discoideum. The results lead us to speculate that the evolution of cell adhesion molecules, which provide efficient cell-cell and cell-substrate binding, probably can explain the rich fossil record of soft-bodied animals, the comparatively poor fossil record of nonskeletal unicellular eukaryotes, and the explosive emergence of the Cambrian diversity of soft-bodied fossils.
Additional Links: PMID-33520185
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@article {pmid33520185,
year = {2021},
author = {Naimark, E and Kirpotin, D and Boeva, N and Gmoshinskiy, V and Kalinina, M and Lyupina, Y and Markov, A and Nikitin, M and Shokurov, A and Volkov, D},
title = {Taphonomic experiments imply a possible link between the evolution of multicellularity and the fossilization potential of soft-bodied organisms.},
journal = {Ecology and evolution},
volume = {11},
number = {2},
pages = {1037-1056},
doi = {10.1002/ece3.7120},
pmid = {33520185},
issn = {2045-7758},
abstract = {The reliability of evolutionary reconstructions based on the fossil record critically depends on our knowledge of the factors affecting the fossilization of soft-bodied organisms. Despite considerable research effort, these factors are still poorly understood. In order to elucidate the main prerequisites for the preservation of soft-bodied organisms, we conducted long-term (1-5 years) taphonomic experiments with the model crustacean Artemia salina buried in five different sediments. The subsequent analysis of the carcasses and sediments revealed that, in our experimental settings, better preservation was associated with the fast deposition of aluminum and silicon on organic tissues. Other elements such as calcium, magnesium, and iron, which can also accumulate quickly on the carcasses, appear to be much less efficient in preventing decay. Next, we asked if the carcasses of uni- and multicellular organisms differ in their ability to accumulate aluminum ions on their surface. The experiments with the flagellate Euglena gracilis and the sponge Spongilla lacustris showed that aluminum ions are more readily deposited onto a multicellular body. This was further confirmed by the experiments with uni- and multicellular stages of the social ameba Dictyostelium discoideum. The results lead us to speculate that the evolution of cell adhesion molecules, which provide efficient cell-cell and cell-substrate binding, probably can explain the rich fossil record of soft-bodied animals, the comparatively poor fossil record of nonskeletal unicellular eukaryotes, and the explosive emergence of the Cambrian diversity of soft-bodied fossils.},
}
RevDate: 2021-01-26
CmpDate: 2021-01-26
Towards understanding the origin of animal development.
Development (Cambridge, England), 147(23): pii:147/23/dev192575.
Almost all animals undergo embryonic development, going from a single-celled zygote to a complex multicellular adult. We know that the patterning and morphogenetic processes involved in development are deeply conserved within the animal kingdom. However, the origins of these developmental processes are just beginning to be unveiled. Here, we focus on how the protist lineages sister to animals are reshaping our view of animal development. Most intriguingly, many of these protistan lineages display transient multicellular structures, which are governed by similar morphogenetic and gene regulatory processes as animal development. We discuss here two potential alternative scenarios to explain the origin of animal embryonic development: either it originated concomitantly at the onset of animals or it evolved from morphogenetic processes already present in their unicellular ancestors. We propose that an integrative study of several unicellular taxa closely related to animals will allow a more refined picture of how the last common ancestor of animals underwent embryonic development.
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@article {pmid33272929,
year = {2020},
author = {Ruiz-Trillo, I and de Mendoza, A},
title = {Towards understanding the origin of animal development.},
journal = {Development (Cambridge, England)},
volume = {147},
number = {23},
pages = {},
doi = {10.1242/dev.192575},
pmid = {33272929},
issn = {1477-9129},
mesh = {Animals ; *Biological Evolution ; Choanoflagellata/genetics/*growth & development ; Embryonic Development/*genetics ; Gene Expression Regulation, Developmental/genetics ; Mammals/genetics ; Morphogenesis/*genetics ; Phylogeny ; Zygote/growth & development ; },
abstract = {Almost all animals undergo embryonic development, going from a single-celled zygote to a complex multicellular adult. We know that the patterning and morphogenetic processes involved in development are deeply conserved within the animal kingdom. However, the origins of these developmental processes are just beginning to be unveiled. Here, we focus on how the protist lineages sister to animals are reshaping our view of animal development. Most intriguingly, many of these protistan lineages display transient multicellular structures, which are governed by similar morphogenetic and gene regulatory processes as animal development. We discuss here two potential alternative scenarios to explain the origin of animal embryonic development: either it originated concomitantly at the onset of animals or it evolved from morphogenetic processes already present in their unicellular ancestors. We propose that an integrative study of several unicellular taxa closely related to animals will allow a more refined picture of how the last common ancestor of animals underwent embryonic development.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Biological Evolution
Choanoflagellata/genetics/*growth & development
Embryonic Development/*genetics
Gene Expression Regulation, Developmental/genetics
Mammals/genetics
Morphogenesis/*genetics
Phylogeny
Zygote/growth & development
RevDate: 2021-01-25
CmpDate: 2021-01-25
Insulin-like growth factor 1 triggers salt secretion machinery in fish under acute salinity stress.
The Journal of endocrinology, 246(3):277-288.
Timely adjustment of osmoregulation upon acute salinity stress is essential for the survival of euryhaline fish. This rapid response is thought to be tightly controlled by hormones; however, there are still questions unanswered. In this work, we tested the hypothesis that the endocrine hormone, insulin-like growth factor 1 (Igf1), a slow-acting hormone, is involved in the activation of salt secretion mechanisms in euryhaline medaka (Oryzias melastigma) during acclimation to acute salinity stress. In response to a 30-ppt seawater (SW) challenge, Na+/Cl- secretion was enhanced within 0.5 h, with concomitant organization of ionocyte multicellular complexes and without changes in expression of major transporters. Igf1 receptor inhibitors significantly impair the Na+/Cl- secretion and ionocyte multicellular complex responses without affecting transporter expression. Thus, Igf1 may activate salt secretion as part of the teleost response to acute salinity stress by exerting effects on transporter function and enhancing the formation of ionocyte multicellular complexes. These findings provide new insights into hormonal control of body fluid ionic/osmotic homeostasis during vertebrate evolution.
Additional Links: PMID-32698133
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@article {pmid32698133,
year = {2020},
author = {Yan, JJ and Lee, YC and Tsou, YL and Tseng, YC and Hwang, PP},
title = {Insulin-like growth factor 1 triggers salt secretion machinery in fish under acute salinity stress.},
journal = {The Journal of endocrinology},
volume = {246},
number = {3},
pages = {277-288},
doi = {10.1530/JOE-20-0053},
pmid = {32698133},
issn = {1479-6805},
mesh = {Animals ; Fish Proteins/metabolism ; Insulin-Like Growth Factor I/antagonists & inhibitors/*metabolism ; Oryzias ; Salinity ; Salt Stress ; Signal Transduction/drug effects ; Sodium Chloride/*pharmacology ; },
abstract = {Timely adjustment of osmoregulation upon acute salinity stress is essential for the survival of euryhaline fish. This rapid response is thought to be tightly controlled by hormones; however, there are still questions unanswered. In this work, we tested the hypothesis that the endocrine hormone, insulin-like growth factor 1 (Igf1), a slow-acting hormone, is involved in the activation of salt secretion mechanisms in euryhaline medaka (Oryzias melastigma) during acclimation to acute salinity stress. In response to a 30-ppt seawater (SW) challenge, Na+/Cl- secretion was enhanced within 0.5 h, with concomitant organization of ionocyte multicellular complexes and without changes in expression of major transporters. Igf1 receptor inhibitors significantly impair the Na+/Cl- secretion and ionocyte multicellular complex responses without affecting transporter expression. Thus, Igf1 may activate salt secretion as part of the teleost response to acute salinity stress by exerting effects on transporter function and enhancing the formation of ionocyte multicellular complexes. These findings provide new insights into hormonal control of body fluid ionic/osmotic homeostasis during vertebrate evolution.},
}
MeSH Terms:
show MeSH Terms
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Animals
Fish Proteins/metabolism
Insulin-Like Growth Factor I/antagonists & inhibitors/*metabolism
Oryzias
Salinity
Salt Stress
Signal Transduction/drug effects
Sodium Chloride/*pharmacology
RevDate: 2021-01-22
Abundantly expressed class of noncoding RNAs conserved through the multicellular evolution of dictyostelid social amoebae.
Genome research pii:gr.272856.120 [Epub ahead of print].
Aggregative multicellularity has evolved multiple times in diverse groups of eukaryotes, exemplified by the well-studied development of dictyostelid social amoebae, e.g. Dictyostelium discoideum However, it is still poorly understood why multicellularity emerged in these amoebae while the great majority of other members of Amoebozoa are unicellular. Previously a novel type of noncoding RNA, Class I RNAs, was identified in D. discoideum and demonstrated to be important for normal multicellular development. Here we investigated Class I RNA evolution and its connection to multicellular development. We identified a large number of new Class I RNA genes by constructing a co-variance model combined with a scoring system based on conserved upstream sequences. Multiple genes were predicted in representatives of each major group of Dictyostelia and expression analysis confirmed that our search approach identifies expressed Class I RNA genes with high accuracy and sensitivity and that the RNAs are developmentally regulated. Further studies showed that Class I RNAs are ubiquitous in Dictyostelia and share highly conserved structure and sequence motifs. In addition, Class I RNA genes appear to be unique to dictyostelid social amoebae since they could not be identified in outgroup genomes, including their closest known relatives. Our results show that Class I RNA is an ancient class of ncRNAs, likely to have been present in the last common ancestor of Dictyostelia dating back at least 600 million years. Based on previous functional analyses and the presented evolutionary investigation, we hypothesize that Class I RNAs were involved in evolution of multicellularity in Dictyostelia.
Additional Links: PMID-33479022
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@article {pmid33479022,
year = {2021},
author = {Kjellin, J and Avesson, L and Reimegård, J and Liao, Z and Eichinger, L and Noegel, A and Glöckner, G and Schaap, P and Söderbom, F},
title = {Abundantly expressed class of noncoding RNAs conserved through the multicellular evolution of dictyostelid social amoebae.},
journal = {Genome research},
volume = {},
number = {},
pages = {},
doi = {10.1101/gr.272856.120},
pmid = {33479022},
issn = {1549-5469},
abstract = {Aggregative multicellularity has evolved multiple times in diverse groups of eukaryotes, exemplified by the well-studied development of dictyostelid social amoebae, e.g. Dictyostelium discoideum However, it is still poorly understood why multicellularity emerged in these amoebae while the great majority of other members of Amoebozoa are unicellular. Previously a novel type of noncoding RNA, Class I RNAs, was identified in D. discoideum and demonstrated to be important for normal multicellular development. Here we investigated Class I RNA evolution and its connection to multicellular development. We identified a large number of new Class I RNA genes by constructing a co-variance model combined with a scoring system based on conserved upstream sequences. Multiple genes were predicted in representatives of each major group of Dictyostelia and expression analysis confirmed that our search approach identifies expressed Class I RNA genes with high accuracy and sensitivity and that the RNAs are developmentally regulated. Further studies showed that Class I RNAs are ubiquitous in Dictyostelia and share highly conserved structure and sequence motifs. In addition, Class I RNA genes appear to be unique to dictyostelid social amoebae since they could not be identified in outgroup genomes, including their closest known relatives. Our results show that Class I RNA is an ancient class of ncRNAs, likely to have been present in the last common ancestor of Dictyostelia dating back at least 600 million years. Based on previous functional analyses and the presented evolutionary investigation, we hypothesize that Class I RNAs were involved in evolution of multicellularity in Dictyostelia.},
}
RevDate: 2021-01-19
CmpDate: 2021-01-19
Regeneration in the sponge Sycon ciliatum partly mimics postlarval development.
Development (Cambridge, England), 147(22): pii:dev.193714.
Somatic cells dissociated from an adult sponge can reorganize and develop into a juvenile-like sponge, a remarkable phenomenon of regeneration. However, the extent to which regeneration recapitulates embryonic developmental pathways has remained enigmatic. We have standardized and established a sponge Sycon ciliatum regeneration protocol from dissociated cells. Morphological analysis demonstrated that dissociated sponge cells follow a series of morphological events resembling postembryonic development. We performed high-throughput sequencing on regenerating samples and compared the data with that from regular postlarval development. Our comparative transcriptomic analysis revealed that sponge regeneration is as equally dynamic as embryogenesis. We found that sponge regeneration is orchestrated by recruiting pathways similar to those utilized in embryonic development. We also demonstrated that sponge regeneration is accompanied by cell death at early stages, revealing the importance of apoptosis in remodelling the primmorphs to initiate re-development. Because sponges are likely to be the first branch of extant multicellular animals, we suggest that this system can be explored to study the genetic features underlying the evolution of multicellularity and regeneration.
Additional Links: PMID-33093150
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@article {pmid33093150,
year = {2020},
author = {Soubigou, A and Ross, EG and Touhami, Y and Chrismas, N and Modepalli, V},
title = {Regeneration in the sponge Sycon ciliatum partly mimics postlarval development.},
journal = {Development (Cambridge, England)},
volume = {147},
number = {22},
pages = {},
doi = {10.1242/dev.193714},
pmid = {33093150},
issn = {1477-9129},
mesh = {Animals ; Embryonic Development/*physiology ; Larva ; Porifera/*embryology ; Regeneration/*physiology ; Transcriptome/*physiology ; },
abstract = {Somatic cells dissociated from an adult sponge can reorganize and develop into a juvenile-like sponge, a remarkable phenomenon of regeneration. However, the extent to which regeneration recapitulates embryonic developmental pathways has remained enigmatic. We have standardized and established a sponge Sycon ciliatum regeneration protocol from dissociated cells. Morphological analysis demonstrated that dissociated sponge cells follow a series of morphological events resembling postembryonic development. We performed high-throughput sequencing on regenerating samples and compared the data with that from regular postlarval development. Our comparative transcriptomic analysis revealed that sponge regeneration is as equally dynamic as embryogenesis. We found that sponge regeneration is orchestrated by recruiting pathways similar to those utilized in embryonic development. We also demonstrated that sponge regeneration is accompanied by cell death at early stages, revealing the importance of apoptosis in remodelling the primmorphs to initiate re-development. Because sponges are likely to be the first branch of extant multicellular animals, we suggest that this system can be explored to study the genetic features underlying the evolution of multicellularity and regeneration.},
}
MeSH Terms:
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Animals
Embryonic Development/*physiology
Larva
Porifera/*embryology
Regeneration/*physiology
Transcriptome/*physiology
RevDate: 2021-01-13
CmpDate: 2021-01-13
The genetic basis for the evolution of soma: mechanistic evidence for the co-option of a stress-induced gene into a developmental master regulator.
Proceedings. Biological sciences, 287(1940):20201414.
In multicellular organisms with specialized cells, the most significant distinction among cell types is between reproductive (germ) cells and non-reproductive/somatic cells (soma). Although soma contributed to the marked increase in complexity of many multicellular lineages, little is known about its evolutionary origins. We have previously suggested that the evolution of genes responsible for the differentiation of somatic cells involved the co-option of life history trade-off genes that in unicellular organisms enhanced survival at a cost to immediate reproduction. In the multicellular green alga, Volvox carteri, cell fate is established early in development by the differential expression of a master regulatory gene known as regA. A closely related RegA-Like Sequence (RLS1) is present in its single-celled relative, Chlamydomonas reinhardtii. RLS1 is expressed in response to stress, and we proposed that an environmentally induced RLS1-like gene was co-opted into a developmental pathway in the lineage leading to V. carteri. However, the exact evolutionary scenario responsible for the postulated co-option event remains to be determined. Here, we show that in addition to being developmentally regulated, regA can also be induced by environmental cues, indicating that regA has maintained its ancestral regulation. We also found that the absence of a functional RegA protein confers increased sensitivity to stress, consistent with RegA having a direct or indirect role in stress responses. Overall, this study (i) provides mechanistic evidence for the co-option of an environmentally induced gene into a major developmental regulator, (ii) supports the view that major morphological innovations can evolve via regulatory changes and (iii) argues for the role of stress in the evolution of multicellular complexity.
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@article {pmid33259762,
year = {2020},
author = {König, SG and Nedelcu, AM},
title = {The genetic basis for the evolution of soma: mechanistic evidence for the co-option of a stress-induced gene into a developmental master regulator.},
journal = {Proceedings. Biological sciences},
volume = {287},
number = {1940},
pages = {20201414},
pmid = {33259762},
issn = {1471-2954},
mesh = {*Biological Evolution ; Chlorophyta/*genetics ; Clonal Evolution/*genetics ; Stress, Physiological/*genetics ; },
abstract = {In multicellular organisms with specialized cells, the most significant distinction among cell types is between reproductive (germ) cells and non-reproductive/somatic cells (soma). Although soma contributed to the marked increase in complexity of many multicellular lineages, little is known about its evolutionary origins. We have previously suggested that the evolution of genes responsible for the differentiation of somatic cells involved the co-option of life history trade-off genes that in unicellular organisms enhanced survival at a cost to immediate reproduction. In the multicellular green alga, Volvox carteri, cell fate is established early in development by the differential expression of a master regulatory gene known as regA. A closely related RegA-Like Sequence (RLS1) is present in its single-celled relative, Chlamydomonas reinhardtii. RLS1 is expressed in response to stress, and we proposed that an environmentally induced RLS1-like gene was co-opted into a developmental pathway in the lineage leading to V. carteri. However, the exact evolutionary scenario responsible for the postulated co-option event remains to be determined. Here, we show that in addition to being developmentally regulated, regA can also be induced by environmental cues, indicating that regA has maintained its ancestral regulation. We also found that the absence of a functional RegA protein confers increased sensitivity to stress, consistent with RegA having a direct or indirect role in stress responses. Overall, this study (i) provides mechanistic evidence for the co-option of an environmentally induced gene into a major developmental regulator, (ii) supports the view that major morphological innovations can evolve via regulatory changes and (iii) argues for the role of stress in the evolution of multicellular complexity.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Biological Evolution
Chlorophyta/*genetics
Clonal Evolution/*genetics
Stress, Physiological/*genetics
RevDate: 2021-01-12
CmpDate: 2021-01-12
Insights into the origin of metazoan multicellularity from predatory unicellular relatives of animals.
BMC biology, 18(1):39.
BACKGROUND: The origin of animals from their unicellular ancestor was one of the most important events in evolutionary history, but the nature and the order of events leading up to the emergence of multicellular animals are still highly uncertain. The diversity and biology of unicellular relatives of animals have strongly informed our understanding of the transition from single-celled organisms to the multicellular Metazoa. Here, we analyze the cellular structures and complex life cycles of the novel unicellular holozoans Pigoraptor and Syssomonas (Opisthokonta), and their implications for the origin of animals.
RESULTS: Syssomonas and Pigoraptor are characterized by complex life cycles with a variety of cell types including flagellates, amoeboflagellates, amoeboid non-flagellar cells, and spherical cysts. The life cycles also include the formation of multicellular aggregations and syncytium-like structures, and an unusual diet for single-celled opisthokonts (partial cell fusion and joint sucking of a large eukaryotic prey), all of which provide new insights into the origin of multicellularity in Metazoa. Several existing models explaining the origin of multicellular animals have been put forward, but these data are interestingly consistent with one, the "synzoospore hypothesis."
CONCLUSIONS: The feeding modes of the ancestral metazoan may have been more complex than previously thought, including not only bacterial prey, but also larger eukaryotic cells and organic structures. The ability to feed on large eukaryotic prey could have been a powerful trigger in the formation and development of both aggregative (e.g., joint feeding, which also implies signaling) and clonal (e.g., hypertrophic growth followed by palintomy) multicellular stages that played important roles in the emergence of multicellular animals.
Additional Links: PMID-32272915
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@article {pmid32272915,
year = {2020},
author = {Tikhonenkov, DV and Hehenberger, E and Esaulov, AS and Belyakova, OI and Mazei, YA and Mylnikov, AP and Keeling, PJ},
title = {Insights into the origin of metazoan multicellularity from predatory unicellular relatives of animals.},
journal = {BMC biology},
volume = {18},
number = {1},
pages = {39},
pmid = {32272915},
issn = {1741-7007},
support = {18-14-00239//Russian Science Foundation/International ; 227301//Natural Sciences and Engineering Research Council of Canada (CA)/International ; },
mesh = {Animals ; *Biological Evolution ; Eukaryota/*physiology ; Evolution, Molecular ; Invertebrates/*physiology ; Phylogeny ; Predatory Behavior ; },
abstract = {BACKGROUND: The origin of animals from their unicellular ancestor was one of the most important events in evolutionary history, but the nature and the order of events leading up to the emergence of multicellular animals are still highly uncertain. The diversity and biology of unicellular relatives of animals have strongly informed our understanding of the transition from single-celled organisms to the multicellular Metazoa. Here, we analyze the cellular structures and complex life cycles of the novel unicellular holozoans Pigoraptor and Syssomonas (Opisthokonta), and their implications for the origin of animals.
RESULTS: Syssomonas and Pigoraptor are characterized by complex life cycles with a variety of cell types including flagellates, amoeboflagellates, amoeboid non-flagellar cells, and spherical cysts. The life cycles also include the formation of multicellular aggregations and syncytium-like structures, and an unusual diet for single-celled opisthokonts (partial cell fusion and joint sucking of a large eukaryotic prey), all of which provide new insights into the origin of multicellularity in Metazoa. Several existing models explaining the origin of multicellular animals have been put forward, but these data are interestingly consistent with one, the "synzoospore hypothesis."
CONCLUSIONS: The feeding modes of the ancestral metazoan may have been more complex than previously thought, including not only bacterial prey, but also larger eukaryotic cells and organic structures. The ability to feed on large eukaryotic prey could have been a powerful trigger in the formation and development of both aggregative (e.g., joint feeding, which also implies signaling) and clonal (e.g., hypertrophic growth followed by palintomy) multicellular stages that played important roles in the emergence of multicellular animals.},
}
MeSH Terms:
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Animals
*Biological Evolution
Eukaryota/*physiology
Evolution, Molecular
Invertebrates/*physiology
Phylogeny
Predatory Behavior
RevDate: 2021-01-13
CmpDate: 2021-01-13
Extracellular Vesicles as Signaling Mediators and Disease Biomarkers across Biological Barriers.
International journal of molecular sciences, 21(7):.
Extracellular vesicles act as shuttle vectors or signal transducers that can deliver specific biological information and have progressively emerged as key regulators of organized communities of cells within multicellular organisms in health and disease. Here, we survey the evolutionary origin, general characteristics, and biological significance of extracellular vesicles as mediators of intercellular signaling, discuss the various subtypes of extracellular vesicles thus far described and the principal methodological approaches to their study, and review the role of extracellular vesicles in tumorigenesis, immunity, non-synaptic neural communication, vascular-neural communication through the blood-brain barrier, renal pathophysiology, and embryo-fetal/maternal communication through the placenta.
Additional Links: PMID-32260425
PubMed:
Citation:
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@article {pmid32260425,
year = {2020},
author = {Simeone, P and Bologna, G and Lanuti, P and Pierdomenico, L and Guagnano, MT and Pieragostino, D and Del Boccio, P and Vergara, D and Marchisio, M and Miscia, S and Mariani-Costantini, R},
title = {Extracellular Vesicles as Signaling Mediators and Disease Biomarkers across Biological Barriers.},
journal = {International journal of molecular sciences},
volume = {21},
number = {7},
pages = {},
pmid = {32260425},
issn = {1422-0067},
mesh = {Biomarkers/*metabolism ; Cell Communication ; Disease/*genetics ; Extracellular Vesicles/genetics/*metabolism ; Genetic Predisposition to Disease ; Humans ; Immunity ; Signal Transduction ; },
abstract = {Extracellular vesicles act as shuttle vectors or signal transducers that can deliver specific biological information and have progressively emerged as key regulators of organized communities of cells within multicellular organisms in health and disease. Here, we survey the evolutionary origin, general characteristics, and biological significance of extracellular vesicles as mediators of intercellular signaling, discuss the various subtypes of extracellular vesicles thus far described and the principal methodological approaches to their study, and review the role of extracellular vesicles in tumorigenesis, immunity, non-synaptic neural communication, vascular-neural communication through the blood-brain barrier, renal pathophysiology, and embryo-fetal/maternal communication through the placenta.},
}
MeSH Terms:
show MeSH Terms
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Biomarkers/*metabolism
Cell Communication
Disease/*genetics
Extracellular Vesicles/genetics/*metabolism
Genetic Predisposition to Disease
Humans
Immunity
Signal Transduction
RevDate: 2021-01-11
CmpDate: 2021-01-11
The role of innate immunity in the protection conferred by a bacterial infection against cancer: study of an invertebrate model.
Scientific reports, 10(1):10106.
All multicellular organisms are exposed to a diversity of infectious agents and to the emergence and proliferation of malignant cells. The protection conferred by some infections against cancer has been recently linked to the production of acquired immunity effectors such as antibodies. However, the evolution of innate immunity as a mechanism to prevent cancer and how it is jeopardized by infections remain poorly investigated. Here, we explored this question by performing experimental infections in two genetically modified invertebrate models (Drosophila melanogaster) that develop invasive or non-invasive neoplastic brain tumors. After quantifying tumor size and antimicrobial peptide gene expression, we found that Drosophila larvae infected with a naturally occurring bacterium had smaller tumors compared to controls and to fungus-infected larvae. This was associated with the upregulation of genes encoding two antimicrobial peptides-diptericin and drosomycin-that are known to be important mediators of tumor cell death. We further confirmed that tumor regression upon infection was associated with an increase in tumor cell death. Thus, our study suggests that infection could have a protective role through the production of antimicrobial peptides that increase tumor cell death. Finally, our study highlights the need to understand the role of innate immune effectors in the complex interactions between infections and cancer cell communities in order to develop innovative cancer treatment strategies.
Additional Links: PMID-32572049
PubMed:
Citation:
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@article {pmid32572049,
year = {2020},
author = {Jacqueline, C and Parvy, JP and Rollin, ML and Faugère, D and Renaud, F and Missé, D and Thomas, F and Roche, B},
title = {The role of innate immunity in the protection conferred by a bacterial infection against cancer: study of an invertebrate model.},
journal = {Scientific reports},
volume = {10},
number = {1},
pages = {10106},
pmid = {32572049},
issn = {2045-2322},
support = {C596/A17196/CRUK_/Cancer Research UK/United Kingdom ; },
mesh = {Animals ; Anti-Bacterial Agents/metabolism ; Antimicrobial Cationic Peptides/*metabolism ; Bacteria/genetics ; Bacterial Infections/metabolism ; Drosophila Proteins/metabolism/pharmacology ; Drosophila melanogaster ; Fungi/genetics ; Gene Expression/genetics ; Immunity, Innate/*physiology ; Invertebrates/genetics ; Larva/metabolism/microbiology ; Neoplasms/*immunology/prevention & control ; },
abstract = {All multicellular organisms are exposed to a diversity of infectious agents and to the emergence and proliferation of malignant cells. The protection conferred by some infections against cancer has been recently linked to the production of acquired immunity effectors such as antibodies. However, the evolution of innate immunity as a mechanism to prevent cancer and how it is jeopardized by infections remain poorly investigated. Here, we explored this question by performing experimental infections in two genetically modified invertebrate models (Drosophila melanogaster) that develop invasive or non-invasive neoplastic brain tumors. After quantifying tumor size and antimicrobial peptide gene expression, we found that Drosophila larvae infected with a naturally occurring bacterium had smaller tumors compared to controls and to fungus-infected larvae. This was associated with the upregulation of genes encoding two antimicrobial peptides-diptericin and drosomycin-that are known to be important mediators of tumor cell death. We further confirmed that tumor regression upon infection was associated with an increase in tumor cell death. Thus, our study suggests that infection could have a protective role through the production of antimicrobial peptides that increase tumor cell death. Finally, our study highlights the need to understand the role of innate immune effectors in the complex interactions between infections and cancer cell communities in order to develop innovative cancer treatment strategies.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
Anti-Bacterial Agents/metabolism
Antimicrobial Cationic Peptides/*metabolism
Bacteria/genetics
Bacterial Infections/metabolism
Drosophila Proteins/metabolism/pharmacology
Drosophila melanogaster
Fungi/genetics
Gene Expression/genetics
Immunity, Innate/*physiology
Invertebrates/genetics
Larva/metabolism/microbiology
Neoplasms/*immunology/prevention & control
RevDate: 2021-01-08
Expanding ecological assessment by integrating microorganisms into routine freshwater biomonitoring.
Water research, 191:116767 pii:S0043-1354(20)31300-2 [Epub ahead of print].
Bioindication has become an indispensable part of water quality monitoring in most countries of the world, with the presence and abundance of bioindicator taxa, mostly multicellular eukaryotes, used for biotic indices. In contrast, microbes (bacteria, archaea and protists) are seldom used as bioindicators in routine assessments, although they have been recognized for their importance in environmental processes. Recently, the use of molecular methods has revealed unexpected diversity within known functional groups and novel metabolic pathways that are particularly important in energy and nutrient cycling. In various habitats, microbial communities respond to eutrophication, metals, and natural or anthropogenic organic pollutants through changes in diversity and function. In this review, we evaluated the common trends in these changes, documenting that they have value as bioindicators and can be used not only for monitoring but also for improving our understanding of the major processes in lotic and lentic environments. Current knowledge provides a solid foundation for exploiting microbial taxa, community structures and diversity, as well as functional genes, in novel monitoring programs. These microbial community measures can also be combined into biotic indices, improving the resolution of individual bioindicators. Here, we assess particular molecular approaches complemented by advanced bioinformatic analysis, as these are the most promising with respect to detailed bioindication value. We conclude that microbial community dynamics are a missing link important for our understanding of rapid changes in the structure and function of aquatic ecosystems, and should be addressed in the future environmental monitoring of freshwater ecosystems.
Additional Links: PMID-33418487
Publisher:
PubMed:
Citation:
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@article {pmid33418487,
year = {2020},
author = {Sagova-Mareckova, M and Boenigk, J and Bouchez, A and Cermakova, K and Chonova, T and Cordier, T and Eisendle, U and Elersek, T and Fazi, S and Fleituch, T and Frühe, L and Gajdosova, M and Graupner, N and Haegerbaeumer, A and Kelly, AM and Kopecky, J and Leese, F and Nõges, P and Orlic, S and Panksep, K and Pawlowski, J and Petrusek, A and Piggott, JJ and Rusch, JC and Salis, R and Schenk, J and Simek, K and Stovicek, A and Strand, DA and Vasquez, MI and Vrålstad, T and Zlatkovic, S and Zupancic, M and Stoeck, T},
title = {Expanding ecological assessment by integrating microorganisms into routine freshwater biomonitoring.},
journal = {Water research},
volume = {191},
number = {},
pages = {116767},
doi = {10.1016/j.watres.2020.116767},
pmid = {33418487},
issn = {1879-2448},
abstract = {Bioindication has become an indispensable part of water quality monitoring in most countries of the world, with the presence and abundance of bioindicator taxa, mostly multicellular eukaryotes, used for biotic indices. In contrast, microbes (bacteria, archaea and protists) are seldom used as bioindicators in routine assessments, although they have been recognized for their importance in environmental processes. Recently, the use of molecular methods has revealed unexpected diversity within known functional groups and novel metabolic pathways that are particularly important in energy and nutrient cycling. In various habitats, microbial communities respond to eutrophication, metals, and natural or anthropogenic organic pollutants through changes in diversity and function. In this review, we evaluated the common trends in these changes, documenting that they have value as bioindicators and can be used not only for monitoring but also for improving our understanding of the major processes in lotic and lentic environments. Current knowledge provides a solid foundation for exploiting microbial taxa, community structures and diversity, as well as functional genes, in novel monitoring programs. These microbial community measures can also be combined into biotic indices, improving the resolution of individual bioindicators. Here, we assess particular molecular approaches complemented by advanced bioinformatic analysis, as these are the most promising with respect to detailed bioindication value. We conclude that microbial community dynamics are a missing link important for our understanding of rapid changes in the structure and function of aquatic ecosystems, and should be addressed in the future environmental monitoring of freshwater ecosystems.},
}
RevDate: 2021-01-08
CmpDate: 2021-01-08
A Screen for Gene Paralogies Delineating Evolutionary Branching Order of Early Metazoa.
G3 (Bethesda, Md.), 10(2):811-826.
The evolutionary diversification of animals is one of Earth's greatest marvels, yet its earliest steps are shrouded in mystery. Animals, the monophyletic clade known as Metazoa, evolved wildly divergent multicellular life strategies featuring ciliated sensory epithelia. In many lineages epithelial sensoria became coupled to increasingly complex nervous systems. Currently, different phylogenetic analyses of single-copy genes support mutually-exclusive possibilities that either Porifera or Ctenophora is sister to all other animals. Resolving this dilemma would advance the ecological and evolutionary understanding of the first animals and the evolution of nervous systems. Here we describe a comparative phylogenetic approach based on gene duplications. We computationally identify and analyze gene families with early metazoan duplications using an approach that mitigates apparent gene loss resulting from the miscalling of paralogs. In the transmembrane channel-like (TMC) family of mechano-transducing channels, we find ancient duplications that define separate clades for Eumetazoa (Placozoa + Cnidaria + Bilateria) vs. Ctenophora, and one duplication that is shared only by Eumetazoa and Porifera. In the Max-like protein X (MLX and MLXIP) family of bHLH-ZIP regulators of metabolism, we find that all major lineages from Eumetazoa and Porifera (sponges) share a duplicated gene pair that is sister to the single-copy gene maintained in Ctenophora. These results suggest a new avenue for deducing deep phylogeny by choosing rather than avoiding ancient gene paralogies.
Additional Links: PMID-31879283
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Citation:
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@article {pmid31879283,
year = {2020},
author = {Erives, A and Fritzsch, B},
title = {A Screen for Gene Paralogies Delineating Evolutionary Branching Order of Early Metazoa.},
journal = {G3 (Bethesda, Md.)},
volume = {10},
number = {2},
pages = {811-826},
pmid = {31879283},
issn = {2160-1836},
support = {R01 AG060504/AG/NIA NIH HHS/United States ; },
mesh = {Animals ; *Evolution, Molecular ; Gene Duplication/radiation effects ; *Genes ; *Genetic Testing/methods ; *Genomics/methods ; Genotype ; Phylogeny ; Plant Proteins ; },
abstract = {The evolutionary diversification of animals is one of Earth's greatest marvels, yet its earliest steps are shrouded in mystery. Animals, the monophyletic clade known as Metazoa, evolved wildly divergent multicellular life strategies featuring ciliated sensory epithelia. In many lineages epithelial sensoria became coupled to increasingly complex nervous systems. Currently, different phylogenetic analyses of single-copy genes support mutually-exclusive possibilities that either Porifera or Ctenophora is sister to all other animals. Resolving this dilemma would advance the ecological and evolutionary understanding of the first animals and the evolution of nervous systems. Here we describe a comparative phylogenetic approach based on gene duplications. We computationally identify and analyze gene families with early metazoan duplications using an approach that mitigates apparent gene loss resulting from the miscalling of paralogs. In the transmembrane channel-like (TMC) family of mechano-transducing channels, we find ancient duplications that define separate clades for Eumetazoa (Placozoa + Cnidaria + Bilateria) vs. Ctenophora, and one duplication that is shared only by Eumetazoa and Porifera. In the Max-like protein X (MLX and MLXIP) family of bHLH-ZIP regulators of metabolism, we find that all major lineages from Eumetazoa and Porifera (sponges) share a duplicated gene pair that is sister to the single-copy gene maintained in Ctenophora. These results suggest a new avenue for deducing deep phylogeny by choosing rather than avoiding ancient gene paralogies.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Evolution, Molecular
Gene Duplication/radiation effects
*Genes
*Genetic Testing/methods
*Genomics/methods
Genotype
Phylogeny
Plant Proteins
RevDate: 2021-01-04
CmpDate: 2021-01-04
Bioactive Plasma Mitochondrial DNA Is Associated With Disease Progression in Scleroderma-Associated Interstitial Lung Disease.
Arthritis & rheumatology (Hoboken, N.J.), 72(11):1905-1915.
OBJECTIVE: Systemic sclerosis-associated interstitial lung disease (SSc-ILD) is characterized by variable clinical outcomes, activation of innate immune pattern-recognition receptors (PRRs), and accumulation of α-smooth muscle actin (α-SMA)-expressing myofibroblasts. The aim of this study was to identify an association between these entities and mitochondrial DNA (mtDNA), an endogenous ligand for the intracellular DNA-sensing PRRs Toll-like receptor 9 (TLR-9) and cyclic GMP-AMP synthase/stimulator of interferon genes (cGAS/STING), which has yet to be determined.
METHODS: Human lung fibroblasts (HLFs) from normal donors and SSc-ILD explants were treated with synthetic CpG DNA and assayed for α-SMA expression and extracellular mtDNA using quantitative polymerase chain reaction for the human MT-ATP6 gene. Plasma MT-ATP6 concentrations were evaluated in 2 independent SSc-ILD cohorts and demographically matched controls. The ability of SSc-ILD and control plasma to induce TLR-9 and cGAS/STING activation was evaluated with commercially available HEK 293 reporter cells. Plasma concentrations of type I interferons (IFNs), interleukin-6 (IL-6), and oxidized DNA were measured using electrochemiluminescence and enzyme-linked immunosorbent assay-based methods. Extracellular vesicles (EVs) precipitated from plasma were evaluated for MT-ATP6 concentrations and proteomics via liquid chromatography mass spectrometry.
RESULTS: Normal HLFs and SSc-ILD fibroblasts developed increased α-SMA expression and MT-ATP6 release following CpG stimulation. Plasma mtDNA concentrations were increased in the 2 SSc-ILD cohorts, reflective of ventilatory decline, and were positively associated with both TLR-9 and cGAS/STING activation as well as type I IFN and IL-6 expression. Plasma mtDNA was not oxidized and was conveyed by EVs displaying a proteomics profile consistent with a multicellular origin.
CONCLUSION: These findings demonstrate a previously unrecognized connection between EV-encapsulated mtDNA, clinical outcomes, and intracellular DNA-sensing PRR activation in SSc-ILD. Further study of these interactions could catalyze novel mechanistic and therapeutic insights into SSc-ILD and related disorders.
Additional Links: PMID-32602227
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PubMed:
Citation:
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@article {pmid32602227,
year = {2020},
author = {Ryu, C and Walia, A and Ortiz, V and Perry, C and Woo, S and Reeves, BC and Sun, H and Winkler, J and Kanyo, JE and Wang, W and Vukmirovic, M and Ristic, N and Stratton, EA and Meena, SR and Minasyan, M and Kurbanov, D and Liu, X and Lam, TT and Farina, G and Gomez, JL and Gulati, M and Herzog, EL},
title = {Bioactive Plasma Mitochondrial DNA Is Associated With Disease Progression in Scleroderma-Associated Interstitial Lung Disease.},
journal = {Arthritis & rheumatology (Hoboken, N.J.)},
volume = {72},
number = {11},
pages = {1905-1915},
doi = {10.1002/art.41418},
pmid = {32602227},
issn = {2326-5205},
support = {U01HL112702/HL/NHLBI NIH HHS/United States ; K01-HL1-25474-03/HL/NHLBI NIH HHS/United States ; R01-HL-109233/HL/NHLBI NIH HHS/United States ; R01-HL-125850/HL/NHLBI NIH HHS/United States ; U01-HL-112702/HL/NHLBI NIH HHS/United States ; S10-OD-018034-01/HL/NHLBI NIH HHS/United States ; },
mesh = {Actins/metabolism ; Cytokines/metabolism ; DNA, Mitochondrial/*blood ; Disease Progression ; Female ; Fibroblasts/metabolism ; HEK293 Cells ; Humans ; Lung Diseases, Interstitial/*blood/etiology ; Male ; Scleroderma, Systemic/*blood/complications ; },
abstract = {OBJECTIVE: Systemic sclerosis-associated interstitial lung disease (SSc-ILD) is characterized by variable clinical outcomes, activation of innate immune pattern-recognition receptors (PRRs), and accumulation of α-smooth muscle actin (α-SMA)-expressing myofibroblasts. The aim of this study was to identify an association between these entities and mitochondrial DNA (mtDNA), an endogenous ligand for the intracellular DNA-sensing PRRs Toll-like receptor 9 (TLR-9) and cyclic GMP-AMP synthase/stimulator of interferon genes (cGAS/STING), which has yet to be determined.
METHODS: Human lung fibroblasts (HLFs) from normal donors and SSc-ILD explants were treated with synthetic CpG DNA and assayed for α-SMA expression and extracellular mtDNA using quantitative polymerase chain reaction for the human MT-ATP6 gene. Plasma MT-ATP6 concentrations were evaluated in 2 independent SSc-ILD cohorts and demographically matched controls. The ability of SSc-ILD and control plasma to induce TLR-9 and cGAS/STING activation was evaluated with commercially available HEK 293 reporter cells. Plasma concentrations of type I interferons (IFNs), interleukin-6 (IL-6), and oxidized DNA were measured using electrochemiluminescence and enzyme-linked immunosorbent assay-based methods. Extracellular vesicles (EVs) precipitated from plasma were evaluated for MT-ATP6 concentrations and proteomics via liquid chromatography mass spectrometry.
RESULTS: Normal HLFs and SSc-ILD fibroblasts developed increased α-SMA expression and MT-ATP6 release following CpG stimulation. Plasma mtDNA concentrations were increased in the 2 SSc-ILD cohorts, reflective of ventilatory decline, and were positively associated with both TLR-9 and cGAS/STING activation as well as type I IFN and IL-6 expression. Plasma mtDNA was not oxidized and was conveyed by EVs displaying a proteomics profile consistent with a multicellular origin.
CONCLUSION: These findings demonstrate a previously unrecognized connection between EV-encapsulated mtDNA, clinical outcomes, and intracellular DNA-sensing PRR activation in SSc-ILD. Further study of these interactions could catalyze novel mechanistic and therapeutic insights into SSc-ILD and related disorders.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Actins/metabolism
Cytokines/metabolism
DNA, Mitochondrial/*blood
Disease Progression
Female
Fibroblasts/metabolism
HEK293 Cells
Humans
Lung Diseases, Interstitial/*blood/etiology
Male
Scleroderma, Systemic/*blood/complications
RevDate: 2021-01-04
CmpDate: 2021-01-04
A sense of place, many times over - pattern formation and evolution of repetitive morphological structures.
Developmental dynamics : an official publication of the American Association of Anatomists, 249(3):313-327.
Fifty years ago, Lewis Wolpert introduced the concept of "positional information" to explain how patterns form in a multicellular embryonic field. Using morphogen gradients, whose continuous distributions of positional values are discretized via thresholds into distinct cellular states, he provided, at the theoretical level, an elegant solution to the "French Flag problem." In the intervening years, many experimental studies have lent support to Wolpert's ideas. However, the embryonic patterning of highly repetitive morphological structures, as often occurring in nature, can reveal limitations in the strict implementation of his initial theory, given the number of distinct threshold values that would have to be specified. Here, we review how positional information is complemented to circumvent these inadequacies, to accommodate tissue growth and pattern periodicity. In particular, we focus on functional anatomical assemblies composed of such structures, like the vertebrate spine or tetrapod digits, where the resulting segmented architecture is intrinsically linked to periodic pattern formation and unidirectional growth. These systems integrate positional information and growth with additional patterning cues that, we suggest, increase robustness and evolvability. We discuss different experimental and theoretical models to study such patterning systems, and how the underlying processes are modulated over evolutionary timescales to enable morphological diversification.
Additional Links: PMID-31702845
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PubMed:
Citation:
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@article {pmid31702845,
year = {2020},
author = {Grall, E and Tschopp, P},
title = {A sense of place, many times over - pattern formation and evolution of repetitive morphological structures.},
journal = {Developmental dynamics : an official publication of the American Association of Anatomists},
volume = {249},
number = {3},
pages = {313-327},
doi = {10.1002/dvdy.131},
pmid = {31702845},
issn = {1097-0177},
mesh = {Animals ; Body Patterning/genetics/*physiology ; Gene Expression Regulation, Developmental/genetics/*physiology ; Humans ; Morphogenesis/genetics/*physiology ; Signal Transduction/genetics/*physiology ; },
abstract = {Fifty years ago, Lewis Wolpert introduced the concept of "positional information" to explain how patterns form in a multicellular embryonic field. Using morphogen gradients, whose continuous distributions of positional values are discretized via thresholds into distinct cellular states, he provided, at the theoretical level, an elegant solution to the "French Flag problem." In the intervening years, many experimental studies have lent support to Wolpert's ideas. However, the embryonic patterning of highly repetitive morphological structures, as often occurring in nature, can reveal limitations in the strict implementation of his initial theory, given the number of distinct threshold values that would have to be specified. Here, we review how positional information is complemented to circumvent these inadequacies, to accommodate tissue growth and pattern periodicity. In particular, we focus on functional anatomical assemblies composed of such structures, like the vertebrate spine or tetrapod digits, where the resulting segmented architecture is intrinsically linked to periodic pattern formation and unidirectional growth. These systems integrate positional information and growth with additional patterning cues that, we suggest, increase robustness and evolvability. We discuss different experimental and theoretical models to study such patterning systems, and how the underlying processes are modulated over evolutionary timescales to enable morphological diversification.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
Body Patterning/genetics/*physiology
Gene Expression Regulation, Developmental/genetics/*physiology
Humans
Morphogenesis/genetics/*physiology
Signal Transduction/genetics/*physiology
RevDate: 2020-12-18
CmpDate: 2020-12-18
Oxygen-sensing mechanisms across eukaryotic kingdoms and their roles in complex multicellularity.
Science (New York, N.Y.), 370(6515):.
Oxygen-sensing mechanisms of eukaryotic multicellular organisms coordinate hypoxic cellular responses in a spatiotemporal manner. Although this capacity partly allows animals and plants to acutely adapt to oxygen deprivation, its functional and historical roots in hypoxia emphasize a broader evolutionary role. For multicellular life-forms that persist in settings with variable oxygen concentrations, the capacity to perceive and modulate responses in and between cells is pivotal. Animals and higher plants represent the most complex life-forms that ever diversified on Earth, and their oxygen-sensing mechanisms demonstrate convergent evolution from a functional perspective. Exploring oxygen-sensing mechanisms across eukaryotic kingdoms can inform us on biological innovations to harness ever-changing oxygen availability at the dawn of complex life and its utilization for their organismal development.
Additional Links: PMID-33093080
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PubMed:
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@article {pmid33093080,
year = {2020},
author = {Hammarlund, EU and Flashman, E and Mohlin, S and Licausi, F},
title = {Oxygen-sensing mechanisms across eukaryotic kingdoms and their roles in complex multicellularity.},
journal = {Science (New York, N.Y.)},
volume = {370},
number = {6515},
pages = {},
doi = {10.1126/science.aba3512},
pmid = {33093080},
issn = {1095-9203},
mesh = {Anaerobiosis ; Animals ; Biological Evolution ; Dioxygenases/genetics/*metabolism ; Eukaryota/*classification/*metabolism ; Fungi ; Oxygen/*metabolism ; Plants ; },
abstract = {Oxygen-sensing mechanisms of eukaryotic multicellular organisms coordinate hypoxic cellular responses in a spatiotemporal manner. Although this capacity partly allows animals and plants to acutely adapt to oxygen deprivation, its functional and historical roots in hypoxia emphasize a broader evolutionary role. For multicellular life-forms that persist in settings with variable oxygen concentrations, the capacity to perceive and modulate responses in and between cells is pivotal. Animals and higher plants represent the most complex life-forms that ever diversified on Earth, and their oxygen-sensing mechanisms demonstrate convergent evolution from a functional perspective. Exploring oxygen-sensing mechanisms across eukaryotic kingdoms can inform us on biological innovations to harness ever-changing oxygen availability at the dawn of complex life and its utilization for their organismal development.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Anaerobiosis
Animals
Biological Evolution
Dioxygenases/genetics/*metabolism
Eukaryota/*classification/*metabolism
Fungi
Oxygen/*metabolism
Plants
RevDate: 2020-12-17
CmpDate: 2020-12-17
The N-space Episenome unifies cellular information space-time within cognition-based evolution.
Progress in biophysics and molecular biology, 150:112-139.
Self-referential cellular homeostasis is maintained by the measured assessment of both internal status and external conditions based within an integrated cellular information field. This cellular field attachment to biologic information space-time coordinates environmental inputs by connecting the cellular senome, as the sum of the sensory experiences of the cell, with its genome and epigenome. In multicellular organisms, individual cellular information fields aggregate into a collective information architectural matrix, termed a N-space Episenome, that enables mutualized organism-wide information management. It is hypothesized that biological organization represents a dual heritable system constituted by both its biological materiality and a conjoining N-space Episenome. It is further proposed that morphogenesis derives from reciprocations between these inter-related facets to yield coordinated multicellular growth and development. The N-space Episenome is conceived as a whole cell informational projection that is heritable, transferable via cell division and essential for the synchronous integration of the diverse self-referential cells that constitute holobionts.
Additional Links: PMID-31415772
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PubMed:
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@article {pmid31415772,
year = {2020},
author = {Miller, WB and Torday, JS and Baluška, F},
title = {The N-space Episenome unifies cellular information space-time within cognition-based evolution.},
journal = {Progress in biophysics and molecular biology},
volume = {150},
number = {},
pages = {112-139},
doi = {10.1016/j.pbiomolbio.2019.08.006},
pmid = {31415772},
issn = {1873-1732},
mesh = {Animals ; *Biological Evolution ; Cell Communication ; Cell Physiological Phenomena ; Cells ; Cognition/*physiology ; Genome ; *Homeostasis ; Humans ; Morphogenesis/*genetics ; Time Factors ; },
abstract = {Self-referential cellular homeostasis is maintained by the measured assessment of both internal status and external conditions based within an integrated cellular information field. This cellular field attachment to biologic information space-time coordinates environmental inputs by connecting the cellular senome, as the sum of the sensory experiences of the cell, with its genome and epigenome. In multicellular organisms, individual cellular information fields aggregate into a collective information architectural matrix, termed a N-space Episenome, that enables mutualized organism-wide information management. It is hypothesized that biological organization represents a dual heritable system constituted by both its biological materiality and a conjoining N-space Episenome. It is further proposed that morphogenesis derives from reciprocations between these inter-related facets to yield coordinated multicellular growth and development. The N-space Episenome is conceived as a whole cell informational projection that is heritable, transferable via cell division and essential for the synchronous integration of the diverse self-referential cells that constitute holobionts.},
}
MeSH Terms:
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Animals
*Biological Evolution
Cell Communication
Cell Physiological Phenomena
Cells
Cognition/*physiology
Genome
*Homeostasis
Humans
Morphogenesis/*genetics
Time Factors
RevDate: 2020-12-15
CmpDate: 2020-12-15
Enhancers, development, and evolution.
Development, growth & differentiation, 62(5):265-268.
A single-celled fertilized egg develops into a complex, multicellular animal through a series of selection processes of developmental pathways. During these processes, regulatory genes exhibit spatiotemporally restricted expression under the control of the species-specific genetic program, and dictate developmental processes from germ layer formation to cellular differentiation. Elucidation of molecular mechanisms underlying developmental processes and also of mechanistic bases for morphological diversification during evolution is one of the central issues in contemporary developmental biology. Progress has been made due to recent technological innovations, such as high-throughput nucleotide sequencing, live-cell imaging, efficient genetic manipulation, and establishment of the organoid system, opening new avenues to the above issues.
Additional Links: PMID-32471018
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PubMed:
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@article {pmid32471018,
year = {2020},
author = {Kuroiwa, A},
title = {Enhancers, development, and evolution.},
journal = {Development, growth & differentiation},
volume = {62},
number = {5},
pages = {265-268},
doi = {10.1111/dgd.12683},
pmid = {32471018},
issn = {1440-169X},
mesh = {Animals ; *Biological Evolution ; Enhancer Elements, Genetic/*genetics ; Gene Expression Regulation, Developmental/*genetics ; Germ Layers ; },
abstract = {A single-celled fertilized egg develops into a complex, multicellular animal through a series of selection processes of developmental pathways. During these processes, regulatory genes exhibit spatiotemporally restricted expression under the control of the species-specific genetic program, and dictate developmental processes from germ layer formation to cellular differentiation. Elucidation of molecular mechanisms underlying developmental processes and also of mechanistic bases for morphological diversification during evolution is one of the central issues in contemporary developmental biology. Progress has been made due to recent technological innovations, such as high-throughput nucleotide sequencing, live-cell imaging, efficient genetic manipulation, and establishment of the organoid system, opening new avenues to the above issues.},
}
MeSH Terms:
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Animals
*Biological Evolution
Enhancer Elements, Genetic/*genetics
Gene Expression Regulation, Developmental/*genetics
Germ Layers
RevDate: 2020-12-15
CmpDate: 2020-12-15
Of mice and plants: Comparative developmental systems biology.
Developmental biology, 460(1):32-39.
Multicellular animals and plants represent independent evolutionary experiments with complex multicellular bodyplans. Differences in their life history, a mobile versus sessile lifestyle, and predominant embryonic versus postembryonic development, have led to the evolution of highly different body plans. However, also many intriguing parallels exist. Extension of the vertebrate body axis and its segmentation into somites bears striking resemblance to plant root growth and the concomittant prepatterning of lateral root competent sites. Likewise, plant shoot phyllotaxis displays similarities with vertebrate limb and digit patterning. Additionally, both plants and animals use complex signalling systems combining systemic and local signals to fine tune and coordinate organ growth across their body. Identification of these striking examples of convergent evolution provides support for the existence of general design principles: the idea that for particular patterning demands, evolution is likely to arrive at highly similar developmental patterning mechanisms. Furthermore, focussing on these parallels may aid in identifying core mechanistic principles, often obscured by the highly complex nature of multiscale patterning processes.
Additional Links: PMID-30395805
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PubMed:
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@article {pmid30395805,
year = {2020},
author = {Ten Tusscher, K},
title = {Of mice and plants: Comparative developmental systems biology.},
journal = {Developmental biology},
volume = {460},
number = {1},
pages = {32-39},
doi = {10.1016/j.ydbio.2018.10.024},
pmid = {30395805},
issn = {1095-564X},
mesh = {Animals ; Body Patterning/*physiology ; Developmental Biology ; Embryonic Development/*physiology ; Gene Expression Regulation, Developmental/*genetics ; Mice ; Models, Biological ; Plant Shoots/*embryology ; Plants ; Signal Transduction/*physiology ; Systems Biology ; },
abstract = {Multicellular animals and plants represent independent evolutionary experiments with complex multicellular bodyplans. Differences in their life history, a mobile versus sessile lifestyle, and predominant embryonic versus postembryonic development, have led to the evolution of highly different body plans. However, also many intriguing parallels exist. Extension of the vertebrate body axis and its segmentation into somites bears striking resemblance to plant root growth and the concomittant prepatterning of lateral root competent sites. Likewise, plant shoot phyllotaxis displays similarities with vertebrate limb and digit patterning. Additionally, both plants and animals use complex signalling systems combining systemic and local signals to fine tune and coordinate organ growth across their body. Identification of these striking examples of convergent evolution provides support for the existence of general design principles: the idea that for particular patterning demands, evolution is likely to arrive at highly similar developmental patterning mechanisms. Furthermore, focussing on these parallels may aid in identifying core mechanistic principles, often obscured by the highly complex nature of multiscale patterning processes.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
Body Patterning/*physiology
Developmental Biology
Embryonic Development/*physiology
Gene Expression Regulation, Developmental/*genetics
Mice
Models, Biological
Plant Shoots/*embryology
Plants
Signal Transduction/*physiology
Systems Biology
RevDate: 2020-12-14
CmpDate: 2020-12-14
Gap junctions amplify spatial variations in cell volume in proliferating tumor spheroids.
Nature communications, 11(1):6148.
Sustained proliferation is a significant driver of cancer progression. Cell-cycle advancement is coupled with cell size, but it remains unclear how multiple cells interact to control their volume in 3D clusters. In this study, we propose a mechano-osmotic model to investigate the evolution of volume dynamics within multicellular systems. Volume control depends on an interplay between multiple cellular constituents, including gap junctions, mechanosensitive ion channels, energy-consuming ion pumps, and the actomyosin cortex, that coordinate to manipulate cellular osmolarity. In connected cells, we show that mechanical loading leads to the emergence of osmotic pressure gradients between cells with consequent increases in cellular ion concentrations driving swelling. We identify how gap junctions can amplify spatial variations in cell volume within multicellular spheroids and, further, describe how the process depends on proliferation-induced solid stress. Our model may provide new insight into the role of gap junctions in breast cancer progression.
Additional Links: PMID-33262337
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@article {pmid33262337,
year = {2020},
author = {McEvoy, E and Han, YL and Guo, M and Shenoy, VB},
title = {Gap junctions amplify spatial variations in cell volume in proliferating tumor spheroids.},
journal = {Nature communications},
volume = {11},
number = {1},
pages = {6148},
pmid = {33262337},
issn = {2041-1723},
mesh = {Breast Neoplasms/chemistry/pathology/*physiopathology ; Cell Line, Tumor ; *Cell Proliferation ; Cell Size ; Disease Progression ; Female ; Gap Junctions/*chemistry ; Humans ; Osmotic Pressure ; Spheroids, Cellular/chemistry/*cytology ; },
abstract = {Sustained proliferation is a significant driver of cancer progression. Cell-cycle advancement is coupled with cell size, but it remains unclear how multiple cells interact to control their volume in 3D clusters. In this study, we propose a mechano-osmotic model to investigate the evolution of volume dynamics within multicellular systems. Volume control depends on an interplay between multiple cellular constituents, including gap junctions, mechanosensitive ion channels, energy-consuming ion pumps, and the actomyosin cortex, that coordinate to manipulate cellular osmolarity. In connected cells, we show that mechanical loading leads to the emergence of osmotic pressure gradients between cells with consequent increases in cellular ion concentrations driving swelling. We identify how gap junctions can amplify spatial variations in cell volume within multicellular spheroids and, further, describe how the process depends on proliferation-induced solid stress. Our model may provide new insight into the role of gap junctions in breast cancer progression.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Breast Neoplasms/chemistry/pathology/*physiopathology
Cell Line, Tumor
*Cell Proliferation
Cell Size
Disease Progression
Female
Gap Junctions/*chemistry
Humans
Osmotic Pressure
Spheroids, Cellular/chemistry/*cytology
RevDate: 2020-12-14
CmpDate: 2020-12-11
Photosynthetic hydrogen production by droplet-based microbial micro-reactors under aerobic conditions.
Nature communications, 11(1):5985.
The spontaneous self-assembly of multicellular ensembles into living materials with synergistic structure and function remains a considerable challenge in biotechnology and synthetic biology. Here, we exploit the aqueous two-phase separation of dextran-in-PEG emulsion micro-droplets for the capture, spatial organization and immobilization of algal cells or algal/bacterial cell communities to produce discrete multicellular spheroids capable of both aerobic (oxygen producing) and hypoxic (hydrogen producing) photosynthesis in daylight under air. We show that localized oxygen depletion results in hydrogen production from the core of the algal microscale reactor, and demonstrate that enhanced levels of hydrogen evolution can be achieved synergistically by spontaneously enclosing the photosynthetic cells within a shell of bacterial cells undergoing aerobic respiration. Our results highlight a promising droplet-based environmentally benign approach to dispersible photosynthetic microbial micro-reactors comprising segregated cellular micro-niches with dual functionality, and provide a step towards photobiological hydrogen production under aerobic conditions.
Additional Links: PMID-33239636
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@article {pmid33239636,
year = {2020},
author = {Xu, Z and Wang, S and Zhao, C and Li, S and Liu, X and Wang, L and Li, M and Huang, X and Mann, S},
title = {Photosynthetic hydrogen production by droplet-based microbial micro-reactors under aerobic conditions.},
journal = {Nature communications},
volume = {11},
number = {1},
pages = {5985},
pmid = {33239636},
issn = {2041-1723},
mesh = {Aerobiosis/physiology ; Bioreactors/*microbiology ; Cell Hypoxia/physiology ; Chlorella/metabolism ; Escherichia coli/metabolism ; Hydrogen/*metabolism ; Industrial Microbiology/*methods ; Microbiota/*physiology ; Oxygen/*metabolism ; Photosynthesis/physiology ; Renewable Energy ; },
abstract = {The spontaneous self-assembly of multicellular ensembles into living materials with synergistic structure and function remains a considerable challenge in biotechnology and synthetic biology. Here, we exploit the aqueous two-phase separation of dextran-in-PEG emulsion micro-droplets for the capture, spatial organization and immobilization of algal cells or algal/bacterial cell communities to produce discrete multicellular spheroids capable of both aerobic (oxygen producing) and hypoxic (hydrogen producing) photosynthesis in daylight under air. We show that localized oxygen depletion results in hydrogen production from the core of the algal microscale reactor, and demonstrate that enhanced levels of hydrogen evolution can be achieved synergistically by spontaneously enclosing the photosynthetic cells within a shell of bacterial cells undergoing aerobic respiration. Our results highlight a promising droplet-based environmentally benign approach to dispersible photosynthetic microbial micro-reactors comprising segregated cellular micro-niches with dual functionality, and provide a step towards photobiological hydrogen production under aerobic conditions.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Aerobiosis/physiology
Bioreactors/*microbiology
Cell Hypoxia/physiology
Chlorella/metabolism
Escherichia coli/metabolism
Hydrogen/*metabolism
Industrial Microbiology/*methods
Microbiota/*physiology
Oxygen/*metabolism
Photosynthesis/physiology
Renewable Energy
RevDate: 2020-12-14
CmpDate: 2020-12-04
OsChz1 acts as a histone chaperone in modulating chromatin organization and genome function in rice.
Nature communications, 11(1):5717.
While the yeast Chz1 acts as a specific histone-chaperone for H2A.Z, functions of CHZ-domain proteins in multicellular eukaryotes remain obscure. Here, we report on the functional characterization of OsChz1, a sole CHZ-domain protein identified in rice. OsChz1 interacts with both the canonical H2A-H2B dimer and the variant H2A.Z-H2B dimer. Within crystal structure the C-terminal region of OsChz1 binds H2A-H2B via an acidic region, pointing to a previously unknown recognition mechanism. Knockout of OsChz1 leads to multiple plant developmental defects. At genome-wide level, loss of OsChz1 causes mis-regulations of thousands of genes and broad alterations of nucleosome occupancy as well as reductions of H2A.Z-enrichment. While OsChz1 associates with chromatin regions enriched of repressive histone marks (H3K27me3 and H3K4me2), its loss does not affect the genome landscape of DNA methylation. Taken together, it is emerging that OsChz1 functions as an important H2A/H2A.Z-H2B chaperone in dynamic regulation of chromatin for higher eukaryote development.
Additional Links: PMID-33177521
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@article {pmid33177521,
year = {2020},
author = {Du, K and Luo, Q and Yin, L and Wu, J and Liu, Y and Gan, J and Dong, A and Shen, WH},
title = {OsChz1 acts as a histone chaperone in modulating chromatin organization and genome function in rice.},
journal = {Nature communications},
volume = {11},
number = {1},
pages = {5717},
pmid = {33177521},
issn = {2041-1723},
mesh = {CRISPR-Cas Systems ; Chromatin/genetics/*metabolism ; DNA Methylation ; Flowers/metabolism ; Gene Expression Regulation, Plant ; Genome, Plant ; Histones/genetics/*metabolism ; Molecular Chaperones/genetics/metabolism ; Mutation ; Nucleosomes/genetics ; Oryza/*genetics/growth & development/metabolism ; Phylogeny ; Plant Proteins/genetics/*metabolism ; Plants, Genetically Modified ; Protein Multimerization ; },
abstract = {While the yeast Chz1 acts as a specific histone-chaperone for H2A.Z, functions of CHZ-domain proteins in multicellular eukaryotes remain obscure. Here, we report on the functional characterization of OsChz1, a sole CHZ-domain protein identified in rice. OsChz1 interacts with both the canonical H2A-H2B dimer and the variant H2A.Z-H2B dimer. Within crystal structure the C-terminal region of OsChz1 binds H2A-H2B via an acidic region, pointing to a previously unknown recognition mechanism. Knockout of OsChz1 leads to multiple plant developmental defects. At genome-wide level, loss of OsChz1 causes mis-regulations of thousands of genes and broad alterations of nucleosome occupancy as well as reductions of H2A.Z-enrichment. While OsChz1 associates with chromatin regions enriched of repressive histone marks (H3K27me3 and H3K4me2), its loss does not affect the genome landscape of DNA methylation. Taken together, it is emerging that OsChz1 functions as an important H2A/H2A.Z-H2B chaperone in dynamic regulation of chromatin for higher eukaryote development.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
CRISPR-Cas Systems
Chromatin/genetics/*metabolism
DNA Methylation
Flowers/metabolism
Gene Expression Regulation, Plant
Genome, Plant
Histones/genetics/*metabolism
Molecular Chaperones/genetics/metabolism
Mutation
Nucleosomes/genetics
Oryza/*genetics/growth & development/metabolism
Phylogeny
Plant Proteins/genetics/*metabolism
Plants, Genetically Modified
Protein Multimerization
RevDate: 2020-12-14
CmpDate: 2020-12-04
Tracing the evolution of nectin and nectin-like cell adhesion molecules.
Scientific reports, 10(1):9434 pii:10.1038/s41598-020-66461-4.
Nectin and nectin-like cell adhesion molecules (collectively referred as nectin family henceforth) are known to mediate cell-cell adhesion and related functions. While current literature suggests that nectins are prevalent in vertebrates, there are no in-depth analyses regarding the evolution of nectin family as a whole. In this work, we examine the evolutionary origin of the nectin family, using selected multicellular metazoans representing diverse clades whose whole genome sequencing data is available. Our results show that this family may have appeared earlier during metazoan evolution than previously believed. Systematic analyses indicate the order in which various members of nectin family seem to have evolved, with some nectin-like molecules appearing first, followed by the evolution of other members. Furthermore, we also found a few possible ancient homologues of nectins. While our study confirms the previous grouping of the nectin family into nectins and nectin-like molecules, it also shows poliovirus receptor (PVR/nectin-like-5) to possess characteristics that are intermediate between these two groups. Interestingly, except for PVR, the other nectins show surprising sequence conservations across species, suggesting evolutionary constraints due to critical roles played by these proteins.
Additional Links: PMID-32523039
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@article {pmid32523039,
year = {2020},
author = {Duraivelan, K and Samanta, D},
title = {Tracing the evolution of nectin and nectin-like cell adhesion molecules.},
journal = {Scientific reports},
volume = {10},
number = {1},
pages = {9434},
doi = {10.1038/s41598-020-66461-4},
pmid = {32523039},
issn = {2045-2322},
mesh = {Animals ; Cell Adhesion/*genetics/physiology ; Cell Adhesion Molecules/*genetics/metabolism ; Cell Adhesion Molecules, Neuronal/genetics/metabolism ; Cell Line ; Computational Biology/methods ; Evolution, Molecular ; Humans ; Nectins/*genetics/metabolism ; },
abstract = {Nectin and nectin-like cell adhesion molecules (collectively referred as nectin family henceforth) are known to mediate cell-cell adhesion and related functions. While current literature suggests that nectins are prevalent in vertebrates, there are no in-depth analyses regarding the evolution of nectin family as a whole. In this work, we examine the evolutionary origin of the nectin family, using selected multicellular metazoans representing diverse clades whose whole genome sequencing data is available. Our results show that this family may have appeared earlier during metazoan evolution than previously believed. Systematic analyses indicate the order in which various members of nectin family seem to have evolved, with some nectin-like molecules appearing first, followed by the evolution of other members. Furthermore, we also found a few possible ancient homologues of nectins. While our study confirms the previous grouping of the nectin family into nectins and nectin-like molecules, it also shows poliovirus receptor (PVR/nectin-like-5) to possess characteristics that are intermediate between these two groups. Interestingly, except for PVR, the other nectins show surprising sequence conservations across species, suggesting evolutionary constraints due to critical roles played by these proteins.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
Cell Adhesion/*genetics/physiology
Cell Adhesion Molecules/*genetics/metabolism
Cell Adhesion Molecules, Neuronal/genetics/metabolism
Cell Line
Computational Biology/methods
Evolution, Molecular
Humans
Nectins/*genetics/metabolism
RevDate: 2020-12-14
CmpDate: 2020-12-04
Cold climate adaptation is a plausible cause for evolution of multicellular sporulation in Dictyostelia.
Scientific reports, 10(1):8797.
Unicellular protozoa that encyst individually upon starvation evolved at least eight times into organisms that instead form multicellular fruiting bodies with spores. The Dictyostelia are the largest and most complex group of such organisms. They can be subdivided into 4 major groups, with many species in groups 1-3 having additionally retained encystment. To understand fitness differences between spores and cysts, we measured long-term survival of spores and cysts under climate-mimicking conditions, investigated spore and cyst ultrastructure, and related fitness characteristics to species ecology. We found that spores and cysts survived 22 °C equally well, but that spores survived wet and dry frost better than cysts, with group 4 spores being most resilient. Spore walls consist of three layers and those of cysts of maximally two, while spores were also more compacted than cysts, with group 4 spores being the most compacted. Group 4 species were frequently isolated from arctic and alpine zones, which was rarely the case for group 1-3 species. We inferred a fossil-calibrated phylogeny of Dictyostelia, which showed that its two major branches diverged 0.52 billion years ago, following several global glaciations. Our results suggest that Dictyostelium multicellular sporulation was a likely adaptation to a cold climate.
Additional Links: PMID-32472019
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@article {pmid32472019,
year = {2020},
author = {Lawal, HM and Schilde, C and Kin, K and Brown, MW and James, J and Prescott, AR and Schaap, P},
title = {Cold climate adaptation is a plausible cause for evolution of multicellular sporulation in Dictyostelia.},
journal = {Scientific reports},
volume = {10},
number = {1},
pages = {8797},
pmid = {32472019},
issn = {2045-2322},
support = {100293/Z/12/Z/WT_/Wellcome Trust/United Kingdom ; BB/K000799/1/BB_/Biotechnology and Biological Sciences Research Council/United Kingdom ; },
mesh = {Acclimatization ; Biological Evolution ; Cold Climate ; Dictyostelium/*classification/*physiology ; Fossils/*parasitology ; Phylogeny ; Spores/physiology ; },
abstract = {Unicellular protozoa that encyst individually upon starvation evolved at least eight times into organisms that instead form multicellular fruiting bodies with spores. The Dictyostelia are the largest and most complex group of such organisms. They can be subdivided into 4 major groups, with many species in groups 1-3 having additionally retained encystment. To understand fitness differences between spores and cysts, we measured long-term survival of spores and cysts under climate-mimicking conditions, investigated spore and cyst ultrastructure, and related fitness characteristics to species ecology. We found that spores and cysts survived 22 °C equally well, but that spores survived wet and dry frost better than cysts, with group 4 spores being most resilient. Spore walls consist of three layers and those of cysts of maximally two, while spores were also more compacted than cysts, with group 4 spores being the most compacted. Group 4 species were frequently isolated from arctic and alpine zones, which was rarely the case for group 1-3 species. We inferred a fossil-calibrated phylogeny of Dictyostelia, which showed that its two major branches diverged 0.52 billion years ago, following several global glaciations. Our results suggest that Dictyostelium multicellular sporulation was a likely adaptation to a cold climate.},
}
MeSH Terms:
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hide MeSH Terms
Acclimatization
Biological Evolution
Cold Climate
Dictyostelium/*classification/*physiology
Fossils/*parasitology
Phylogeny
Spores/physiology
RevDate: 2020-12-14
CmpDate: 2020-12-04
Multicellular growth of the Basidiomycota phytopathogen fungus Sporisorium reilianum induced by acid conditions.
Folia microbiologica, 65(3):511-521.
Fungi are considered model organisms for the analysis of important phenomena of eukaryotes. For example, some of them have been described as models to understand the phenomenon of multicellularity acquisition by different unicellular organisms phylogenetically distant. Interestingly, in this work, we describe the multicellular development in the model fungus S. reilianum. We observed that Sporisorium reilianum, a Basidiomycota cereal pathogen that at neutral pH grows with a yeast-like morphology during its saprophytic haploid stage, when incubated at acid pH grew in the form of multicellular clusters. The multicellularity observed in S. reilianum was of clonal type, where buds of "stem" cells growing as yeasts remain joined by their cell wall septa, after cytokinesis. The elaboration and analysis of a regulatory network of S. reilianum showed that the putative zinc finger transcription factor CBQ73544.1 regulates a number of genes involved in cell cycle, cellular division, signal transduction pathways, and biogenesis of cell wall. Interestingly, homologous of these genes have been found to be regulated during Saccharomyces cerevisiae multicellular growth. In adddition, some of these genes were found to be negatively regulated during multicellularity of S. reilianum. With these data, we suggest that S. reilianum is an interesting model for the study of multicellular development.
Additional Links: PMID-31721091
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@article {pmid31721091,
year = {2020},
author = {Martínez-Soto, D and Velez-Haro, JM and León-Ramírez, CG and Galán-Vásquez, E and Chávez-Munguía, B and Ruiz-Herrera, J},
title = {Multicellular growth of the Basidiomycota phytopathogen fungus Sporisorium reilianum induced by acid conditions.},
journal = {Folia microbiologica},
volume = {65},
number = {3},
pages = {511-521},
doi = {10.1007/s12223-019-00755-7},
pmid = {31721091},
issn = {1874-9356},
mesh = {Acids/*pharmacology ; Basidiomycota/drug effects/*genetics/*growth & development ; Cell Cycle/drug effects ; Cell Division/drug effects ; Fungal Proteins/*genetics ; Hydrogen-Ion Concentration ; Phylogeny ; Signal Transduction/drug effects ; },
abstract = {Fungi are considered model organisms for the analysis of important phenomena of eukaryotes. For example, some of them have been described as models to understand the phenomenon of multicellularity acquisition by different unicellular organisms phylogenetically distant. Interestingly, in this work, we describe the multicellular development in the model fungus S. reilianum. We observed that Sporisorium reilianum, a Basidiomycota cereal pathogen that at neutral pH grows with a yeast-like morphology during its saprophytic haploid stage, when incubated at acid pH grew in the form of multicellular clusters. The multicellularity observed in S. reilianum was of clonal type, where buds of "stem" cells growing as yeasts remain joined by their cell wall septa, after cytokinesis. The elaboration and analysis of a regulatory network of S. reilianum showed that the putative zinc finger transcription factor CBQ73544.1 regulates a number of genes involved in cell cycle, cellular division, signal transduction pathways, and biogenesis of cell wall. Interestingly, homologous of these genes have been found to be regulated during Saccharomyces cerevisiae multicellular growth. In adddition, some of these genes were found to be negatively regulated during multicellularity of S. reilianum. With these data, we suggest that S. reilianum is an interesting model for the study of multicellular development.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Acids/*pharmacology
Basidiomycota/drug effects/*genetics/*growth & development
Cell Cycle/drug effects
Cell Division/drug effects
Fungal Proteins/*genetics
Hydrogen-Ion Concentration
Phylogeny
Signal Transduction/drug effects
RevDate: 2020-12-14
CmpDate: 2020-12-08
Do cells use passwords in cell-state transitions? Is cell signaling sometimes encrypted?.
Theory in biosciences = Theorie in den Biowissenschaften, 139(1):87-93.
Organisms must maintain proper regulation including defense and healing. Life-threatening problems may be caused by pathogens or by a multicellular organism's own cells through cancer or autoimmune disorders. Life evolved solutions to these problems that can be conceptualized through the lens of information security, which is a well-developed field in computer science. Here I argue that taking an information security view of cells is not merely semantics, but useful to explain features of signaling, regulation, and defense. An information security perspective also offers a conduit for cross-fertilization of advanced ideas from computer science and the potential for biology to inform computer science. First, I consider whether cells use passwords, i.e., initiation sequences that are required for subsequent signals to have effects, by analyzing the concept of pioneer transcription factors in chromatin regulation and cellular reprogramming. Second, I consider whether cells may encrypt signal transduction cascades. Encryption could benefit cells by making it more difficult for pathogens or oncogenes to hijack cell networks. By using numerous molecules, cells may gain a security advantage in particular against viruses, whose genome sizes are typically under selection pressure. I provide a simple conceptual argument for how cells may perform encryption through posttranslational modifications, complex formation, and chromatin accessibility. I invoke information theory to provide a criterion of an entropy spike to assess whether a signaling cascade has encryption-like features. I discuss how the frequently invoked concept of context dependency may oversimplify more advanced features of cell signaling networks, such as encryption. Therefore, by considering that biochemical networks may be even more complex than commonly realized we may be better able to understand defenses against pathogens and pathologies.
Additional Links: PMID-31175621
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@article {pmid31175621,
year = {2020},
author = {Root, A},
title = {Do cells use passwords in cell-state transitions? Is cell signaling sometimes encrypted?.},
journal = {Theory in biosciences = Theorie in den Biowissenschaften},
volume = {139},
number = {1},
pages = {87-93},
pmid = {31175621},
issn = {1611-7530},
mesh = {Algorithms ; Animals ; Autoimmune Diseases/*metabolism ; Biological Evolution ; Biological Phenomena ; Chromatin/metabolism ; Computational Biology ; Entropy ; Environment ; Genome ; Humans ; Immune System ; *Models, Biological ; Neoplasms/*metabolism ; Neurons/metabolism ; Semantics ; *Signal Transduction ; },
abstract = {Organisms must maintain proper regulation including defense and healing. Life-threatening problems may be caused by pathogens or by a multicellular organism's own cells through cancer or autoimmune disorders. Life evolved solutions to these problems that can be conceptualized through the lens of information security, which is a well-developed field in computer science. Here I argue that taking an information security view of cells is not merely semantics, but useful to explain features of signaling, regulation, and defense. An information security perspective also offers a conduit for cross-fertilization of advanced ideas from computer science and the potential for biology to inform computer science. First, I consider whether cells use passwords, i.e., initiation sequences that are required for subsequent signals to have effects, by analyzing the concept of pioneer transcription factors in chromatin regulation and cellular reprogramming. Second, I consider whether cells may encrypt signal transduction cascades. Encryption could benefit cells by making it more difficult for pathogens or oncogenes to hijack cell networks. By using numerous molecules, cells may gain a security advantage in particular against viruses, whose genome sizes are typically under selection pressure. I provide a simple conceptual argument for how cells may perform encryption through posttranslational modifications, complex formation, and chromatin accessibility. I invoke information theory to provide a criterion of an entropy spike to assess whether a signaling cascade has encryption-like features. I discuss how the frequently invoked concept of context dependency may oversimplify more advanced features of cell signaling networks, such as encryption. Therefore, by considering that biochemical networks may be even more complex than commonly realized we may be better able to understand defenses against pathogens and pathologies.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Algorithms
Animals
Autoimmune Diseases/*metabolism
Biological Evolution
Biological Phenomena
Chromatin/metabolism
Computational Biology
Entropy
Environment
Genome
Humans
Immune System
*Models, Biological
Neoplasms/*metabolism
Neurons/metabolism
Semantics
*Signal Transduction
RevDate: 2020-12-11
P53 induces senescence in the unstable progeny of aneuploid cells.
Cell cycle (Georgetown, Tex.) [Epub ahead of print].
Aneuploidy is the condition of having an imbalanced karyotype, which is associated with tumor initiation, evolution, and acquisition of drug-resistant features, possibly by generating heterogeneous populations of cells with distinct genotypes and phenotypes. Multicellular eukaryotes have therefore evolved a range of extrinsic and cell-autonomous mechanisms for restraining proliferation of aneuploid cells, including activation of the tumor suppressor protein p53. However, accumulating evidence indicates that a subset of aneuploid cells can escape p53-mediated growth restriction and continue proliferating in vitro. Here we show that such aneuploid cell lines display a robust modal karyotype and low frequency of chromosomal aberrations despite ongoing chromosome instability. Indeed, while these aneuploid cells are able to survive for extended periods in vitro, their chromosomally unstable progeny remain subject to p53-induced senescence and growth restriction, leading to subsequent elimination from the aneuploid pool. This mechanism helps maintain low levels of heterogeneity in aneuploid populations and may prevent detrimental evolutionary processes such as cancer progression and development of drug resistance.
Additional Links: PMID-33305692
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@article {pmid33305692,
year = {2020},
author = {Giam, M and Wong, CK and Low, JS and Sinelli, M and Dreesen, O and Rancati, G},
title = {P53 induces senescence in the unstable progeny of aneuploid cells.},
journal = {Cell cycle (Georgetown, Tex.)},
volume = {},
number = {},
pages = {1-13},
doi = {10.1080/15384101.2020.1850968},
pmid = {33305692},
issn = {1551-4005},
abstract = {Aneuploidy is the condition of having an imbalanced karyotype, which is associated with tumor initiation, evolution, and acquisition of drug-resistant features, possibly by generating heterogeneous populations of cells with distinct genotypes and phenotypes. Multicellular eukaryotes have therefore evolved a range of extrinsic and cell-autonomous mechanisms for restraining proliferation of aneuploid cells, including activation of the tumor suppressor protein p53. However, accumulating evidence indicates that a subset of aneuploid cells can escape p53-mediated growth restriction and continue proliferating in vitro. Here we show that such aneuploid cell lines display a robust modal karyotype and low frequency of chromosomal aberrations despite ongoing chromosome instability. Indeed, while these aneuploid cells are able to survive for extended periods in vitro, their chromosomally unstable progeny remain subject to p53-induced senescence and growth restriction, leading to subsequent elimination from the aneuploid pool. This mechanism helps maintain low levels of heterogeneity in aneuploid populations and may prevent detrimental evolutionary processes such as cancer progression and development of drug resistance.},
}
RevDate: 2020-12-03
Comparative Analysis of ROS Network Genes in Extremophile Eukaryotes.
International journal of molecular sciences, 21(23): pii:ijms21239131.
The reactive oxygen species (ROS) gene network, consisting of both ROS-generating and detoxifying enzymes, adjusts ROS levels in response to various stimuli. We performed a cross-kingdom comparison of ROS gene networks to investigate how they have evolved across all Eukaryotes, including protists, fungi, plants and animals. We included the genomes of 16 extremotolerant Eukaryotes to gain insight into ROS gene evolution in organisms that experience extreme stress conditions. Our analysis focused on ROS genes found in all Eukaryotes (such as catalases, superoxide dismutases, glutathione reductases, peroxidases and glutathione peroxidase/peroxiredoxins) as well as those specific to certain groups, such as ascorbate peroxidases, dehydroascorbate/monodehydroascorbate reductases in plants and other photosynthetic organisms. ROS-producing NADPH oxidases (NOX) were found in most multicellular organisms, although several NOX-like genes were identified in unicellular or filamentous species. However, despite the extreme conditions experienced by extremophile species, we found no evidence for expansion of ROS-related gene families in these species compared to other Eukaryotes. Tardigrades and rotifers do show ROS gene expansions that could be related to their extreme lifestyles, although a high rate of lineage-specific horizontal gene transfer events, coupled with recent tetraploidy in rotifers, could explain this observation. This suggests that the basal Eukaryotic ROS scavenging systems are sufficient to maintain ROS homeostasis even under the most extreme conditions.
Additional Links: PMID-33266251
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@article {pmid33266251,
year = {2020},
author = {Lyall, R and Nikoloski, Z and Gechev, T},
title = {Comparative Analysis of ROS Network Genes in Extremophile Eukaryotes.},
journal = {International journal of molecular sciences},
volume = {21},
number = {23},
pages = {},
doi = {10.3390/ijms21239131},
pmid = {33266251},
issn = {1422-0067},
support = {SGA-CSA No. 739582//Project PlantaSYST, European Union's Horizon 2020 Research & Innovation Programme/ ; GA No. 823746//Project RESIST, European Union's Horizon 2020 Research & Innovation Programme/ ; BG05M2OP001-1.003-001-C01//European Regional Development Fund/ ; },
abstract = {The reactive oxygen species (ROS) gene network, consisting of both ROS-generating and detoxifying enzymes, adjusts ROS levels in response to various stimuli. We performed a cross-kingdom comparison of ROS gene networks to investigate how they have evolved across all Eukaryotes, including protists, fungi, plants and animals. We included the genomes of 16 extremotolerant Eukaryotes to gain insight into ROS gene evolution in organisms that experience extreme stress conditions. Our analysis focused on ROS genes found in all Eukaryotes (such as catalases, superoxide dismutases, glutathione reductases, peroxidases and glutathione peroxidase/peroxiredoxins) as well as those specific to certain groups, such as ascorbate peroxidases, dehydroascorbate/monodehydroascorbate reductases in plants and other photosynthetic organisms. ROS-producing NADPH oxidases (NOX) were found in most multicellular organisms, although several NOX-like genes were identified in unicellular or filamentous species. However, despite the extreme conditions experienced by extremophile species, we found no evidence for expansion of ROS-related gene families in these species compared to other Eukaryotes. Tardigrades and rotifers do show ROS gene expansions that could be related to their extreme lifestyles, although a high rate of lineage-specific horizontal gene transfer events, coupled with recent tetraploidy in rotifers, could explain this observation. This suggests that the basal Eukaryotic ROS scavenging systems are sufficient to maintain ROS homeostasis even under the most extreme conditions.},
}
RevDate: 2020-12-02
Symbiotic Origin of Apoptosis.
Results and problems in cell differentiation, 69:253-280.
The progress of evolutionary biology has revealed that symbiosis played a basic role in the evolution of complex eukaryotic organisms, including humans. Mitochondria are actually simplified endosymbiotic bacteria currently playing the role of cellular organelles. Mitochondrial domestication occurred at the very beginning of eukaryotic evolution. Mitochondria have two different basic functions: they produce energy using oxidative respiration, and they initiate different forms of apoptotic programmed/regulated cell death. Apoptotic programmed cell death may have different cytological forms. Mechanisms of apoptotic programmed cell death exist even in the unicellular organisms, and they play a basic role in the development of complex multicellular organisms, such as fungi, green plants, and animals. Multicellularity was independently established many times among eukaryotes. There are indications that apoptotic programmed cell death is a trait required for the establishment of multicellularity. Regulated cell death is initiated by many different parallel biochemical pathways. It is generally accepted that apoptosis evolved during mitochondrial domestication. However, there are different hypothetical models of the origin of apoptosis. The phylogenetic studies of my group indicate that apoptosis probably evolved during an evolutionary arms race between host ancestral eukaryotic predators and ancestral prey mitochondria (named protomitochondria). Protomitochondrial prey produced many different toxins as a defense against predators. From these toxins evolved extant apoptotic factors. There are indications that aerobic respiration and apoptosis co-evolved and are functionally linked in extant organisms. Perturbations of apoptosis and oxidative respiration are frequently observed during neoplastic transition. Our group showed that perturbations of apoptosis in yeasts also cause perturbations of oxidative respiration.
Additional Links: PMID-33263876
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PubMed:
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@article {pmid33263876,
year = {2020},
author = {Kaczanowski, S},
title = {Symbiotic Origin of Apoptosis.},
journal = {Results and problems in cell differentiation},
volume = {69},
number = {},
pages = {253-280},
doi = {10.1007/978-3-030-51849-3_10},
pmid = {33263876},
issn = {0080-1844},
abstract = {The progress of evolutionary biology has revealed that symbiosis played a basic role in the evolution of complex eukaryotic organisms, including humans. Mitochondria are actually simplified endosymbiotic bacteria currently playing the role of cellular organelles. Mitochondrial domestication occurred at the very beginning of eukaryotic evolution. Mitochondria have two different basic functions: they produce energy using oxidative respiration, and they initiate different forms of apoptotic programmed/regulated cell death. Apoptotic programmed cell death may have different cytological forms. Mechanisms of apoptotic programmed cell death exist even in the unicellular organisms, and they play a basic role in the development of complex multicellular organisms, such as fungi, green plants, and animals. Multicellularity was independently established many times among eukaryotes. There are indications that apoptotic programmed cell death is a trait required for the establishment of multicellularity. Regulated cell death is initiated by many different parallel biochemical pathways. It is generally accepted that apoptosis evolved during mitochondrial domestication. However, there are different hypothetical models of the origin of apoptosis. The phylogenetic studies of my group indicate that apoptosis probably evolved during an evolutionary arms race between host ancestral eukaryotic predators and ancestral prey mitochondria (named protomitochondria). Protomitochondrial prey produced many different toxins as a defense against predators. From these toxins evolved extant apoptotic factors. There are indications that aerobic respiration and apoptosis co-evolved and are functionally linked in extant organisms. Perturbations of apoptosis and oxidative respiration are frequently observed during neoplastic transition. Our group showed that perturbations of apoptosis in yeasts also cause perturbations of oxidative respiration.},
}
RevDate: 2020-11-19
Transmissible cancers and the evolution of sex under the Red Queen hypothesis.
PLoS biology, 18(11):e3000916 pii:PBIOLOGY-D-20-00851.
The predominance of sexual reproduction in eukaryotes remains paradoxical in evolutionary theory. Of the hypotheses proposed to resolve this paradox, the 'Red Queen hypothesis' emphasises the potential of antagonistic interactions to cause fluctuating selection, which favours the evolution and maintenance of sex. Whereas empirical and theoretical developments have focused on host-parasite interactions, the premises of the Red Queen theory apply equally well to any type of antagonistic interactions. Recently, it has been suggested that early multicellular organisms with basic anticancer defences were presumably plagued by antagonistic interactions with transmissible cancers and that this could have played a pivotal role in the evolution of sex. Here, we dissect this argument using a population genetic model. One fundamental aspect distinguishing transmissible cancers from other parasites is the continual production of cancerous cell lines from hosts' own tissues. We show that this influx dampens fluctuating selection and therefore makes the evolution of sex more difficult than in standard Red Queen models. Although coevolutionary cycling can remain sufficient to select for sex under some parameter regions of our model, we show that the size of those regions shrinks once we account for epidemiological constraints. Altogether, our results suggest that horizontal transmission of cancerous cells is unlikely to cause fluctuating selection favouring sexual reproduction. Nonetheless, we confirm that vertical transmission of cancerous cells can promote the evolution of sex through a separate mechanism, known as similarity selection, that does not depend on coevolutionary fluctuations.
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@article {pmid33211684,
year = {2020},
author = {Aubier, TG and Galipaud, M and Erten, EY and Kokko, H},
title = {Transmissible cancers and the evolution of sex under the Red Queen hypothesis.},
journal = {PLoS biology},
volume = {18},
number = {11},
pages = {e3000916},
doi = {10.1371/journal.pbio.3000916},
pmid = {33211684},
issn = {1545-7885},
abstract = {The predominance of sexual reproduction in eukaryotes remains paradoxical in evolutionary theory. Of the hypotheses proposed to resolve this paradox, the 'Red Queen hypothesis' emphasises the potential of antagonistic interactions to cause fluctuating selection, which favours the evolution and maintenance of sex. Whereas empirical and theoretical developments have focused on host-parasite interactions, the premises of the Red Queen theory apply equally well to any type of antagonistic interactions. Recently, it has been suggested that early multicellular organisms with basic anticancer defences were presumably plagued by antagonistic interactions with transmissible cancers and that this could have played a pivotal role in the evolution of sex. Here, we dissect this argument using a population genetic model. One fundamental aspect distinguishing transmissible cancers from other parasites is the continual production of cancerous cell lines from hosts' own tissues. We show that this influx dampens fluctuating selection and therefore makes the evolution of sex more difficult than in standard Red Queen models. Although coevolutionary cycling can remain sufficient to select for sex under some parameter regions of our model, we show that the size of those regions shrinks once we account for epidemiological constraints. Altogether, our results suggest that horizontal transmission of cancerous cells is unlikely to cause fluctuating selection favouring sexual reproduction. Nonetheless, we confirm that vertical transmission of cancerous cells can promote the evolution of sex through a separate mechanism, known as similarity selection, that does not depend on coevolutionary fluctuations.},
}
RevDate: 2020-11-20
CmpDate: 2020-11-20
[Environment and immunity-Allergies and autoimmune diseases from epidemiological perspective].
Nihon eiseigaku zasshi. Japanese journal of hygiene, 75(0):.
Immunity, which denotes the protection of multicellular organisms against various bacterial and viral infections, is an essential protective mechanism for living organisms. Allergy is a reaction to a foreign substance existing in the environment that is basically not a component of the self. Additionally, autoimmune diseases are associated with the dysfunction in the recognition of self and non-self, and are pathological conditions caused by immune cells attacking their own tissues and cells. In this paper, we outline the current status of immunity with respect to the environment from the epidemiological perspective with regard to the following: (1) evolution and immunity, (2) allergy, (3) autoantibodies, (4) autoimmune diseases, (5) relationships of immunity with the environment, allergy, autoantibodies, and autoimmune diseases, and (6) celiac disease.
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@article {pmid33148926,
year = {2020},
author = {Katoh, T and Satoh, M},
title = {[Environment and immunity-Allergies and autoimmune diseases from epidemiological perspective].},
journal = {Nihon eiseigaku zasshi. Japanese journal of hygiene},
volume = {75},
number = {0},
pages = {},
doi = {10.1265/jjh.20005},
pmid = {33148926},
issn = {1882-6482},
mesh = {Adolescent ; Adult ; Aged ; Autoantibodies ; Autoimmune Diseases/epidemiology/*immunology ; *Autoimmunity ; Biological Evolution ; Celiac Disease/immunology ; Child ; Child, Preschool ; Environment ; Female ; Humans ; Hypersensitivity/epidemiology/*immunology ; Infant ; Male ; Middle Aged ; Young Adult ; },
abstract = {Immunity, which denotes the protection of multicellular organisms against various bacterial and viral infections, is an essential protective mechanism for living organisms. Allergy is a reaction to a foreign substance existing in the environment that is basically not a component of the self. Additionally, autoimmune diseases are associated with the dysfunction in the recognition of self and non-self, and are pathological conditions caused by immune cells attacking their own tissues and cells. In this paper, we outline the current status of immunity with respect to the environment from the epidemiological perspective with regard to the following: (1) evolution and immunity, (2) allergy, (3) autoantibodies, (4) autoimmune diseases, (5) relationships of immunity with the environment, allergy, autoantibodies, and autoimmune diseases, and (6) celiac disease.},
}
MeSH Terms:
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hide MeSH Terms
Adolescent
Adult
Aged
Autoantibodies
Autoimmune Diseases/epidemiology/*immunology
*Autoimmunity
Biological Evolution
Celiac Disease/immunology
Child
Child, Preschool
Environment
Female
Humans
Hypersensitivity/epidemiology/*immunology
Infant
Male
Middle Aged
Young Adult
RevDate: 2020-11-28
The Plant Target of Rapamycin: A Conduc TOR of Nutrition and Metabolism in Photosynthetic Organisms.
Genes, 11(11):.
Living organisms possess many mechanisms to sense nutrients and favorable conditions, which allow them to grow and develop. Photosynthetic organisms are very diverse, from green unicellular algae to multicellular flowering plants, but most of them are sessile and thus unable to escape from the biotic and abiotic stresses they experience. The Target of Rapamycin (TOR) signaling pathway is conserved in all eukaryotes and acts as a central regulatory hub between growth and extrinsic factors, such as nutrients or stress. However, relatively little is known about the regulations and roles of this pathway in plants and algae. Although some features of the TOR pathway seem to have been highly conserved throughout evolution, others clearly differ in plants, perhaps reflecting adaptations to different lifestyles and the rewiring of this primordial signaling module to adapt to specific requirements. Indeed, TOR is involved in plant responses to a vast array of signals including nutrients, hormones, light, stresses or pathogens. In this review, we will summarize recent studies that address the regulations of TOR by nutrients in photosynthetic organisms, and the roles of TOR in controlling important metabolic pathways, highlighting similarities and differences with the other eukaryotes.
Additional Links: PMID-33138108
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@article {pmid33138108,
year = {2020},
author = {Ingargiola, C and Turqueto Duarte, G and Robaglia, C and Leprince, AS and Meyer, C},
title = {The Plant Target of Rapamycin: A Conduc TOR of Nutrition and Metabolism in Photosynthetic Organisms.},
journal = {Genes},
volume = {11},
number = {11},
pages = {},
pmid = {33138108},
issn = {2073-4425},
support = {ECO201806006346//Fondation pour la Recherche Médicale/ ; ANR-17-EUR-0007, EUR SPS-GSR//Agence Nationale de la Recherche/ ; FP7-609398//Seventh Framework Programme/ ; },
abstract = {Living organisms possess many mechanisms to sense nutrients and favorable conditions, which allow them to grow and develop. Photosynthetic organisms are very diverse, from green unicellular algae to multicellular flowering plants, but most of them are sessile and thus unable to escape from the biotic and abiotic stresses they experience. The Target of Rapamycin (TOR) signaling pathway is conserved in all eukaryotes and acts as a central regulatory hub between growth and extrinsic factors, such as nutrients or stress. However, relatively little is known about the regulations and roles of this pathway in plants and algae. Although some features of the TOR pathway seem to have been highly conserved throughout evolution, others clearly differ in plants, perhaps reflecting adaptations to different lifestyles and the rewiring of this primordial signaling module to adapt to specific requirements. Indeed, TOR is involved in plant responses to a vast array of signals including nutrients, hormones, light, stresses or pathogens. In this review, we will summarize recent studies that address the regulations of TOR by nutrients in photosynthetic organisms, and the roles of TOR in controlling important metabolic pathways, highlighting similarities and differences with the other eukaryotes.},
}
RevDate: 2020-10-20
The Distribution of Genes Associated With Regulated Cell Death Is Decoupled From the Mitochondrial Phenotypes Within Unicellular Eukaryotic Hosts.
Frontiers in cell and developmental biology, 8:536389.
Genetically regulated cell death (RCD) occurs in all domains of life. In eukaryotes, the evolutionary origin of the mitochondrion and of certain forms of RCD, in particular apoptosis, are thought to coincide, suggesting a central general role for mitochondria in cellular suicide. We tested this mitochondrial centrality hypothesis across a dataset of 67 species of protists, presenting 5 classes of mitochondrial phenotypes, including functional mitochondria, metabolically diversified mitochondria, functionally reduced mitochondria (Mitochondrion Related Organelle or MRO) and even complete absence of mitochondria. We investigated the distribution of genes associated with various forms of RCD. No homologs for described mammalian regulators of regulated necrosis could be identified in our set of 67 unicellular taxa. Protists with MRO and the secondarily a mitochondriate Monocercomonoides exilis display heterogeneous reductions of apoptosis gene sets with respect to typical mitochondriate protists. Remarkably, despite the total lack of mitochondria in M. exilis, apoptosis-associated genes could still be identified. These same species of protists with MRO and M. exilis harbored non-reduced autophagic cell death gene sets. Moreover, transiently multicellular protist taxa appeared enriched in apoptotic and autophagy associated genes compared to free-living protists. This analysis suggests that genes associated with apoptosis in animals and the presence of the mitochondria are significant yet non-essential biological components for RCD in protists. More generally, our results support the hypothesis of a selection for RCD, including both apoptosis and autophagy, as a developmental mechanism linked to multicellularity.
Additional Links: PMID-33072737
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@article {pmid33072737,
year = {2020},
author = {Teulière, J and Bernard, G and Bapteste, E},
title = {The Distribution of Genes Associated With Regulated Cell Death Is Decoupled From the Mitochondrial Phenotypes Within Unicellular Eukaryotic Hosts.},
journal = {Frontiers in cell and developmental biology},
volume = {8},
number = {},
pages = {536389},
pmid = {33072737},
issn = {2296-634X},
abstract = {Genetically regulated cell death (RCD) occurs in all domains of life. In eukaryotes, the evolutionary origin of the mitochondrion and of certain forms of RCD, in particular apoptosis, are thought to coincide, suggesting a central general role for mitochondria in cellular suicide. We tested this mitochondrial centrality hypothesis across a dataset of 67 species of protists, presenting 5 classes of mitochondrial phenotypes, including functional mitochondria, metabolically diversified mitochondria, functionally reduced mitochondria (Mitochondrion Related Organelle or MRO) and even complete absence of mitochondria. We investigated the distribution of genes associated with various forms of RCD. No homologs for described mammalian regulators of regulated necrosis could be identified in our set of 67 unicellular taxa. Protists with MRO and the secondarily a mitochondriate Monocercomonoides exilis display heterogeneous reductions of apoptosis gene sets with respect to typical mitochondriate protists. Remarkably, despite the total lack of mitochondria in M. exilis, apoptosis-associated genes could still be identified. These same species of protists with MRO and M. exilis harbored non-reduced autophagic cell death gene sets. Moreover, transiently multicellular protist taxa appeared enriched in apoptotic and autophagy associated genes compared to free-living protists. This analysis suggests that genes associated with apoptosis in animals and the presence of the mitochondria are significant yet non-essential biological components for RCD in protists. More generally, our results support the hypothesis of a selection for RCD, including both apoptosis and autophagy, as a developmental mechanism linked to multicellularity.},
}
RevDate: 2020-11-27
Functional Long Non-coding RNAs Evolve from Junk Transcripts.
Cell, 183(5):1151-1161.
Transcriptome studies reveal pervasive transcription of complex genomes, such as those of mammals. Despite popular arguments for functionality of most, if not all, of these transcripts, genome-wide analysis of selective constraints indicates that most of the produced RNA are junk. However, junk is not garbage. On the contrary, junk transcripts provide the raw material for the evolution of diverse long non-coding (lnc) RNAs by non-adaptive mechanisms, such as constructive neutral evolution. The generation of many novel functional entities, such as lncRNAs, that fuels organismal complexity does not seem to be driven by strong positive selection. Rather, the weak selection regime that dominates the evolution of most multicellular eukaryotes provides ample material for functional innovation with relatively little adaptation involved.
Additional Links: PMID-33068526
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PubMed:
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@article {pmid33068526,
year = {2020},
author = {Palazzo, AF and Koonin, EV},
title = {Functional Long Non-coding RNAs Evolve from Junk Transcripts.},
journal = {Cell},
volume = {183},
number = {5},
pages = {1151-1161},
doi = {10.1016/j.cell.2020.09.047},
pmid = {33068526},
issn = {1097-4172},
abstract = {Transcriptome studies reveal pervasive transcription of complex genomes, such as those of mammals. Despite popular arguments for functionality of most, if not all, of these transcripts, genome-wide analysis of selective constraints indicates that most of the produced RNA are junk. However, junk is not garbage. On the contrary, junk transcripts provide the raw material for the evolution of diverse long non-coding (lnc) RNAs by non-adaptive mechanisms, such as constructive neutral evolution. The generation of many novel functional entities, such as lncRNAs, that fuels organismal complexity does not seem to be driven by strong positive selection. Rather, the weak selection regime that dominates the evolution of most multicellular eukaryotes provides ample material for functional innovation with relatively little adaptation involved.},
}
RevDate: 2020-11-26
CmpDate: 2020-11-26
Transcriptome data reveal conserved patterns of fruiting body development and response to heat stress in the mushroom-forming fungus Flammulina filiformis.
PloS one, 15(10):e0239890.
Mushroom-forming fungi are complex multicellular organisms that form the basis of a large industry, yet, our understanding of the mechanisms of mushroom development and its responses to various stresses remains limited. The winter mushroom (Flammulina filiformis) is cultivated at a large commercial scale in East Asia and is a species with a preference for low temperatures. This study investigated fruiting body development in F. filiformis by comparing transcriptomes of 4 developmental stages, and compared the developmental genes to a 200-genome dataset to identify conserved genes involved in fruiting body development, and examined the response of heat sensitive and -resistant strains to heat stress. Our data revealed widely conserved genes involved in primordium development of F. filiformis, many of which originated before the emergence of the Agaricomycetes, indicating co-option for complex multicellularity during evolution. We also revealed several notable fruiting-specific genes, including the genes with conserved stipe-specific expression patterns and the others which related to sexual development, water absorption, basidium formation and sporulation, among others. Comparative analysis revealed that heat stress induced more genes in the heat resistant strain (M1) than in the heat sensitive one (XR). Of particular importance are the hsp70, hsp90 and fes1 genes, which may facilitate the adjustment to heat stress in the early stages of fruiting body development. These data highlighted novel genes involved in complex multicellular development in fungi and aid further studies on gene function and efforts to improve the productivity and heat tolerance in mushroom-forming fungi.
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@article {pmid33064719,
year = {2020},
author = {Liu, XB and Xia, EH and Li, M and Cui, YY and Wang, PM and Zhang, JX and Xie, BG and Xu, JP and Yan, JJ and Li, J and Nagy, LG and Yang, ZL},
title = {Transcriptome data reveal conserved patterns of fruiting body development and response to heat stress in the mushroom-forming fungus Flammulina filiformis.},
journal = {PloS one},
volume = {15},
number = {10},
pages = {e0239890},
pmid = {33064719},
issn = {1932-6203},
mesh = {Agaricales/*genetics/growth & development/metabolism ; Conserved Sequence ; *Evolution, Molecular ; Fruiting Bodies, Fungal/genetics/*growth & development/metabolism ; Fungal Proteins/genetics/metabolism ; Heat-Shock Proteins/genetics/metabolism ; *Heat-Shock Response ; *Transcriptome ; },
abstract = {Mushroom-forming fungi are complex multicellular organisms that form the basis of a large industry, yet, our understanding of the mechanisms of mushroom development and its responses to various stresses remains limited. The winter mushroom (Flammulina filiformis) is cultivated at a large commercial scale in East Asia and is a species with a preference for low temperatures. This study investigated fruiting body development in F. filiformis by comparing transcriptomes of 4 developmental stages, and compared the developmental genes to a 200-genome dataset to identify conserved genes involved in fruiting body development, and examined the response of heat sensitive and -resistant strains to heat stress. Our data revealed widely conserved genes involved in primordium development of F. filiformis, many of which originated before the emergence of the Agaricomycetes, indicating co-option for complex multicellularity during evolution. We also revealed several notable fruiting-specific genes, including the genes with conserved stipe-specific expression patterns and the others which related to sexual development, water absorption, basidium formation and sporulation, among others. Comparative analysis revealed that heat stress induced more genes in the heat resistant strain (M1) than in the heat sensitive one (XR). Of particular importance are the hsp70, hsp90 and fes1 genes, which may facilitate the adjustment to heat stress in the early stages of fruiting body development. These data highlighted novel genes involved in complex multicellular development in fungi and aid further studies on gene function and efforts to improve the productivity and heat tolerance in mushroom-forming fungi.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Agaricales/*genetics/growth & development/metabolism
Conserved Sequence
*Evolution, Molecular
Fruiting Bodies, Fungal/genetics/*growth & development/metabolism
Fungal Proteins/genetics/metabolism
Heat-Shock Proteins/genetics/metabolism
*Heat-Shock Response
*Transcriptome
RevDate: 2020-10-27
CmpDate: 2020-10-27
Engineering synthetic morphogen systems that can program multicellular patterning.
Science (New York, N.Y.), 370(6514):327-331.
In metazoan tissues, cells decide their fates by sensing positional information provided by specialized morphogen proteins. To explore what features are sufficient for positional encoding, we asked whether arbitrary molecules (e.g., green fluorescent protein or mCherry) could be converted into synthetic morphogens. Synthetic morphogens expressed from a localized source formed a gradient when trapped by surface-anchoring proteins, and they could be sensed by synthetic receptors. Despite their simplicity, these morphogen systems yielded patterns reminiscent of those observed in vivo. Gradients could be reshaped by altering anchor density or by providing a source of competing inhibitor. Gradient interpretation could be altered by adding feedback loops or morphogen cascades to receiver cell response circuits. Orthogonal cell-cell communication systems provide insight into morphogen evolution and a platform for engineering tissues.
Additional Links: PMID-33060357
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PubMed:
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@article {pmid33060357,
year = {2020},
author = {Toda, S and McKeithan, WL and Hakkinen, TJ and Lopez, P and Klein, OD and Lim, WA},
title = {Engineering synthetic morphogen systems that can program multicellular patterning.},
journal = {Science (New York, N.Y.)},
volume = {370},
number = {6514},
pages = {327-331},
doi = {10.1126/science.abc0033},
pmid = {33060357},
issn = {1095-9203},
support = {F32 DK123939/DK/NIDDK NIH HHS/United States ; R01 DE028496/DE/NIDCR NIH HHS/United States ; R35 DE026602/DE/NIDCR NIH HHS/United States ; /HHMI/Howard Hughes Medical Institute/United States ; },
mesh = {Animals ; *Body Patterning ; Drosophila melanogaster/growth & development ; Fibroblasts ; Green Fluorescent Proteins/genetics/*metabolism ; Protein Engineering ; Receptors, Notch/genetics/metabolism ; Tissue Engineering/*methods ; },
abstract = {In metazoan tissues, cells decide their fates by sensing positional information provided by specialized morphogen proteins. To explore what features are sufficient for positional encoding, we asked whether arbitrary molecules (e.g., green fluorescent protein or mCherry) could be converted into synthetic morphogens. Synthetic morphogens expressed from a localized source formed a gradient when trapped by surface-anchoring proteins, and they could be sensed by synthetic receptors. Despite their simplicity, these morphogen systems yielded patterns reminiscent of those observed in vivo. Gradients could be reshaped by altering anchor density or by providing a source of competing inhibitor. Gradient interpretation could be altered by adding feedback loops or morphogen cascades to receiver cell response circuits. Orthogonal cell-cell communication systems provide insight into morphogen evolution and a platform for engineering tissues.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Body Patterning
Drosophila melanogaster/growth & development
Fibroblasts
Green Fluorescent Proteins/genetics/*metabolism
Protein Engineering
Receptors, Notch/genetics/metabolism
Tissue Engineering/*methods
RevDate: 2020-10-10
The algal selenoproteomes.
BMC genomics, 21(1):699.
BACKGROUND: Selenium is an essential trace element, and selenocysteine (Sec, U) is its predominant form in vivo. Proteins that contain Sec are selenoproteins, whose special structural features include not only the TGA codon encoding Sec but also the SECIS element in mRNA and the conservation of the Sec-flanking region. These unique features have led to the development of a series of bioinformatics methods to predict and research selenoprotein genes. There have been some studies and reports on the evolution and distribution of selenoprotein genes in prokaryotes and multicellular eukaryotes, but the systematic analysis of single-cell eukaryotes, especially algae, has been very limited.
RESULTS: In this study, we predicted selenoprotein genes in 137 species of algae by using a program we previously developed. More than 1000 selenoprotein genes were obtained. A database website was built to record these algae selenoprotein genes (www.selenoprotein.com). These genes belong to 42 selenoprotein families, including three novel selenoprotein gene families.
CONCLUSIONS: This study reveals the primordial state of the eukaryotic selenoproteome. It is an important clue to explore the significance of selenium for primordial eukaryotes and to determine the complete evolutionary spectrum of selenoproteins in all life forms.
Additional Links: PMID-33028229
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@article {pmid33028229,
year = {2020},
author = {Jiang, L and Lu, Y and Zheng, L and Li, G and Chen, L and Zhang, M and Ni, J and Liu, Q and Zhang, Y},
title = {The algal selenoproteomes.},
journal = {BMC genomics},
volume = {21},
number = {1},
pages = {699},
pmid = {33028229},
issn = {1471-2164},
support = {31401129//National Natural Science Foundation of China/ ; },
abstract = {BACKGROUND: Selenium is an essential trace element, and selenocysteine (Sec, U) is its predominant form in vivo. Proteins that contain Sec are selenoproteins, whose special structural features include not only the TGA codon encoding Sec but also the SECIS element in mRNA and the conservation of the Sec-flanking region. These unique features have led to the development of a series of bioinformatics methods to predict and research selenoprotein genes. There have been some studies and reports on the evolution and distribution of selenoprotein genes in prokaryotes and multicellular eukaryotes, but the systematic analysis of single-cell eukaryotes, especially algae, has been very limited.
RESULTS: In this study, we predicted selenoprotein genes in 137 species of algae by using a program we previously developed. More than 1000 selenoprotein genes were obtained. A database website was built to record these algae selenoprotein genes (www.selenoprotein.com). These genes belong to 42 selenoprotein families, including three novel selenoprotein gene families.
CONCLUSIONS: This study reveals the primordial state of the eukaryotic selenoproteome. It is an important clue to explore the significance of selenium for primordial eukaryotes and to determine the complete evolutionary spectrum of selenoproteins in all life forms.},
}
RevDate: 2020-10-20
Deep phylogeny of cancer drivers and compensatory mutations.
Communications biology, 3(1):551.
Driver mutations (DM) are the genetic impetus for most cancers. The DM are assumed to be deleterious in species evolution, being eliminated by purifying selection unless compensated by other mutations. We present deep phylogenies for 84 cancer driver genes and investigate the prevalence of 434 DM across gene-species trees. The DM are rare in species evolution, and 181 are completely absent, validating their negative fitness effect. The DM are more common in unicellular than in multicellular eukaryotes, suggesting a link between these mutations and cell proliferation control. 18 DM appear as the ancestral state in one or more major clades, including 3 among mammals. We identify within-gene, compensatory mutations for 98 DM and infer likely interactions between the DM and compensatory sites in protein structures. These findings elucidate the evolutionary status of DM and are expected to advance the understanding of the functions and evolution of oncogenes and tumor suppressors.
Additional Links: PMID-33009502
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@article {pmid33009502,
year = {2020},
author = {Rochman, ND and Wolf, YI and Koonin, EV},
title = {Deep phylogeny of cancer drivers and compensatory mutations.},
journal = {Communications biology},
volume = {3},
number = {1},
pages = {551},
pmid = {33009502},
issn = {2399-3642},
abstract = {Driver mutations (DM) are the genetic impetus for most cancers. The DM are assumed to be deleterious in species evolution, being eliminated by purifying selection unless compensated by other mutations. We present deep phylogenies for 84 cancer driver genes and investigate the prevalence of 434 DM across gene-species trees. The DM are rare in species evolution, and 181 are completely absent, validating their negative fitness effect. The DM are more common in unicellular than in multicellular eukaryotes, suggesting a link between these mutations and cell proliferation control. 18 DM appear as the ancestral state in one or more major clades, including 3 among mammals. We identify within-gene, compensatory mutations for 98 DM and infer likely interactions between the DM and compensatory sites in protein structures. These findings elucidate the evolutionary status of DM and are expected to advance the understanding of the functions and evolution of oncogenes and tumor suppressors.},
}
RevDate: 2020-09-26
Toward the Discovery of Host-Defense Peptides in Plants.
Frontiers in immunology, 11:1825.
Defense peptides protect multicellular eukaryotes from infections. In biomedical sciences, a dominant conceptual framework refers to defense peptides as host-defense peptides (HDPs), which are bifunctional peptides with both direct antimicrobial and immunomodulatory activities. No HDP has been reported in plants so far, and the very concept of HDP has not been captured yet by the plant science community. Plant science thus lacks the conceptual framework that would coordinate research efforts aimed at discovering plant HDPs. In this perspective article, I used bibliometric and literature survey approaches to raise awareness about the HDP concept among plant scientists, and to encourage research efforts aimed at discovering plant HDPs. Such discovery would enrich our comprehension of the function and evolution of the plant immune system, and provide us with novel molecular tools to develop innovative strategies to control crop diseases.
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@article {pmid32973760,
year = {2020},
author = {Petre, B},
title = {Toward the Discovery of Host-Defense Peptides in Plants.},
journal = {Frontiers in immunology},
volume = {11},
number = {},
pages = {1825},
pmid = {32973760},
issn = {1664-3224},
abstract = {Defense peptides protect multicellular eukaryotes from infections. In biomedical sciences, a dominant conceptual framework refers to defense peptides as host-defense peptides (HDPs), which are bifunctional peptides with both direct antimicrobial and immunomodulatory activities. No HDP has been reported in plants so far, and the very concept of HDP has not been captured yet by the plant science community. Plant science thus lacks the conceptual framework that would coordinate research efforts aimed at discovering plant HDPs. In this perspective article, I used bibliometric and literature survey approaches to raise awareness about the HDP concept among plant scientists, and to encourage research efforts aimed at discovering plant HDPs. Such discovery would enrich our comprehension of the function and evolution of the plant immune system, and provide us with novel molecular tools to develop innovative strategies to control crop diseases.},
}
RevDate: 2020-10-02
CmpDate: 2020-09-30
Entamoeba and Giardia parasites implicated as hosts of CRESS viruses.
Nature communications, 11(1):4620.
Metagenomic techniques have enabled genome sequencing of unknown viruses without isolation in cell culture, but information on the virus host is often lacking, preventing viral characterisation. High-throughput methods capable of identifying virus hosts based on genomic data alone would aid evaluation of their medical or biological relevance. Here, we address this by linking metagenomic discovery of three virus families in human stool samples with determination of probable hosts. Recombination between viruses provides evidence of a shared host, in which genetic exchange occurs. We utilise networks of viral recombination to delimit virus-host clusters, which are then anchored to specific hosts using (1) statistical association to a host organism in clinical samples, (2) endogenous viral elements in host genomes, and (3) evidence of host small RNA responses to these elements. This analysis suggests two CRESS virus families (Naryaviridae and Nenyaviridae) infect Entamoeba parasites, while a third (Vilyaviridae) infects Giardia duodenalis. The trio supplements five CRESS virus families already known to infect eukaryotes, extending the CRESS virus host range to protozoa. Phylogenetic analysis implies CRESS viruses infecting multicellular life have evolved independently on at least three occasions.
Additional Links: PMID-32934242
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@article {pmid32934242,
year = {2020},
author = {Kinsella, CM and Bart, A and Deijs, M and Broekhuizen, P and Kaczorowska, J and Jebbink, MF and van Gool, T and Cotten, M and van der Hoek, L},
title = {Entamoeba and Giardia parasites implicated as hosts of CRESS viruses.},
journal = {Nature communications},
volume = {11},
number = {1},
pages = {4620},
pmid = {32934242},
issn = {2041-1723},
mesh = {Adult ; Cohort Studies ; Entamoeba/*virology ; Feces/parasitology/virology ; Female ; Genome, Viral ; Giardia/*virology ; Host Specificity ; Humans ; Male ; Middle Aged ; Phylogeny ; Virus Physiological Phenomena ; Viruses/classification/genetics ; Young Adult ; },
abstract = {Metagenomic techniques have enabled genome sequencing of unknown viruses without isolation in cell culture, but information on the virus host is often lacking, preventing viral characterisation. High-throughput methods capable of identifying virus hosts based on genomic data alone would aid evaluation of their medical or biological relevance. Here, we address this by linking metagenomic discovery of three virus families in human stool samples with determination of probable hosts. Recombination between viruses provides evidence of a shared host, in which genetic exchange occurs. We utilise networks of viral recombination to delimit virus-host clusters, which are then anchored to specific hosts using (1) statistical association to a host organism in clinical samples, (2) endogenous viral elements in host genomes, and (3) evidence of host small RNA responses to these elements. This analysis suggests two CRESS virus families (Naryaviridae and Nenyaviridae) infect Entamoeba parasites, while a third (Vilyaviridae) infects Giardia duodenalis. The trio supplements five CRESS virus families already known to infect eukaryotes, extending the CRESS virus host range to protozoa. Phylogenetic analysis implies CRESS viruses infecting multicellular life have evolved independently on at least three occasions.},
}
MeSH Terms:
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Adult
Cohort Studies
Entamoeba/*virology
Feces/parasitology/virology
Female
Genome, Viral
Giardia/*virology
Host Specificity
Humans
Male
Middle Aged
Phylogeny
Virus Physiological Phenomena
Viruses/classification/genetics
Young Adult
RevDate: 2020-09-15
The evolution of universal adaptations of life is driven by universal properties of matter: energy, entropy, and interaction.
F1000Research, 9:626.
The evolution of multicellular eukaryotes expresses two sorts of adaptations: local adaptations like fur or feathers, which characterize species in particular environments, and universal adaptations like microbiomes or sexual reproduction, which characterize most multicellulars in any environment. We reason that the mechanisms driving the universal adaptations of multicellulars should themselves be universal, and propose a mechanism based on properties of matter and systems: energy, entropy, and interaction. Energy from the sun, earth and beyond creates new arrangements and interactions. Metabolic networks channel some of this energy to form cooperating, interactive arrangements. Entropy, used here as a term for all forces that dismantle ordered structures (rather than as a physical quantity), acts as a selective force. Entropy selects for arrangements that resist it long enough to replicate, and dismantles those that do not. Interactions, energy-charged and dynamic, restrain entropy and enable survival and propagation of integrated living systems. This fosters survival-of-the-fitted - those entities that resist entropic destruction - and not only of the fittest - the entities with the greatest reproductive success. The "unit" of evolution is not a discrete entity, such as a gene, individual, or species; what evolves are collections of related interactions at multiple scales. Survival-of-the-fitted explains universal adaptations, including resident microbiomes, sexual reproduction, continuous diversification, programmed turnover, seemingly wasteful phenotypes, altruism, co-evolving environmental niches, and advancing complexity. Indeed survival-of-the-fittest may be a particular case of the survival-of-the-fitted mechanism, promoting local adaptations that express reproductive advantages in addition to resisting entropy. Survival-of-the-fitted accounts for phenomena that have been attributed to neutral evolution: in the face of entropy, there is no neutrality; all variations are challenged by ubiquitous energy and entropy, retaining those that are "fit enough". We propose experiments to test predictions of the survival-of-the-fitted theory, and discuss implications for the wellbeing of humans and the biosphere.
Additional Links: PMID-32802320
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@article {pmid32802320,
year = {2020},
author = {Cohen, IR and Marron, A},
title = {The evolution of universal adaptations of life is driven by universal properties of matter: energy, entropy, and interaction.},
journal = {F1000Research},
volume = {9},
number = {},
pages = {626},
doi = {10.12688/f1000research.24447.3},
pmid = {32802320},
issn = {2046-1402},
abstract = {The evolution of multicellular eukaryotes expresses two sorts of adaptations: local adaptations like fur or feathers, which characterize species in particular environments, and universal adaptations like microbiomes or sexual reproduction, which characterize most multicellulars in any environment. We reason that the mechanisms driving the universal adaptations of multicellulars should themselves be universal, and propose a mechanism based on properties of matter and systems: energy, entropy, and interaction. Energy from the sun, earth and beyond creates new arrangements and interactions. Metabolic networks channel some of this energy to form cooperating, interactive arrangements. Entropy, used here as a term for all forces that dismantle ordered structures (rather than as a physical quantity), acts as a selective force. Entropy selects for arrangements that resist it long enough to replicate, and dismantles those that do not. Interactions, energy-charged and dynamic, restrain entropy and enable survival and propagation of integrated living systems. This fosters survival-of-the-fitted - those entities that resist entropic destruction - and not only of the fittest - the entities with the greatest reproductive success. The "unit" of evolution is not a discrete entity, such as a gene, individual, or species; what evolves are collections of related interactions at multiple scales. Survival-of-the-fitted explains universal adaptations, including resident microbiomes, sexual reproduction, continuous diversification, programmed turnover, seemingly wasteful phenotypes, altruism, co-evolving environmental niches, and advancing complexity. Indeed survival-of-the-fittest may be a particular case of the survival-of-the-fitted mechanism, promoting local adaptations that express reproductive advantages in addition to resisting entropy. Survival-of-the-fitted accounts for phenomena that have been attributed to neutral evolution: in the face of entropy, there is no neutrality; all variations are challenged by ubiquitous energy and entropy, retaining those that are "fit enough". We propose experiments to test predictions of the survival-of-the-fitted theory, and discuss implications for the wellbeing of humans and the biosphere.},
}
RevDate: 2020-11-23
Structural characterization and computational analysis of PDZ domains in Monosiga brevicollis.
Protein science : a publication of the Protein Society, 29(11):2226-2244.
Identification of the molecular networks that facilitated the evolution of multicellular animals from their unicellular ancestors is a fundamental problem in evolutionary cellular biology. Choanoflagellates are recognized as the closest extant nonmetazoan ancestors to animals. These unicellular eukaryotes can adopt a multicellular-like "rosette" state. Therefore, they are compelling models for the study of early multicellularity. Comparative studies revealed that a number of putative human orthologs are present in choanoflagellate genomes, suggesting that a subset of these genes were necessary for the emergence of multicellularity. However, previous work is largely based on sequence alignments alone, which does not confirm structural nor functional similarity. Here, we focus on the PDZ domain, a peptide-binding domain which plays critical roles in myriad cellular signaling networks and which underwent a gene family expansion in metazoan lineages. Using a customized sequence similarity search algorithm, we identified 178 PDZ domains in the Monosiga brevicollis proteome. This includes 11 previously unidentified sequences, which we analyzed using Rosetta and homology modeling. To assess conservation of protein structure, we solved high-resolution crystal structures of representative M. brevicollis PDZ domains that are homologous to human Dlg1 PDZ2, Dlg1 PDZ3, GIPC, and SHANK1 PDZ domains. To assess functional conservation, we calculated binding affinities for mbGIPC, mbSHANK1, mbSNX27, and mbDLG-3 PDZ domains from M. brevicollis. Overall, we find that peptide selectivity is generally conserved between these two disparate organisms, with one possible exception, mbDLG-3. Overall, our results provide novel insight into signaling pathways in a choanoflagellate model of primitive multicellularity.
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@article {pmid32914530,
year = {2020},
author = {Gao, M and Mackley, IGP and Mesbahi-Vasey, S and Bamonte, HA and Struyvenberg, SA and Landolt, L and Pederson, NJ and Williams, LI and Bahl, CD and Brooks, L and Amacher, JF},
title = {Structural characterization and computational analysis of PDZ domains in Monosiga brevicollis.},
journal = {Protein science : a publication of the Protein Society},
volume = {29},
number = {11},
pages = {2226-2244},
pmid = {32914530},
issn = {1469-896X},
support = {S10OD021832/NH/NIH HHS/United States ; S10 OD021832/OD/NIH HHS/United States ; /HHMI/Howard Hughes Medical Institute/United States ; },
abstract = {Identification of the molecular networks that facilitated the evolution of multicellular animals from their unicellular ancestors is a fundamental problem in evolutionary cellular biology. Choanoflagellates are recognized as the closest extant nonmetazoan ancestors to animals. These unicellular eukaryotes can adopt a multicellular-like "rosette" state. Therefore, they are compelling models for the study of early multicellularity. Comparative studies revealed that a number of putative human orthologs are present in choanoflagellate genomes, suggesting that a subset of these genes were necessary for the emergence of multicellularity. However, previous work is largely based on sequence alignments alone, which does not confirm structural nor functional similarity. Here, we focus on the PDZ domain, a peptide-binding domain which plays critical roles in myriad cellular signaling networks and which underwent a gene family expansion in metazoan lineages. Using a customized sequence similarity search algorithm, we identified 178 PDZ domains in the Monosiga brevicollis proteome. This includes 11 previously unidentified sequences, which we analyzed using Rosetta and homology modeling. To assess conservation of protein structure, we solved high-resolution crystal structures of representative M. brevicollis PDZ domains that are homologous to human Dlg1 PDZ2, Dlg1 PDZ3, GIPC, and SHANK1 PDZ domains. To assess functional conservation, we calculated binding affinities for mbGIPC, mbSHANK1, mbSNX27, and mbDLG-3 PDZ domains from M. brevicollis. Overall, we find that peptide selectivity is generally conserved between these two disparate organisms, with one possible exception, mbDLG-3. Overall, our results provide novel insight into signaling pathways in a choanoflagellate model of primitive multicellularity.},
}
RevDate: 2020-10-01
CmpDate: 2020-09-21
Amalgamated cross-species transcriptomes reveal organ-specific propensity in gene expression evolution.
Nature communications, 11(1):4459.
The origins of multicellular physiology are tied to evolution of gene expression. Genes can shift expression as organisms evolve, but how ancestral expression influences altered descendant expression is not well understood. To examine this, we amalgamate 1,903 RNA-seq datasets from 182 research projects, including 6 organs in 21 vertebrate species. Quality control eliminates project-specific biases, and expression shifts are reconstructed using gene-family-wise phylogenetic Ornstein-Uhlenbeck models. Expression shifts following gene duplication result in more drastic changes in expression properties than shifts without gene duplication. The expression properties are tightly coupled with protein evolutionary rate, depending on whether and how gene duplication occurred. Fluxes in expression patterns among organs are nonrandom, forming modular connections that are reshaped by gene duplication. Thus, if expression shifts, ancestral expression in some organs induces a strong propensity for expression in particular organs in descendants. Regardless of whether the shifts are adaptive or not, this supports a major role for what might be termed preadaptive pathways of gene expression evolution.
Additional Links: PMID-32900997
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@article {pmid32900997,
year = {2020},
author = {Fukushima, K and Pollock, DD},
title = {Amalgamated cross-species transcriptomes reveal organ-specific propensity in gene expression evolution.},
journal = {Nature communications},
volume = {11},
number = {1},
pages = {4459},
pmid = {32900997},
issn = {2041-1723},
support = {R01 GM083127/GM/NIGMS NIH HHS/United States ; },
mesh = {Animals ; Databases, Nucleic Acid ; *Evolution, Molecular ; Female ; Gene Duplication ; Humans ; Male ; Models, Genetic ; Multigene Family ; Organ Specificity ; Phylogeny ; Proteins/genetics ; RNA-Seq ; Species Specificity ; *Transcriptome ; Vertebrates/classification/genetics ; },
abstract = {The origins of multicellular physiology are tied to evolution of gene expression. Genes can shift expression as organisms evolve, but how ancestral expression influences altered descendant expression is not well understood. To examine this, we amalgamate 1,903 RNA-seq datasets from 182 research projects, including 6 organs in 21 vertebrate species. Quality control eliminates project-specific biases, and expression shifts are reconstructed using gene-family-wise phylogenetic Ornstein-Uhlenbeck models. Expression shifts following gene duplication result in more drastic changes in expression properties than shifts without gene duplication. The expression properties are tightly coupled with protein evolutionary rate, depending on whether and how gene duplication occurred. Fluxes in expression patterns among organs are nonrandom, forming modular connections that are reshaped by gene duplication. Thus, if expression shifts, ancestral expression in some organs induces a strong propensity for expression in particular organs in descendants. Regardless of whether the shifts are adaptive or not, this supports a major role for what might be termed preadaptive pathways of gene expression evolution.},
}
MeSH Terms:
show MeSH Terms
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Animals
Databases, Nucleic Acid
*Evolution, Molecular
Female
Gene Duplication
Humans
Male
Models, Genetic
Multigene Family
Organ Specificity
Phylogeny
Proteins/genetics
RNA-Seq
Species Specificity
*Transcriptome
Vertebrates/classification/genetics
RevDate: 2020-11-30
A model of autowave self-organization as a hierarchy of active media in the biological evolution.
Bio Systems, 198:104234.
Within the framework of the active media concept, we develop a biophysical model of autowave self-organization which is treated as a hierarchy of active media in the evolution of the biosphere. We also propose a mathematical model of the autowave process of speciation in a flow of mutations for the three main taxonometric groups (prokaryotes, unicellular and multicellular eukaryotes) with a naturally determined lower boundary of living matter (the appearance of prokaryotes) and an open upper boundary for the formation of new species. It is shown that the fluctuation-bifurcation description of the evolution for the formation of new taxonometric groups as a trajectory of transformation of small fluctuations into giant ones adequately reflects the process of self-organization during the formation of taxa. The major concepts of biological evolution, conditions of hierarchy formation as a fundamental manifestation of self-organization and complexity in the evolution of biological systems are considered.
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@article {pmid32889101,
year = {2020},
author = {Sidorova, A and Tverdislov, V and Levashova, N and Garaeva, A},
title = {A model of autowave self-organization as a hierarchy of active media in the biological evolution.},
journal = {Bio Systems},
volume = {198},
number = {},
pages = {104234},
doi = {10.1016/j.biosystems.2020.104234},
pmid = {32889101},
issn = {1872-8324},
abstract = {Within the framework of the active media concept, we develop a biophysical model of autowave self-organization which is treated as a hierarchy of active media in the evolution of the biosphere. We also propose a mathematical model of the autowave process of speciation in a flow of mutations for the three main taxonometric groups (prokaryotes, unicellular and multicellular eukaryotes) with a naturally determined lower boundary of living matter (the appearance of prokaryotes) and an open upper boundary for the formation of new species. It is shown that the fluctuation-bifurcation description of the evolution for the formation of new taxonometric groups as a trajectory of transformation of small fluctuations into giant ones adequately reflects the process of self-organization during the formation of taxa. The major concepts of biological evolution, conditions of hierarchy formation as a fundamental manifestation of self-organization and complexity in the evolution of biological systems are considered.},
}
RevDate: 2020-09-01
Embryo-like features in developing Bacillus subtilis biofilms.
Molecular biology and evolution pii:5900268 [Epub ahead of print].
Correspondence between evolution and development has been discussed for more than two centuries. Recent work reveals that phylogeny-ontogeny correlations are indeed present in developmental transcriptomes of eukaryotic clades with complex multicellularity. Nevertheless, it has been largely ignored that the pervasive presence of phylogeny-ontogeny correlations is a hallmark of development in eukaryotes. This perspective opens a possibility to look for similar parallelisms in biological settings where developmental logic and multicellular complexity are more obscure. For instance, it has been increasingly recognized that multicellular behaviour underlies biofilm formation in bacteria. However, it remains unclear whether bacterial biofilm growth shares some basic principles with development in complex eukaryotes. Here we show that the ontogeny of growing Bacillus subtilis biofilms recapitulates phylogeny at the expression level. Using time-resolved transcriptome and proteome profiles, we found that biofilm ontogeny correlates with the evolutionary measures, in a way that evolutionary younger and more diverged genes were increasingly expressed towards later timepoints of biofilm growth. Molecular and morphological signatures also revealed that biofilm growth is highly regulated and organized into discrete ontogenetic stages, analogous to those of eukaryotic embryos. Together, this suggests that biofilm formation in Bacillus is a bona fide developmental process comparable to organismal development in animals, plants and fungi. Given that most cells on Earth reside in the form of biofilms and that biofilms represent the oldest known fossils, we anticipate that the widely-adopted vision of the first life as a single-cell and free-living organism needs rethinking.
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@article {pmid32871001,
year = {2020},
author = {Futo, M and Opašić, L and Koska, S and Čorak, N and Široki, T and Ravikumar, V and Thorsell, A and Lenuzzi, M and Kifer, D and Domazet-Lošo, M and Vlahoviček, K and Mijakovic, I and Domazet-Lošo, T},
title = {Embryo-like features in developing Bacillus subtilis biofilms.},
journal = {Molecular biology and evolution},
volume = {},
number = {},
pages = {},
doi = {10.1093/molbev/msaa217},
pmid = {32871001},
issn = {1537-1719},
abstract = {Correspondence between evolution and development has been discussed for more than two centuries. Recent work reveals that phylogeny-ontogeny correlations are indeed present in developmental transcriptomes of eukaryotic clades with complex multicellularity. Nevertheless, it has been largely ignored that the pervasive presence of phylogeny-ontogeny correlations is a hallmark of development in eukaryotes. This perspective opens a possibility to look for similar parallelisms in biological settings where developmental logic and multicellular complexity are more obscure. For instance, it has been increasingly recognized that multicellular behaviour underlies biofilm formation in bacteria. However, it remains unclear whether bacterial biofilm growth shares some basic principles with development in complex eukaryotes. Here we show that the ontogeny of growing Bacillus subtilis biofilms recapitulates phylogeny at the expression level. Using time-resolved transcriptome and proteome profiles, we found that biofilm ontogeny correlates with the evolutionary measures, in a way that evolutionary younger and more diverged genes were increasingly expressed towards later timepoints of biofilm growth. Molecular and morphological signatures also revealed that biofilm growth is highly regulated and organized into discrete ontogenetic stages, analogous to those of eukaryotic embryos. Together, this suggests that biofilm formation in Bacillus is a bona fide developmental process comparable to organismal development in animals, plants and fungi. Given that most cells on Earth reside in the form of biofilms and that biofilms represent the oldest known fossils, we anticipate that the widely-adopted vision of the first life as a single-cell and free-living organism needs rethinking.},
}
RevDate: 2020-10-28
CmpDate: 2020-10-28
Enhancer evolutionary co-option through shared chromatin accessibility input.
Proceedings of the National Academy of Sciences of the United States of America, 117(34):20636-20644.
The diversity of forms in multicellular organisms originates largely from the spatial redeployment of developmental genes [S. B. Carroll, Cell 134, 25-36 (2008)]. Several scenarios can explain the emergence of cis-regulatory elements that govern novel aspects of a gene expression pattern [M. Rebeiz, M. Tsiantis, Curr. Opin. Genet. Dev. 45, 115-123 (2017)]. One scenario, enhancer co-option, holds that a DNA sequence producing an ancestral regulatory activity also becomes the template for a new regulatory activity, sharing regulatory information. While enhancer co-option might fuel morphological diversification, it has rarely been documented [W. J. Glassford et al., Dev. Cell 34, 520-531 (2015)]. Moreover, if two regulatory activities are borne from the same sequence, their modularity, considered a defining feature of enhancers [J. Banerji, L. Olson, W. Schaffner, Cell 33, 729-740 (1983)], might be affected by pleiotropy. Sequence overlap may thereby play a determinant role in enhancer function and evolution. Here, we investigated this problem with two regulatory activities of the Drosophila gene yellow, the novel spot enhancer and the ancestral wing blade enhancer. We used precise and comprehensive quantification of each activity in Drosophila wings to systematically map their sequences along the locus. We show that the spot enhancer has co-opted the sequences of the wing blade enhancer. We also identified a pleiotropic site necessary for DNA accessibility of a shared regulatory region. While the evolutionary steps leading to the derived activity are still unknown, such pleiotropy suggests that enhancer accessibility could be one of the molecular mechanisms seeding evolutionary co-option.
Additional Links: PMID-32778581
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@article {pmid32778581,
year = {2020},
author = {Xin, Y and Le Poul, Y and Ling, L and Museridze, M and Mühling, B and Jaenichen, R and Osipova, E and Gompel, N},
title = {Enhancer evolutionary co-option through shared chromatin accessibility input.},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {117},
number = {34},
pages = {20636-20644},
pmid = {32778581},
issn = {1091-6490},
mesh = {Animals ; Biological Evolution ; Chromatin/genetics/metabolism ; Drosophila Proteins/*genetics/metabolism ; Drosophila melanogaster/genetics ; Enhancer Elements, Genetic/*genetics ; Evolution, Molecular ; Gene Expression Regulation, Developmental/*genetics ; Regulatory Elements, Transcriptional/genetics ; Wings, Animal/metabolism ; },
abstract = {The diversity of forms in multicellular organisms originates largely from the spatial redeployment of developmental genes [S. B. Carroll, Cell 134, 25-36 (2008)]. Several scenarios can explain the emergence of cis-regulatory elements that govern novel aspects of a gene expression pattern [M. Rebeiz, M. Tsiantis, Curr. Opin. Genet. Dev. 45, 115-123 (2017)]. One scenario, enhancer co-option, holds that a DNA sequence producing an ancestral regulatory activity also becomes the template for a new regulatory activity, sharing regulatory information. While enhancer co-option might fuel morphological diversification, it has rarely been documented [W. J. Glassford et al., Dev. Cell 34, 520-531 (2015)]. Moreover, if two regulatory activities are borne from the same sequence, their modularity, considered a defining feature of enhancers [J. Banerji, L. Olson, W. Schaffner, Cell 33, 729-740 (1983)], might be affected by pleiotropy. Sequence overlap may thereby play a determinant role in enhancer function and evolution. Here, we investigated this problem with two regulatory activities of the Drosophila gene yellow, the novel spot enhancer and the ancestral wing blade enhancer. We used precise and comprehensive quantification of each activity in Drosophila wings to systematically map their sequences along the locus. We show that the spot enhancer has co-opted the sequences of the wing blade enhancer. We also identified a pleiotropic site necessary for DNA accessibility of a shared regulatory region. While the evolutionary steps leading to the derived activity are still unknown, such pleiotropy suggests that enhancer accessibility could be one of the molecular mechanisms seeding evolutionary co-option.},
}
MeSH Terms:
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Animals
Biological Evolution
Chromatin/genetics/metabolism
Drosophila Proteins/*genetics/metabolism
Drosophila melanogaster/genetics
Enhancer Elements, Genetic/*genetics
Evolution, Molecular
Gene Expression Regulation, Developmental/*genetics
Regulatory Elements, Transcriptional/genetics
Wings, Animal/metabolism
RevDate: 2020-08-10
Insights From the Ecology of Information to Cancer Control.
Cancer control : journal of the Moffitt Cancer Center, 27(3):1073274820945980.
Uniquely in nature, living systems must acquire, store, and act upon information. The survival and replicative fate of each normal cell in a multicellular organism is determined solely by information obtained from its surrounding tissue. In contrast, cancer cells as single-cell eukaryotes live in a disrupted, heterogeneous environment with opportunities and hazards. Thus, cancer cells, unlike normal somatic cells, must constantly obtain information from their environment to ensure survival and proliferation. In this study, we build upon a simple mathematical modeling framework developed to predict (1) how information promotes population persistence in a highly heterogeneous environment and (2) how disruption of information resulting from habitat fragmentation increases the probability of population extinction. Because (1) tumors grow in a highly heterogeneous microenvironment and (2) many cancer therapies fragment tumors into isolated, small cancer cell populations, we identify parallels between these 2 systems and develop ideas for cancer cure based on lessons gleaned from Anthropocene extinctions. In many Anthropocene extinctions, such as that of the North American heath hen (Tympanuchus cupido cupido), a large and widespread population was initially reduced and fragmented owing to overexploitation by humans (a "first strike"). After this, the small surviving populations are vulnerable to extinction from environmental or demographic stochastic disturbances (a "second strike"). Following this analogy, after a tumor is fragmented into small populations of isolated cancer cells by an initial therapy, additional treatment can be applied with the intent of extinction (cure). Disrupting a cancer cell's ability to acquire and use information in a heterogeneous environment may be an important tactic for causing extinction following an effective initial therapy. Thus, information, from the scale of cells within tumors to that of species within ecosystems, can be used to identify vulnerabilities to extinction and opportunities for novel treatment strategies.
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@article {pmid32762341,
year = {2020},
author = {Whelan, CJ and Avdieiev, SS and Gatenby, RA},
title = {Insights From the Ecology of Information to Cancer Control.},
journal = {Cancer control : journal of the Moffitt Cancer Center},
volume = {27},
number = {3},
pages = {1073274820945980},
doi = {10.1177/1073274820945980},
pmid = {32762341},
issn = {1526-2359},
abstract = {Uniquely in nature, living systems must acquire, store, and act upon information. The survival and replicative fate of each normal cell in a multicellular organism is determined solely by information obtained from its surrounding tissue. In contrast, cancer cells as single-cell eukaryotes live in a disrupted, heterogeneous environment with opportunities and hazards. Thus, cancer cells, unlike normal somatic cells, must constantly obtain information from their environment to ensure survival and proliferation. In this study, we build upon a simple mathematical modeling framework developed to predict (1) how information promotes population persistence in a highly heterogeneous environment and (2) how disruption of information resulting from habitat fragmentation increases the probability of population extinction. Because (1) tumors grow in a highly heterogeneous microenvironment and (2) many cancer therapies fragment tumors into isolated, small cancer cell populations, we identify parallels between these 2 systems and develop ideas for cancer cure based on lessons gleaned from Anthropocene extinctions. In many Anthropocene extinctions, such as that of the North American heath hen (Tympanuchus cupido cupido), a large and widespread population was initially reduced and fragmented owing to overexploitation by humans (a "first strike"). After this, the small surviving populations are vulnerable to extinction from environmental or demographic stochastic disturbances (a "second strike"). Following this analogy, after a tumor is fragmented into small populations of isolated cancer cells by an initial therapy, additional treatment can be applied with the intent of extinction (cure). Disrupting a cancer cell's ability to acquire and use information in a heterogeneous environment may be an important tactic for causing extinction following an effective initial therapy. Thus, information, from the scale of cells within tumors to that of species within ecosystems, can be used to identify vulnerabilities to extinction and opportunities for novel treatment strategies.},
}
RevDate: 2020-09-02
CmpDate: 2020-09-02
The evolution of multicellular complexity: the role of relatedness and environmental constraints.
Proceedings. Biological sciences, 287(1931):20192963.
A major challenge in evolutionary biology has been to explain the variation in multicellularity across the many independently evolved multicellular lineages, from slime moulds to vertebrates. Social evolution theory has highlighted the key role of relatedness in determining multicellular complexity and obligateness; however, there is a need to extend this to a broader perspective incorporating the role of the environment. In this paper, we formally test Bonner's 1998 hypothesis that the environment is crucial in determining the course of multicellular evolution, with aggregative multicellularity evolving more frequently on land and clonal multicellularity more frequently in water. Using a combination of scaling theory and phylogenetic comparative analyses, we describe multicellular organizational complexity across 139 species spanning 14 independent transitions to multicellularity and investigate the role of the environment in determining multicellular group formation and in imposing constraints on multicellular evolution. Our results, showing that the physical environment has impacted the way in which multicellular groups form, highlight that environmental conditions might have affected the major evolutionary transition to obligate multicellularity.
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@article {pmid32693719,
year = {2020},
author = {Fisher, RM and Shik, JZ and Boomsma, JJ},
title = {The evolution of multicellular complexity: the role of relatedness and environmental constraints.},
journal = {Proceedings. Biological sciences},
volume = {287},
number = {1931},
pages = {20192963},
pmid = {32693719},
issn = {1471-2954},
mesh = {Animals ; *Biological Evolution ; Phylogeny ; },
abstract = {A major challenge in evolutionary biology has been to explain the variation in multicellularity across the many independently evolved multicellular lineages, from slime moulds to vertebrates. Social evolution theory has highlighted the key role of relatedness in determining multicellular complexity and obligateness; however, there is a need to extend this to a broader perspective incorporating the role of the environment. In this paper, we formally test Bonner's 1998 hypothesis that the environment is crucial in determining the course of multicellular evolution, with aggregative multicellularity evolving more frequently on land and clonal multicellularity more frequently in water. Using a combination of scaling theory and phylogenetic comparative analyses, we describe multicellular organizational complexity across 139 species spanning 14 independent transitions to multicellularity and investigate the role of the environment in determining multicellular group formation and in imposing constraints on multicellular evolution. Our results, showing that the physical environment has impacted the way in which multicellular groups form, highlight that environmental conditions might have affected the major evolutionary transition to obligate multicellularity.},
}
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Animals
*Biological Evolution
Phylogeny
RevDate: 2020-11-20
Evolution of Regulated Transcription.
Cells, 9(7):.
The genomes of all organisms abound with various cis-regulatory elements, which control gene activity. Transcriptional enhancers are a key group of such elements in eukaryotes and are DNA regions that form physical contacts with gene promoters and precisely orchestrate gene expression programs. Here, we follow gradual evolution of this regulatory system and discuss its features in different organisms. In eubacteria, an enhancer-like element is often a single regulatory element, is usually proximal to the core promoter, and is occupied by one or a few activators. Activation of gene expression in archaea is accompanied by the recruitment of an activator to several enhancer-like sites in the upstream promoter region. In eukaryotes, activation of expression is accompanied by the recruitment of activators to multiple enhancers, which may be distant from the core promoter, and the activators act through coactivators. The role of the general DNA architecture in transcription control increases in evolution. As a whole, it can be seen that enhancers of multicellular eukaryotes evolved from the corresponding prototypic enhancer-like regulatory elements with the gradually increasing genome size of organisms.
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@article {pmid32664620,
year = {2020},
author = {Bylino, OV and Ibragimov, AN and Shidlovskii, YV},
title = {Evolution of Regulated Transcription.},
journal = {Cells},
volume = {9},
number = {7},
pages = {},
pmid = {32664620},
issn = {2073-4409},
abstract = {The genomes of all organisms abound with various cis-regulatory elements, which control gene activity. Transcriptional enhancers are a key group of such elements in eukaryotes and are DNA regions that form physical contacts with gene promoters and precisely orchestrate gene expression programs. Here, we follow gradual evolution of this regulatory system and discuss its features in different organisms. In eubacteria, an enhancer-like element is often a single regulatory element, is usually proximal to the core promoter, and is occupied by one or a few activators. Activation of gene expression in archaea is accompanied by the recruitment of an activator to several enhancer-like sites in the upstream promoter region. In eukaryotes, activation of expression is accompanied by the recruitment of activators to multiple enhancers, which may be distant from the core promoter, and the activators act through coactivators. The role of the general DNA architecture in transcription control increases in evolution. As a whole, it can be seen that enhancers of multicellular eukaryotes evolved from the corresponding prototypic enhancer-like regulatory elements with the gradually increasing genome size of organisms.},
}
RevDate: 2020-08-09
Exaptive Evolution of Target of Rapamycin Signaling in Multicellular Eukaryotes.
Developmental cell, 54(2):142-155.
Target of rapamycin (TOR) is a protein kinase that coordinates metabolism with nutrient and energy availability in eukaryotes. TOR and its primary interactors, RAPTOR and LST8, have been remarkably evolutionarily static since they arose in the unicellular last common ancestor of plants, fungi, and animals, but the upstream regulatory mechanisms and downstream effectors of TOR signaling have evolved considerable diversity in these separate lineages. Here, I focus on the roles of exaptation and adaptation in the evolution of novel signaling axes in the TOR network in multicellular eukaryotes, concentrating especially on amino acid sensing, cell-cell signaling, and cell differentiation.
Additional Links: PMID-32649861
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@article {pmid32649861,
year = {2020},
author = {Brunkard, JO},
title = {Exaptive Evolution of Target of Rapamycin Signaling in Multicellular Eukaryotes.},
journal = {Developmental cell},
volume = {54},
number = {2},
pages = {142-155},
doi = {10.1016/j.devcel.2020.06.022},
pmid = {32649861},
issn = {1878-1551},
support = {DP5 OD023072/OD/NIH HHS/United States ; },
abstract = {Target of rapamycin (TOR) is a protein kinase that coordinates metabolism with nutrient and energy availability in eukaryotes. TOR and its primary interactors, RAPTOR and LST8, have been remarkably evolutionarily static since they arose in the unicellular last common ancestor of plants, fungi, and animals, but the upstream regulatory mechanisms and downstream effectors of TOR signaling have evolved considerable diversity in these separate lineages. Here, I focus on the roles of exaptation and adaptation in the evolution of novel signaling axes in the TOR network in multicellular eukaryotes, concentrating especially on amino acid sensing, cell-cell signaling, and cell differentiation.},
}
RevDate: 2020-08-12
CmpDate: 2020-08-12
Meta-population structure and the evolutionary transition to multicellularity.
Ecology letters, 23(9):1380-1390.
The evolutionary transition to multicellularity has occurred on numerous occasions, but transitions to complex life forms are rare. Here, using experimental bacterial populations as proxies for nascent multicellular organisms, we manipulate ecological factors shaping the evolution of groups. Groups were propagated under regimes requiring reproduction via a life cycle replete with developmental and dispersal (propagule) phases, but in one treatment lineages never mixed, whereas in a second treatment, cells from different lineages experienced intense competition during the dispersal phase. The latter treatment favoured traits promoting cell growth at the expense of traits underlying group fitness - a finding that is supported by results from a mathematical model. Our results show that the transition to multicellularity benefits from ecological conditions that maintain discreteness not just of the group (soma) phase, but also of the dispersal (germline) phase.
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@article {pmid32643307,
year = {2020},
author = {Rose, CJ and Hammerschmidt, K and Pichugin, Y and Rainey, PB},
title = {Meta-population structure and the evolutionary transition to multicellularity.},
journal = {Ecology letters},
volume = {23},
number = {9},
pages = {1380-1390},
doi = {10.1111/ele.13570},
pmid = {32643307},
issn = {1461-0248},
support = {//Marsden Fund Council from government funding administered by the Royal Society of New Zealand/ ; //Marsden Fund/ ; //Royal Society/ ; },
mesh = {Animals ; *Biological Evolution ; Life Cycle Stages ; Phenotype ; *Reproduction ; },
abstract = {The evolutionary transition to multicellularity has occurred on numerous occasions, but transitions to complex life forms are rare. Here, using experimental bacterial populations as proxies for nascent multicellular organisms, we manipulate ecological factors shaping the evolution of groups. Groups were propagated under regimes requiring reproduction via a life cycle replete with developmental and dispersal (propagule) phases, but in one treatment lineages never mixed, whereas in a second treatment, cells from different lineages experienced intense competition during the dispersal phase. The latter treatment favoured traits promoting cell growth at the expense of traits underlying group fitness - a finding that is supported by results from a mathematical model. Our results show that the transition to multicellularity benefits from ecological conditions that maintain discreteness not just of the group (soma) phase, but also of the dispersal (germline) phase.},
}
MeSH Terms:
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Animals
*Biological Evolution
Life Cycle Stages
Phenotype
*Reproduction
RevDate: 2020-09-28
Volvox and volvocine green algae.
EvoDevo, 11:13.
The transition of life from single cells to more complex multicellular forms has occurred at least two dozen times among eukaryotes and is one of the major evolutionary transitions, but the early steps that enabled multicellular life to evolve and thrive remain poorly understood. Volvocine green algae are a taxonomic group that is uniquely suited to investigating the step-wise acquisition of multicellular organization. The multicellular volvocine species Volvox carteri exhibits many hallmarks of complex multicellularity including complete germ-soma division of labor, asymmetric cell divisions, coordinated tissue-level morphogenesis, and dimorphic sexes-none of which have obvious analogs in its closest unicellular relative, the model alga Chlamydomonas reinhardtii. Here, I summarize some of the key questions and areas of study that are being addressed with Volvox carteri and how increasing genomic information and methodologies for volvocine algae are opening up the entire group as an integrated experimental system for exploring the evolution of multicellularity and more.
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@article {pmid32626570,
year = {2020},
author = {Umen, JG},
title = {Volvox and volvocine green algae.},
journal = {EvoDevo},
volume = {11},
number = {},
pages = {13},
pmid = {32626570},
issn = {2041-9139},
abstract = {The transition of life from single cells to more complex multicellular forms has occurred at least two dozen times among eukaryotes and is one of the major evolutionary transitions, but the early steps that enabled multicellular life to evolve and thrive remain poorly understood. Volvocine green algae are a taxonomic group that is uniquely suited to investigating the step-wise acquisition of multicellular organization. The multicellular volvocine species Volvox carteri exhibits many hallmarks of complex multicellularity including complete germ-soma division of labor, asymmetric cell divisions, coordinated tissue-level morphogenesis, and dimorphic sexes-none of which have obvious analogs in its closest unicellular relative, the model alga Chlamydomonas reinhardtii. Here, I summarize some of the key questions and areas of study that are being addressed with Volvox carteri and how increasing genomic information and methodologies for volvocine algae are opening up the entire group as an integrated experimental system for exploring the evolution of multicellularity and more.},
}
RevDate: 2020-08-25
Selection Shapes Synonymous Stop Codon Use in Mammals.
Journal of molecular evolution, 88(7):549-561.
Phylogenetic models of the evolution of protein-coding sequences can provide insights into the selection pressures that have shaped them. In the application of these models synonymous nucleotide substitutions, which do not alter the encoded amino acid, are often assumed to have limited functional consequences and used as a proxy for the neutral rate of evolution. The ratio of nonsynonymous to synonymous substitution rates is then used to categorize the selective regime that applies to the protein (e.g., purifying selection, neutral evolution, diversifying selection). Here, we extend the Muse and Gaut model of codon evolution to explore the extent of purifying selection acting on substitutions between synonymous stop codons. Using a large collection of coding sequence alignments, we estimate that a high proportion (approximately 57%) of mammalian genes are affected by selection acting on stop codon preference. This proportion varies substantially by codon, with UGA stop codons far more likely to be conserved. Genes with evidence of selection acting on synonymous stop codons have distinctive characteristics, compared to unconserved genes with the same stop codon, including longer [Formula: see text] untranslated regions (UTRs) and shorter mRNA half-life. The coding regions of these genes are also much more likely to be under strong purifying selection pressure. Our results suggest that the preference for UGA stop codons found in many multicellular eukaryotes is selective rather than mutational in origin.
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@article {pmid32617614,
year = {2020},
author = {Seoighe, C and Kiniry, SJ and Peters, A and Baranov, PV and Yang, H},
title = {Selection Shapes Synonymous Stop Codon Use in Mammals.},
journal = {Journal of molecular evolution},
volume = {88},
number = {7},
pages = {549-561},
doi = {10.1007/s00239-020-09957-x},
pmid = {32617614},
issn = {1432-1432},
support = {210692/Z/18/Z//SFI-HRB-Wellcome Trust Biomedical Research Partnership/ ; 16/IA/4612/SFI_/Science Foundation Ireland/Ireland ; },
abstract = {Phylogenetic models of the evolution of protein-coding sequences can provide insights into the selection pressures that have shaped them. In the application of these models synonymous nucleotide substitutions, which do not alter the encoded amino acid, are often assumed to have limited functional consequences and used as a proxy for the neutral rate of evolution. The ratio of nonsynonymous to synonymous substitution rates is then used to categorize the selective regime that applies to the protein (e.g., purifying selection, neutral evolution, diversifying selection). Here, we extend the Muse and Gaut model of codon evolution to explore the extent of purifying selection acting on substitutions between synonymous stop codons. Using a large collection of coding sequence alignments, we estimate that a high proportion (approximately 57%) of mammalian genes are affected by selection acting on stop codon preference. This proportion varies substantially by codon, with UGA stop codons far more likely to be conserved. Genes with evidence of selection acting on synonymous stop codons have distinctive characteristics, compared to unconserved genes with the same stop codon, including longer [Formula: see text] untranslated regions (UTRs) and shorter mRNA half-life. The coding regions of these genes are also much more likely to be under strong purifying selection pressure. Our results suggest that the preference for UGA stop codons found in many multicellular eukaryotes is selective rather than mutational in origin.},
}
RevDate: 2020-12-01
CmpDate: 2020-12-01
Do food trichomes occur in Pinguicula (Lentibulariaceae) flowers?.
Annals of botany, 126(6):1039-1048.
BACKGROUND AND AIMS: Floral food bodies (including edible trichomes) are a form of floral reward for pollinators. This type of nutritive reward has been recorded in several angiosperm families: Annonaceae, Araceae, Calycanthaceae, Eupomatiaceae, Himantandraceae, Nymphaeaceae, Orchidaceae, Pandanaceae and Winteraceae. Although these bodies are very diverse in their structure, their cells contain food material: starch grains, protein bodies or lipid droplets. In Pinguicula flowers, there are numerous multicellular clavate trichomes. Previous authors have proposed that these trichomes in the Pinguicula flower play the role of 'futterhaare' ('feeding hairs') and are eaten by pollinators. The main aim of this study was to investigate whether the floral non-glandular trichomes of Pinguicula contain food reserves and thus are a reward for pollinators. The trichomes from the Pinguicula groups, which differ in their taxonomy (species from the subgenera: Temnoceras, Pinguicula and Isoloba) as well as the types of their pollinators (butterflies/flies and bees/hummingbirds), were examined. Thus, it was determined whether there are any connections between the occurrence of food trichomes and phylogeny position or pollination biology. Additionally, we determined the phylogenetic history of edible trichomes and pollinator evolution in the Pinguicula species.
METHODS: The species that were sampled were: Pinguicula moctezumae, P. esseriana, P. moranensis, P. emarginata, P. rectifolia, P. mesophytica, P. hemiepiphytica, P. agnata, P. albida, P. ibarrae, P. martinezii, P. filifolia, P. gigantea, P. lusitanica, P. alpina and P. vulgaris. Light microscopy, histochemistry, and scanning and transmission electron microscopy were used to address our aims with a phylogenetic perspective based on matK/trnK DNA sequences.
KEY RESULTS: No accumulation of protein bodies or lipid droplets was recorded in the floral non-glandular trichomes of any of the analysed species. Starch grains occurred in the cells of the trichomes of the bee-/fly-pollinated species: P. agnata, P. albida, P. ibarrae, P. martinezii, P. filifolia and P. gigantea, but not in P. alpina or P. vulgaris. Moreover, starch grains were not recorded in the cells of the trichomes of the Pinguicula species that have long spurs, which are pollinated by Lepidoptera (P. moctezumae, P. esseriana, P. moranensis, P. emarginata and P. rectifolia) or birds (P. mesophytica and P. hemiepihytica), or in species with a small and whitish corolla that self-pollinate (P. lusitanica). The results on the occurrence of edible trichomes and pollinator syndromes were mapped onto a phylogenetic reconstruction of the genus.
CONCLUSION: Floral non-glandular trichomes play the role of edible trichomes in some Pinguicula species (P. agnata, P. albida, P. ibarrae, P. martinezii, P. filifolia and P. gigantea), which are mainly classified as bee-pollinated species that had originated from Central and South America. It seems that in the Pinguicula that are pollinated by other pollinator groups (Lepidoptera and hummingbirds), the non-glandular trichomes in the flowers play a role other than that of a floral reward for their pollinators. Edible trichomes are symplesiomorphic for the Pinguicula species, and thus do not support a monophyletic group such as a synapomorphy. Nevertheless, edible trichomes are derived and are possibly a specialization for fly and bee pollinators by acting as a food reward for these visitors.
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@article {pmid32592586,
year = {2020},
author = {Lustofin, K and Świątek, P and Stolarczyk, P and Miranda, VFO and Płachno, BJ},
title = {Do food trichomes occur in Pinguicula (Lentibulariaceae) flowers?.},
journal = {Annals of botany},
volume = {126},
number = {6},
pages = {1039-1048},
pmid = {32592586},
issn = {1095-8290},
mesh = {Animals ; Bees ; *Flowers ; Phylogeny ; Pollination ; South America ; *Trichomes ; },
abstract = {BACKGROUND AND AIMS: Floral food bodies (including edible trichomes) are a form of floral reward for pollinators. This type of nutritive reward has been recorded in several angiosperm families: Annonaceae, Araceae, Calycanthaceae, Eupomatiaceae, Himantandraceae, Nymphaeaceae, Orchidaceae, Pandanaceae and Winteraceae. Although these bodies are very diverse in their structure, their cells contain food material: starch grains, protein bodies or lipid droplets. In Pinguicula flowers, there are numerous multicellular clavate trichomes. Previous authors have proposed that these trichomes in the Pinguicula flower play the role of 'futterhaare' ('feeding hairs') and are eaten by pollinators. The main aim of this study was to investigate whether the floral non-glandular trichomes of Pinguicula contain food reserves and thus are a reward for pollinators. The trichomes from the Pinguicula groups, which differ in their taxonomy (species from the subgenera: Temnoceras, Pinguicula and Isoloba) as well as the types of their pollinators (butterflies/flies and bees/hummingbirds), were examined. Thus, it was determined whether there are any connections between the occurrence of food trichomes and phylogeny position or pollination biology. Additionally, we determined the phylogenetic history of edible trichomes and pollinator evolution in the Pinguicula species.
METHODS: The species that were sampled were: Pinguicula moctezumae, P. esseriana, P. moranensis, P. emarginata, P. rectifolia, P. mesophytica, P. hemiepiphytica, P. agnata, P. albida, P. ibarrae, P. martinezii, P. filifolia, P. gigantea, P. lusitanica, P. alpina and P. vulgaris. Light microscopy, histochemistry, and scanning and transmission electron microscopy were used to address our aims with a phylogenetic perspective based on matK/trnK DNA sequences.
KEY RESULTS: No accumulation of protein bodies or lipid droplets was recorded in the floral non-glandular trichomes of any of the analysed species. Starch grains occurred in the cells of the trichomes of the bee-/fly-pollinated species: P. agnata, P. albida, P. ibarrae, P. martinezii, P. filifolia and P. gigantea, but not in P. alpina or P. vulgaris. Moreover, starch grains were not recorded in the cells of the trichomes of the Pinguicula species that have long spurs, which are pollinated by Lepidoptera (P. moctezumae, P. esseriana, P. moranensis, P. emarginata and P. rectifolia) or birds (P. mesophytica and P. hemiepihytica), or in species with a small and whitish corolla that self-pollinate (P. lusitanica). The results on the occurrence of edible trichomes and pollinator syndromes were mapped onto a phylogenetic reconstruction of the genus.
CONCLUSION: Floral non-glandular trichomes play the role of edible trichomes in some Pinguicula species (P. agnata, P. albida, P. ibarrae, P. martinezii, P. filifolia and P. gigantea), which are mainly classified as bee-pollinated species that had originated from Central and South America. It seems that in the Pinguicula that are pollinated by other pollinator groups (Lepidoptera and hummingbirds), the non-glandular trichomes in the flowers play a role other than that of a floral reward for their pollinators. Edible trichomes are symplesiomorphic for the Pinguicula species, and thus do not support a monophyletic group such as a synapomorphy. Nevertheless, edible trichomes are derived and are possibly a specialization for fly and bee pollinators by acting as a food reward for these visitors.},
}
MeSH Terms:
show MeSH Terms
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Animals
Bees
*Flowers
Phylogeny
Pollination
South America
*Trichomes
RevDate: 2020-11-23
Lateral Gene Transfer Acts As an Evolutionary Shortcut to Efficient C4 Biochemistry.
Molecular biology and evolution, 37(11):3094-3104.
The adaptation of proteins for novel functions often requires changes in their kinetics via amino acid replacement. This process can require multiple mutations, and therefore extended periods of selection. The transfer of genes among distinct species might speed up the process, by providing proteins already adapted for the novel function. However, this hypothesis remains untested in multicellular eukaryotes. The grass Alloteropsis is an ideal system to test this hypothesis due to its diversity of genes encoding phosphoenolpyruvate carboxylase, an enzyme that catalyzes one of the key reactions in the C4 pathway. Different accessions of Alloteropsis either use native isoforms relatively recently co-opted from other functions or isoforms that were laterally acquired from distantly related species that evolved the C4 trait much earlier. By comparing the enzyme kinetics, we show that native isoforms with few amino acid replacements have substrate KM values similar to the non-C4 ancestral form, but exhibit marked increases in catalytic efficiency. The co-option of native isoforms was therefore followed by rapid catalytic improvements, which appear to rely on standing genetic variation observed within one species. Native C4 isoforms with more amino acid replacements exhibit additional changes in affinities, suggesting that the initial catalytic improvements are followed by gradual modifications. Finally, laterally acquired genes show both strong increases in catalytic efficiency and important changes in substrate handling. We conclude that the transfer of genes among distant species sharing the same physiological novelty creates an evolutionary shortcut toward more efficient enzymes, effectively accelerating evolution.
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@article {pmid32521019,
year = {2020},
author = {Phansopa, C and Dunning, LT and Reid, JD and Christin, PA},
title = {Lateral Gene Transfer Acts As an Evolutionary Shortcut to Efficient C4 Biochemistry.},
journal = {Molecular biology and evolution},
volume = {37},
number = {11},
pages = {3094-3104},
doi = {10.1093/molbev/msaa143},
pmid = {32521019},
issn = {1537-1719},
abstract = {The adaptation of proteins for novel functions often requires changes in their kinetics via amino acid replacement. This process can require multiple mutations, and therefore extended periods of selection. The transfer of genes among distinct species might speed up the process, by providing proteins already adapted for the novel function. However, this hypothesis remains untested in multicellular eukaryotes. The grass Alloteropsis is an ideal system to test this hypothesis due to its diversity of genes encoding phosphoenolpyruvate carboxylase, an enzyme that catalyzes one of the key reactions in the C4 pathway. Different accessions of Alloteropsis either use native isoforms relatively recently co-opted from other functions or isoforms that were laterally acquired from distantly related species that evolved the C4 trait much earlier. By comparing the enzyme kinetics, we show that native isoforms with few amino acid replacements have substrate KM values similar to the non-C4 ancestral form, but exhibit marked increases in catalytic efficiency. The co-option of native isoforms was therefore followed by rapid catalytic improvements, which appear to rely on standing genetic variation observed within one species. Native C4 isoforms with more amino acid replacements exhibit additional changes in affinities, suggesting that the initial catalytic improvements are followed by gradual modifications. Finally, laterally acquired genes show both strong increases in catalytic efficiency and important changes in substrate handling. We conclude that the transfer of genes among distant species sharing the same physiological novelty creates an evolutionary shortcut toward more efficient enzymes, effectively accelerating evolution.},
}
RevDate: 2020-08-05
CmpDate: 2020-08-05
Chytrid rhizoid morphogenesis resembles hyphal development in multicellular fungi and is adaptive to resource availability.
Proceedings. Biological sciences, 287(1928):20200433.
Key to the ecological prominence of fungi is their distinctive cell biology, our understanding of which has been principally based on dikaryan hyphal and yeast forms. The early-diverging Chytridiomycota (chytrids) are ecologically important and a significant component of fungal diversity, yet their cell biology remains poorly understood. Unlike dikaryan hyphae, chytrids typically attach to substrates and feed osmotrophically via anucleate rhizoids. The evolution of fungal hyphae appears to have occurred from rhizoid-bearing lineages and it has been hypothesized that a rhizoid-like structure was the precursor to multicellular hyphae. Here, we show in a unicellular chytrid, Rhizoclosmatium globosum, that rhizoid development exhibits striking similarities with dikaryan hyphae and is adaptive to resource availability. Rhizoid morphogenesis exhibits analogous patterns to hyphal growth and is controlled by β-glucan-dependent cell wall synthesis and actin polymerization. Chytrid rhizoids growing from individual cells also demonstrate adaptive morphological plasticity in response to resource availability, developing a searching phenotype when carbon starved and spatial differentiation when interacting with particulate organic matter. We demonstrate that the adaptive cell biology and associated developmental plasticity considered characteristic of hyphal fungi are shared more widely across the Kingdom Fungi and therefore could be conserved from their most recent common ancestor.
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@article {pmid32517626,
year = {2020},
author = {Laundon, D and Chrismas, N and Wheeler, G and Cunliffe, M},
title = {Chytrid rhizoid morphogenesis resembles hyphal development in multicellular fungi and is adaptive to resource availability.},
journal = {Proceedings. Biological sciences},
volume = {287},
number = {1928},
pages = {20200433},
pmid = {32517626},
issn = {1471-2954},
mesh = {Chytridiomycota/*physiology ; Fungi ; Hyphae/*growth & development ; Morphogenesis ; },
abstract = {Key to the ecological prominence of fungi is their distinctive cell biology, our understanding of which has been principally based on dikaryan hyphal and yeast forms. The early-diverging Chytridiomycota (chytrids) are ecologically important and a significant component of fungal diversity, yet their cell biology remains poorly understood. Unlike dikaryan hyphae, chytrids typically attach to substrates and feed osmotrophically via anucleate rhizoids. The evolution of fungal hyphae appears to have occurred from rhizoid-bearing lineages and it has been hypothesized that a rhizoid-like structure was the precursor to multicellular hyphae. Here, we show in a unicellular chytrid, Rhizoclosmatium globosum, that rhizoid development exhibits striking similarities with dikaryan hyphae and is adaptive to resource availability. Rhizoid morphogenesis exhibits analogous patterns to hyphal growth and is controlled by β-glucan-dependent cell wall synthesis and actin polymerization. Chytrid rhizoids growing from individual cells also demonstrate adaptive morphological plasticity in response to resource availability, developing a searching phenotype when carbon starved and spatial differentiation when interacting with particulate organic matter. We demonstrate that the adaptive cell biology and associated developmental plasticity considered characteristic of hyphal fungi are shared more widely across the Kingdom Fungi and therefore could be conserved from their most recent common ancestor.},
}
MeSH Terms:
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Chytridiomycota/*physiology
Fungi
Hyphae/*growth & development
Morphogenesis
RevDate: 2020-09-11
CmpDate: 2020-06-12
The human genetic determinism of life-threatening infectious diseases: genetic heterogeneity and physiological homogeneity?.
Human genetics, 139(6-7):681-694.
Multicellular eukaryotes emerged late in evolution from an ocean of viruses, bacteria, archaea, and unicellular eukaryotes. These macroorganisms are exposed to and infected by a tremendous diversity of microorganisms. Those that are large enough can even be infected by multicellular fungi and parasites. Each interaction is unique, if only because it operates between two unique living organisms, in an infinite diversity of circumstances. This is neatly illustrated by the extraordinarily high level of interindividual clinical variability in human infections, even for a given pathogen, ranging from a total absence of clinical manifestations to death. We discuss here the idea that the determinism of human life-threatening infectious diseases can be governed by single-gene inborn errors of immunity, which are rarely Mendelian and frequently display incomplete penetrance. We briefly review the evidence in support of this notion obtained over the last two decades, referring to a number of focused and thorough reviews published by eminent colleagues in this issue of Human Genetics. It seems that almost any life-threatening infectious disease can be driven by at least one, and, perhaps, a great many diverse monogenic inborn errors, which may nonetheless be immunologically related. While the proportions of monogenic cases remain unknown, a picture in which genetic heterogeneity is combined with physiological homogeneity is emerging from these studies. A preliminary sketch of the human genetic architecture of severe infectious diseases is perhaps in sight.
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@article {pmid32462426,
year = {2020},
author = {Casanova, JL and Abel, L},
title = {The human genetic determinism of life-threatening infectious diseases: genetic heterogeneity and physiological homogeneity?.},
journal = {Human genetics},
volume = {139},
number = {6-7},
pages = {681-694},
pmid = {32462426},
issn = {1432-1203},
support = {UL1 TR001866/TR/NCATS NIH HHS/United States ; R21 AI137371/AI/NIAID NIH HHS/United States ; R37 AI095983/AI/NIAID NIH HHS/United States ; R01 AI127564/AI/NIAID NIH HHS/United States ; R01 NS072381/NS/NINDS NIH HHS/United States ; U19 AI111143/AI/NIAID NIH HHS/United States ; R01 AI088364/AI/NIAID NIH HHS/United States ; P01 AI061093/AI/NIAID NIH HHS/United States ; },
mesh = {Communicable Diseases/*genetics/immunology/*pathology ; *Genetic Heterogeneity ; *Genetic Predisposition to Disease ; Humans ; Models, Genetic ; },
abstract = {Multicellular eukaryotes emerged late in evolution from an ocean of viruses, bacteria, archaea, and unicellular eukaryotes. These macroorganisms are exposed to and infected by a tremendous diversity of microorganisms. Those that are large enough can even be infected by multicellular fungi and parasites. Each interaction is unique, if only because it operates between two unique living organisms, in an infinite diversity of circumstances. This is neatly illustrated by the extraordinarily high level of interindividual clinical variability in human infections, even for a given pathogen, ranging from a total absence of clinical manifestations to death. We discuss here the idea that the determinism of human life-threatening infectious diseases can be governed by single-gene inborn errors of immunity, which are rarely Mendelian and frequently display incomplete penetrance. We briefly review the evidence in support of this notion obtained over the last two decades, referring to a number of focused and thorough reviews published by eminent colleagues in this issue of Human Genetics. It seems that almost any life-threatening infectious disease can be driven by at least one, and, perhaps, a great many diverse monogenic inborn errors, which may nonetheless be immunologically related. While the proportions of monogenic cases remain unknown, a picture in which genetic heterogeneity is combined with physiological homogeneity is emerging from these studies. A preliminary sketch of the human genetic architecture of severe infectious diseases is perhaps in sight.},
}
MeSH Terms:
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Communicable Diseases/*genetics/immunology/*pathology
*Genetic Heterogeneity
*Genetic Predisposition to Disease
Humans
Models, Genetic
RevDate: 2020-09-21
Does Formation of Multicellular Colonies by Choanoflagellates Affect Their Susceptibility to Capture by Passive Protozoan Predators?.
The Journal of eukaryotic microbiology, 67(5):555-565.
Microbial eukaryotes, critical links in aquatic food webs, are unicellular, but some, such as choanoflagellates, form multicellular colonies. Are there consequences to predator avoidance of being unicellular vs. forming larger colonies? Choanoflagellates share a common ancestor with animals and are used as model organisms to study the evolution of multicellularity. Escape in size from protozoan predators is suggested as a selective factor favoring evolution of multicellularity. Heterotrophic protozoans are categorized as suspension feeders, motile raptors, or passive predators that eat swimming prey which bump into them. We focused on passive predation and measured the mechanisms responsible for the susceptibility of unicellular vs. multicellular choanoflagellates, Salpingoeca helianthica, to capture by passive heliozoan predators, Actinosphaerium nucleofilum, which trap prey on axopodia radiating from the cell body. Microvideography showed that unicellular and colonial choanoflagellates entered the predator's capture zone at similar frequencies, but a greater proportion of colonies contacted axopodia. However, more colonies than single cells were lost during transport by axopodia to the cell body. Thus, feeding efficiency (proportion of prey entering the capture zone that were engulfed in phagosomes) was the same for unicellular and multicellular prey, suggesting that colony formation is not an effective defense against such passive predators.
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@article {pmid32455487,
year = {2020},
author = {Kumler, WE and Jorge, J and Kim, PM and Iftekhar, N and Koehl, MAR},
title = {Does Formation of Multicellular Colonies by Choanoflagellates Affect Their Susceptibility to Capture by Passive Protozoan Predators?.},
journal = {The Journal of eukaryotic microbiology},
volume = {67},
number = {5},
pages = {555-565},
doi = {10.1111/jeu.12808},
pmid = {32455487},
issn = {1550-7408},
support = {//Berkeley Undergraduate Research Apprentice Program (URAP)/ ; IOS-1655318//National Science Foundation/ ; //Berkeley Summer Undergraduate Research Fellowships (SURF)/ ; },
abstract = {Microbial eukaryotes, critical links in aquatic food webs, are unicellular, but some, such as choanoflagellates, form multicellular colonies. Are there consequences to predator avoidance of being unicellular vs. forming larger colonies? Choanoflagellates share a common ancestor with animals and are used as model organisms to study the evolution of multicellularity. Escape in size from protozoan predators is suggested as a selective factor favoring evolution of multicellularity. Heterotrophic protozoans are categorized as suspension feeders, motile raptors, or passive predators that eat swimming prey which bump into them. We focused on passive predation and measured the mechanisms responsible for the susceptibility of unicellular vs. multicellular choanoflagellates, Salpingoeca helianthica, to capture by passive heliozoan predators, Actinosphaerium nucleofilum, which trap prey on axopodia radiating from the cell body. Microvideography showed that unicellular and colonial choanoflagellates entered the predator's capture zone at similar frequencies, but a greater proportion of colonies contacted axopodia. However, more colonies than single cells were lost during transport by axopodia to the cell body. Thus, feeding efficiency (proportion of prey entering the capture zone that were engulfed in phagosomes) was the same for unicellular and multicellular prey, suggesting that colony formation is not an effective defense against such passive predators.},
}
RevDate: 2020-08-24
CmpDate: 2020-08-24
A mechanistic explanation of the transition to simple multicellularity in fungi.
Nature communications, 11(1):2594 pii:10.1038/s41467-020-16072-4.
Development of multicellularity was one of the major transitions in evolution and occurred independently multiple times in algae, plants, animals, and fungi. However recent comparative genome analyses suggest that fungi followed a different route to other eukaryotic lineages. To understand the driving forces behind the transition from unicellular fungi to hyphal forms of growth, we develop a comparative model of osmotrophic resource acquisition. This predicts that whenever the local resource is immobile, hard-to-digest, and nutrient poor, hyphal osmotrophs outcompete motile or autolytic unicellular osmotrophs. This hyphal advantage arises because transporting nutrients via a contiguous cytoplasm enables continued exploitation of remaining resources after local depletion of essential nutrients, and more efficient use of costly exoenzymes. The model provides a mechanistic explanation for the origins of multicellular hyphal organisms, and explains why fungi, rather than unicellular bacteria, evolved to dominate decay of recalcitrant, nutrient poor substrates such as leaf litter or wood.
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@article {pmid32444651,
year = {2020},
author = {Heaton, LLM and Jones, NS and Fricker, MD},
title = {A mechanistic explanation of the transition to simple multicellularity in fungi.},
journal = {Nature communications},
volume = {11},
number = {1},
pages = {2594},
doi = {10.1038/s41467-020-16072-4},
pmid = {32444651},
issn = {2041-1723},
mesh = {Carbon/metabolism ; Cytoplasm/metabolism ; Fungi/*cytology/growth & development/*physiology ; Hyphae/cytology/growth & development ; *Models, Biological ; Nitrogen/metabolism ; Phosphorus/metabolism ; },
abstract = {Development of multicellularity was one of the major transitions in evolution and occurred independently multiple times in algae, plants, animals, and fungi. However recent comparative genome analyses suggest that fungi followed a different route to other eukaryotic lineages. To understand the driving forces behind the transition from unicellular fungi to hyphal forms of growth, we develop a comparative model of osmotrophic resource acquisition. This predicts that whenever the local resource is immobile, hard-to-digest, and nutrient poor, hyphal osmotrophs outcompete motile or autolytic unicellular osmotrophs. This hyphal advantage arises because transporting nutrients via a contiguous cytoplasm enables continued exploitation of remaining resources after local depletion of essential nutrients, and more efficient use of costly exoenzymes. The model provides a mechanistic explanation for the origins of multicellular hyphal organisms, and explains why fungi, rather than unicellular bacteria, evolved to dominate decay of recalcitrant, nutrient poor substrates such as leaf litter or wood.},
}
MeSH Terms:
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Carbon/metabolism
Cytoplasm/metabolism
Fungi/*cytology/growth & development/*physiology
Hyphae/cytology/growth & development
*Models, Biological
Nitrogen/metabolism
Phosphorus/metabolism
RevDate: 2020-08-11
Oxygen, life forms, and the evolution of sexes in multicellular eukaryotes.
Heredity, 125(1-2):1-14.
The evolutionary advantage of different sexual systems in multicellular eukaryotes is still not well understood, because the differentiation into male and female individuals halves offspring production compared with asexuality. Here we propose that various physiological adaptations to oxidative stress could have forged sessility versus motility, and consequently the evolution of sexual systems in multicellular animals, plants, and fungi. Photosynthesis causes substantial amounts of oxidative stress in photoautotrophic plants and, likewise, oxidative chemistry of polymer breakdown, cellulose and lignin, for saprotrophic fungi. In both cases, its extent precludes motility, an additional source of oxidative stress. Sessile life form and the lack of neuronal systems, however, limit options for mate recognition and adult sexual selection, resulting in inefficient mate-searching systems. Hence, sessility requires that all individuals can produce offspring, which is achieved by hermaphroditism in plants and/or by multiple mating types in fungi. In animals, motility requires neuronal systems, and muscle activity, both of which are highly sensitive to oxidative damage. As a consequence, motility has evolved in animals as heterotrophic organisms that (1) are not photosynthetically active, and (2) are not primary decomposers. Adaptations to motility provide prerequisites for an active mating behavior and efficient mate-searching systems. These benefits compensate for the "cost of males", and may explain the early evolution of sex chromosomes in metazoans. We conclude that different sexual systems evolved under the indirect physiological constraints of lifestyles.
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@article {pmid32415185,
year = {2020},
author = {Hörandl, E and Hadacek, F},
title = {Oxygen, life forms, and the evolution of sexes in multicellular eukaryotes.},
journal = {Heredity},
volume = {125},
number = {1-2},
pages = {1-14},
pmid = {32415185},
issn = {1365-2540},
abstract = {The evolutionary advantage of different sexual systems in multicellular eukaryotes is still not well understood, because the differentiation into male and female individuals halves offspring production compared with asexuality. Here we propose that various physiological adaptations to oxidative stress could have forged sessility versus motility, and consequently the evolution of sexual systems in multicellular animals, plants, and fungi. Photosynthesis causes substantial amounts of oxidative stress in photoautotrophic plants and, likewise, oxidative chemistry of polymer breakdown, cellulose and lignin, for saprotrophic fungi. In both cases, its extent precludes motility, an additional source of oxidative stress. Sessile life form and the lack of neuronal systems, however, limit options for mate recognition and adult sexual selection, resulting in inefficient mate-searching systems. Hence, sessility requires that all individuals can produce offspring, which is achieved by hermaphroditism in plants and/or by multiple mating types in fungi. In animals, motility requires neuronal systems, and muscle activity, both of which are highly sensitive to oxidative damage. As a consequence, motility has evolved in animals as heterotrophic organisms that (1) are not photosynthetically active, and (2) are not primary decomposers. Adaptations to motility provide prerequisites for an active mating behavior and efficient mate-searching systems. These benefits compensate for the "cost of males", and may explain the early evolution of sex chromosomes in metazoans. We conclude that different sexual systems evolved under the indirect physiological constraints of lifestyles.},
}
RevDate: 2020-07-17
CmpDate: 2020-07-17
Recent advances in understanding mitochondrial genome diversity.
F1000Research, 9:.
Ever since its discovery, the double-stranded DNA contained in the mitochondria of eukaryotes has fascinated researchers because of its bacterial endosymbiotic origin, crucial role in encoding subunits of the respiratory complexes, compact nature, and specific inheritance mechanisms. In the last few years, high-throughput sequencing techniques have accelerated the sequencing of mitochondrial genomes (mitogenomes) and uncovered the great diversity of organizations, gene contents, and modes of replication and transcription found in living eukaryotes. Some early divergent lineages of unicellular eukaryotes retain certain synteny and gene content resembling those observed in the genomes of alphaproteobacteria (the inferred closest living group of mitochondria), whereas others adapted to anaerobic environments have drastically reduced or even lost the mitogenome. In the three main multicellular lineages of eukaryotes, mitogenomes have pursued diverse evolutionary trajectories in which different types of molecules (circular versus linear and single versus multipartite), gene structures (with or without self-splicing introns), gene contents, gene orders, genetic codes, and transfer RNA editing mechanisms have been selected. Whereas animals have evolved a rather compact mitochondrial genome between 11 and 50 Kb in length with a highly conserved gene content in bilaterians, plants exhibit large mitochondrial genomes of 66 Kb to 11.3 Mb with large intergenic repetitions prone to recombination, and fungal mitogenomes have intermediate sizes of 12 to 236 Kb.
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@article {pmid32399193,
year = {2020},
author = {Zardoya, R},
title = {Recent advances in understanding mitochondrial genome diversity.},
journal = {F1000Research},
volume = {9},
number = {},
pages = {},
pmid = {32399193},
issn = {2046-1402},
mesh = {Animals ; *Evolution, Molecular ; Fungi/genetics ; *Genome, Mitochondrial ; Introns ; Mitochondria ; Plants/genetics ; RNA Editing ; },
abstract = {Ever since its discovery, the double-stranded DNA contained in the mitochondria of eukaryotes has fascinated researchers because of its bacterial endosymbiotic origin, crucial role in encoding subunits of the respiratory complexes, compact nature, and specific inheritance mechanisms. In the last few years, high-throughput sequencing techniques have accelerated the sequencing of mitochondrial genomes (mitogenomes) and uncovered the great diversity of organizations, gene contents, and modes of replication and transcription found in living eukaryotes. Some early divergent lineages of unicellular eukaryotes retain certain synteny and gene content resembling those observed in the genomes of alphaproteobacteria (the inferred closest living group of mitochondria), whereas others adapted to anaerobic environments have drastically reduced or even lost the mitogenome. In the three main multicellular lineages of eukaryotes, mitogenomes have pursued diverse evolutionary trajectories in which different types of molecules (circular versus linear and single versus multipartite), gene structures (with or without self-splicing introns), gene contents, gene orders, genetic codes, and transfer RNA editing mechanisms have been selected. Whereas animals have evolved a rather compact mitochondrial genome between 11 and 50 Kb in length with a highly conserved gene content in bilaterians, plants exhibit large mitochondrial genomes of 66 Kb to 11.3 Mb with large intergenic repetitions prone to recombination, and fungal mitogenomes have intermediate sizes of 12 to 236 Kb.},
}
MeSH Terms:
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Animals
*Evolution, Molecular
Fungi/genetics
*Genome, Mitochondrial
Introns
Mitochondria
Plants/genetics
RNA Editing
RevDate: 2020-05-18
CmpDate: 2020-05-12
Antimicrobial peptides: Application informed by evolution.
Science (New York, N.Y.), 368(6490):.
Antimicrobial peptides (AMPs) are essential components of immune defenses of multicellular organisms and are currently in development as anti-infective drugs. AMPs have been classically assumed to have broad-spectrum activity and simple kinetics, but recent evidence suggests an unexpected degree of specificity and a high capacity for synergies. Deeper evaluation of the molecular evolution and population genetics of AMP genes reveals more evidence for adaptive maintenance of polymorphism in AMP genes than has previously been appreciated, as well as adaptive loss of AMP activity. AMPs exhibit pharmacodynamic properties that reduce the evolution of resistance in target microbes, and AMPs may synergize with one another and with conventional antibiotics. Both of these properties make AMPs attractive for translational applications. However, if AMPs are to be used clinically, it is crucial to understand their natural biology in order to lessen the risk of collateral harm and avoid the crisis of resistance now facing conventional antibiotics.
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@article {pmid32355003,
year = {2020},
author = {Lazzaro, BP and Zasloff, M and Rolff, J},
title = {Antimicrobial peptides: Application informed by evolution.},
journal = {Science (New York, N.Y.)},
volume = {368},
number = {6490},
pages = {},
doi = {10.1126/science.aau5480},
pmid = {32355003},
issn = {1095-9203},
support = {R01 AI141385/AI/NIAID NIH HHS/United States ; /ERC_/European Research Council/International ; },
mesh = {Animals ; Anti-Bacterial Agents/*pharmacology ; Antimicrobial Cationic Peptides/chemistry/*genetics/*pharmacology ; Drosophila Proteins/genetics/pharmacology ; *Drug Resistance, Bacterial ; Drug Synergism ; *Evolution, Molecular ; Humans ; Polymorphism, Genetic ; Translational Medical Research ; },
abstract = {Antimicrobial peptides (AMPs) are essential components of immune defenses of multicellular organisms and are currently in development as anti-infective drugs. AMPs have been classically assumed to have broad-spectrum activity and simple kinetics, but recent evidence suggests an unexpected degree of specificity and a high capacity for synergies. Deeper evaluation of the molecular evolution and population genetics of AMP genes reveals more evidence for adaptive maintenance of polymorphism in AMP genes than has previously been appreciated, as well as adaptive loss of AMP activity. AMPs exhibit pharmacodynamic properties that reduce the evolution of resistance in target microbes, and AMPs may synergize with one another and with conventional antibiotics. Both of these properties make AMPs attractive for translational applications. However, if AMPs are to be used clinically, it is crucial to understand their natural biology in order to lessen the risk of collateral harm and avoid the crisis of resistance now facing conventional antibiotics.},
}
MeSH Terms:
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Animals
Anti-Bacterial Agents/*pharmacology
Antimicrobial Cationic Peptides/chemistry/*genetics/*pharmacology
Drosophila Proteins/genetics/pharmacology
*Drug Resistance, Bacterial
Drug Synergism
*Evolution, Molecular
Humans
Polymorphism, Genetic
Translational Medical Research
RevDate: 2020-11-20
Phenotypic Comparability from Genotypic Variability among Physically Structured Microbial Consortia.
Integrative and comparative biology, 60(2):288-303.
Microbiomes represent the collective bacteria, archaea, protist, fungi, and virus communities living in or on individual organisms that are typically multicellular eukaryotes. Such consortia have become recognized as having significant impacts on the development, health, and disease status of their hosts. Since understanding the mechanistic connections between an individual's genetic makeup and their complete set of traits (i.e., genome to phenome) requires consideration at different levels of biological organization, this should include interactions with, and the organization of, microbial consortia. To understand microbial consortia organization, we elucidated the genetic constituents among phenotypically similar (and hypothesized functionally-analogous) layers (i.e., top orange, second orange, pink, and green layers) in the unique laminated orange cyanobacterial-bacterial crusts endemic to Hawaii's anchialine ecosystem. High-throughput amplicon sequencing of ribosomal RNA hypervariable regions (i.e., Bacteria-specific V6 and Eukarya-biased V9) revealed microbial richness increasing by crust layer depth, with samples of a given layer more similar to different layers from the same geographic site than to their phenotypically-analogous layer from different sites. Furthermore, samples from sites on the same island were more similar to each other, regardless of which layer they originated from, than to analogous layers from another island. However, cyanobacterial and algal taxa were abundant in all surface and bottom layers, with anaerobic and chemoautotrophic taxa concentrated in the middle two layers, suggesting crust oxygenation from both above and below. Thus, the arrangement of oxygenated vs. anoxygenated niches in these orange crusts is functionally distinct relative to other laminated cyanobacterial-bacterial communities examined to date, with convergent evolution due to similar environmental conditions a likely driver for these phenotypically comparable but genetically distinct microbial consortia.
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@article {pmid32353148,
year = {2020},
author = {Hoffman, SK and Seitz, KW and Havird, JC and Weese, DA and Santos, SR},
title = {Phenotypic Comparability from Genotypic Variability among Physically Structured Microbial Consortia.},
journal = {Integrative and comparative biology},
volume = {60},
number = {2},
pages = {288-303},
doi = {10.1093/icb/icaa022},
pmid = {32353148},
issn = {1557-7023},
abstract = {Microbiomes represent the collective bacteria, archaea, protist, fungi, and virus communities living in or on individual organisms that are typically multicellular eukaryotes. Such consortia have become recognized as having significant impacts on the development, health, and disease status of their hosts. Since understanding the mechanistic connections between an individual's genetic makeup and their complete set of traits (i.e., genome to phenome) requires consideration at different levels of biological organization, this should include interactions with, and the organization of, microbial consortia. To understand microbial consortia organization, we elucidated the genetic constituents among phenotypically similar (and hypothesized functionally-analogous) layers (i.e., top orange, second orange, pink, and green layers) in the unique laminated orange cyanobacterial-bacterial crusts endemic to Hawaii's anchialine ecosystem. High-throughput amplicon sequencing of ribosomal RNA hypervariable regions (i.e., Bacteria-specific V6 and Eukarya-biased V9) revealed microbial richness increasing by crust layer depth, with samples of a given layer more similar to different layers from the same geographic site than to their phenotypically-analogous layer from different sites. Furthermore, samples from sites on the same island were more similar to each other, regardless of which layer they originated from, than to analogous layers from another island. However, cyanobacterial and algal taxa were abundant in all surface and bottom layers, with anaerobic and chemoautotrophic taxa concentrated in the middle two layers, suggesting crust oxygenation from both above and below. Thus, the arrangement of oxygenated vs. anoxygenated niches in these orange crusts is functionally distinct relative to other laminated cyanobacterial-bacterial communities examined to date, with convergent evolution due to similar environmental conditions a likely driver for these phenotypically comparable but genetically distinct microbial consortia.},
}
RevDate: 2020-11-16
CmpDate: 2020-11-16
Fundamental control of grade-specific colorectal cancer morphology by Src regulation of ezrin-centrosome engagement.
The Journal of pathology, 251(3):310-322.
The phenotypic spectrum of colorectal cancer (CRC) is remarkably diverse, with seemingly endless variations in cell shape, mitotic figures and multicellular configurations. Despite this morphological complexity, histological grading of collective phenotype patterns provides robust prognostic stratification in CRC. Although mechanistic understanding is incomplete, previous studies have shown that the cortical protein ezrin controls diversification of cell shape, mitotic figure geometry and multicellular architecture, in 3D organotypic CRC cultures. Because ezrin is a substrate of Src tyrosine kinase that is frequently overexpressed in CRC, we investigated Src regulation of ezrin and morphogenic growth in 3D CRC cultures. Here we show that Src perturbations disrupt CRC epithelial spatial organisation. Aberrant Src activity suppresses formation of the cortical ezrin cap that anchors interphase centrosomes. In CRC cells with a normal centrosome number, these events lead to mitotic spindle misorientation, perturbation of cell cleavage, abnormal epithelial stratification, apical membrane misalignment, multilumen formation and evolution of cribriform multicellular morphology, a feature of low-grade cancer. In isogenic CRC cells with centrosome amplification, aberrant Src signalling promotes multipolar mitotic spindle formation, pleomorphism and morphological features of high-grade cancer. Translational studies in archival human CRC revealed associations between Src intensity, multipolar mitotic spindle frequency and high-grade cancer morphology. Collectively, our study reveals Src regulation of CRC morphogenic growth via ezrin-centrosome engagement and uncovers combined perturbations underlying transition to high-grade CRC morphology. © 2020 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.
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@article {pmid32315081,
year = {2020},
author = {Rainey, L and Deevi, RK and McClements, J and Khawaja, H and Watson, CJ and Roudier, M and Van Schaeybroeck, S and Campbell, FC},
title = {Fundamental control of grade-specific colorectal cancer morphology by Src regulation of ezrin-centrosome engagement.},
journal = {The Journal of pathology},
volume = {251},
number = {3},
pages = {310-322},
doi = {10.1002/path.5452},
pmid = {32315081},
issn = {1096-9896},
support = {MR/L015110/1/MRC_/Medical Research Council/United Kingdom ; L015110/MRC_/Medical Research Council/United Kingdom ; },
mesh = {Caco-2 Cells ; Centrosome/*enzymology/pathology ; Colorectal Neoplasms/*enzymology/genetics/pathology ; Cytoskeletal Proteins/genetics/*metabolism ; Focal Adhesion Kinase 1/genetics/metabolism ; HCT116 Cells ; Humans ; *Mitosis ; Neoplasm Grading ; PTEN Phosphohydrolase/genetics/metabolism ; Signal Transduction ; src-Family Kinases/genetics/*metabolism ; },
abstract = {The phenotypic spectrum of colorectal cancer (CRC) is remarkably diverse, with seemingly endless variations in cell shape, mitotic figures and multicellular configurations. Despite this morphological complexity, histological grading of collective phenotype patterns provides robust prognostic stratification in CRC. Although mechanistic understanding is incomplete, previous studies have shown that the cortical protein ezrin controls diversification of cell shape, mitotic figure geometry and multicellular architecture, in 3D organotypic CRC cultures. Because ezrin is a substrate of Src tyrosine kinase that is frequently overexpressed in CRC, we investigated Src regulation of ezrin and morphogenic growth in 3D CRC cultures. Here we show that Src perturbations disrupt CRC epithelial spatial organisation. Aberrant Src activity suppresses formation of the cortical ezrin cap that anchors interphase centrosomes. In CRC cells with a normal centrosome number, these events lead to mitotic spindle misorientation, perturbation of cell cleavage, abnormal epithelial stratification, apical membrane misalignment, multilumen formation and evolution of cribriform multicellular morphology, a feature of low-grade cancer. In isogenic CRC cells with centrosome amplification, aberrant Src signalling promotes multipolar mitotic spindle formation, pleomorphism and morphological features of high-grade cancer. Translational studies in archival human CRC revealed associations between Src intensity, multipolar mitotic spindle frequency and high-grade cancer morphology. Collectively, our study reveals Src regulation of CRC morphogenic growth via ezrin-centrosome engagement and uncovers combined perturbations underlying transition to high-grade CRC morphology. © 2020 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Caco-2 Cells
Centrosome/*enzymology/pathology
Colorectal Neoplasms/*enzymology/genetics/pathology
Cytoskeletal Proteins/genetics/*metabolism
Focal Adhesion Kinase 1/genetics/metabolism
HCT116 Cells
Humans
*Mitosis
Neoplasm Grading
PTEN Phosphohydrolase/genetics/metabolism
Signal Transduction
src-Family Kinases/genetics/*metabolism
RevDate: 2020-09-28
Tracing the Origin of Planktonic Protists in an Ancient Lake.
Microorganisms, 8(4):.
Ancient lakes are among the most interesting models for evolution studies because their biodiversity is the result of a complex combination of migration and speciation. Here, we investigate the origin of single celled planktonic eukaryotes from the oldest lake in the world-Lake Baikal (Russia). By using 18S rDNA metabarcoding, we recovered 1414 Operational Taxonomic Units (OTUs) belonging to protists populating surface waters (1-50 m) and representing pico/nano-sized cells. The recovered communities resembled other lacustrine freshwater assemblages found elsewhere, especially the taxonomically unclassified protists. However, our results suggest that a fraction of Baikal protists could belong to glacial relicts and have close relationships with marine/brackish species. Moreover, our results suggest that rapid radiation may have occurred among some protist taxa, partially mirroring what was already shown for multicellular organisms in Lake Baikal. We found 16% of the OTUs belonging to potential species flocks in Stramenopiles, Alveolata, Opisthokonta, Archaeplastida, Rhizaria, and Hacrobia. Putative flocks predominated in Chrysophytes, which are highly diverse in Lake Baikal. Also, the 18S rDNA of a number of species (7% of the total) differed >10% from other known sequences. These taxa as well as those belonging to the flocks may be endemic to Lake Baikal. Overall, our study points to novel diversity of planktonic protists in Lake Baikal, some of which may have emerged in situ after evolutionary diversification.
Additional Links: PMID-32283732
PubMed:
Citation:
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@article {pmid32283732,
year = {2020},
author = {Annenkova, NV and Giner, CR and Logares, R},
title = {Tracing the Origin of Planktonic Protists in an Ancient Lake.},
journal = {Microorganisms},
volume = {8},
number = {4},
pages = {},
pmid = {32283732},
issn = {2076-2607},
support = {18-74-00054//Russian Science Foundation/ ; 0345-2016-0009//Russian state assignment/ ; RYC-2013-12554//Ministerio de Economía y Competitividad/ ; },
abstract = {Ancient lakes are among the most interesting models for evolution studies because their biodiversity is the result of a complex combination of migration and speciation. Here, we investigate the origin of single celled planktonic eukaryotes from the oldest lake in the world-Lake Baikal (Russia). By using 18S rDNA metabarcoding, we recovered 1414 Operational Taxonomic Units (OTUs) belonging to protists populating surface waters (1-50 m) and representing pico/nano-sized cells. The recovered communities resembled other lacustrine freshwater assemblages found elsewhere, especially the taxonomically unclassified protists. However, our results suggest that a fraction of Baikal protists could belong to glacial relicts and have close relationships with marine/brackish species. Moreover, our results suggest that rapid radiation may have occurred among some protist taxa, partially mirroring what was already shown for multicellular organisms in Lake Baikal. We found 16% of the OTUs belonging to potential species flocks in Stramenopiles, Alveolata, Opisthokonta, Archaeplastida, Rhizaria, and Hacrobia. Putative flocks predominated in Chrysophytes, which are highly diverse in Lake Baikal. Also, the 18S rDNA of a number of species (7% of the total) differed >10% from other known sequences. These taxa as well as those belonging to the flocks may be endemic to Lake Baikal. Overall, our study points to novel diversity of planktonic protists in Lake Baikal, some of which may have emerged in situ after evolutionary diversification.},
}
RevDate: 2020-07-20
CmpDate: 2020-07-20
How to fit in: The learning principles of cell differentiation.
PLoS computational biology, 16(4):e1006811.
Cell differentiation in multicellular organisms requires cells to respond to complex combinations of extracellular cues, such as morphogen concentrations. Some models of phenotypic plasticity conceptualise the response as a relatively simple function of a single environmental cues (e.g. a linear function of one cue), which facilitates rigorous analysis. Conversely, more mechanistic models such those implementing GRNs allows for a more general class of response functions but makes analysis more difficult. Therefore, a general theory describing how cells integrate multi-dimensional signals is lacking. In this work, we propose a theoretical framework for understanding the relationships between environmental cues (inputs) and phenotypic responses (outputs) underlying cell plasticity. We describe the relationship between environment and cell phenotype using logical functions, making the evolution of cell plasticity equivalent to a simple categorisation learning task. This abstraction allows us to apply principles derived from learning theory to understand the evolution of multi-dimensional plasticity. Our results show that natural selection is capable of discovering adaptive forms of cell plasticity associated with complex logical functions. However, developmental dynamics cause simpler functions to evolve more readily than complex ones. By using conceptual tools derived from learning theory we show that this developmental bias can be interpreted as a learning bias in the acquisition of plasticity functions. Because of that bias, the evolution of plasticity enables cells, under some circumstances, to display appropriate plastic responses to environmental conditions that they have not experienced in their evolutionary past. This is possible when the selective environment mirrors the bias of the developmental dynamics favouring the acquisition of simple plasticity functions-an example of the necessary conditions for generalisation in learning systems. These results illustrate the functional parallelisms between learning in neural networks and the action of natural selection on environmentally sensitive gene regulatory networks. This offers a theoretical framework for the evolution of plastic responses that integrate information from multiple cues, a phenomenon that underpins the evolution of multicellularity and developmental robustness.
Additional Links: PMID-32282832
PubMed:
Citation:
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@article {pmid32282832,
year = {2020},
author = {Brun-Usan, M and Thies, C and Watson, RA},
title = {How to fit in: The learning principles of cell differentiation.},
journal = {PLoS computational biology},
volume = {16},
number = {4},
pages = {e1006811},
pmid = {32282832},
issn = {1553-7358},
mesh = {Adaptation, Physiological/*genetics ; Animals ; Biological Evolution ; *Cell Differentiation ; Computer Simulation ; Developmental Biology/*methods ; Environment ; Gene Regulatory Networks ; Genetic Variation ; Learning ; Models, Biological ; Phenotype ; Selection, Genetic ; },
abstract = {Cell differentiation in multicellular organisms requires cells to respond to complex combinations of extracellular cues, such as morphogen concentrations. Some models of phenotypic plasticity conceptualise the response as a relatively simple function of a single environmental cues (e.g. a linear function of one cue), which facilitates rigorous analysis. Conversely, more mechanistic models such those implementing GRNs allows for a more general class of response functions but makes analysis more difficult. Therefore, a general theory describing how cells integrate multi-dimensional signals is lacking. In this work, we propose a theoretical framework for understanding the relationships between environmental cues (inputs) and phenotypic responses (outputs) underlying cell plasticity. We describe the relationship between environment and cell phenotype using logical functions, making the evolution of cell plasticity equivalent to a simple categorisation learning task. This abstraction allows us to apply principles derived from learning theory to understand the evolution of multi-dimensional plasticity. Our results show that natural selection is capable of discovering adaptive forms of cell plasticity associated with complex logical functions. However, developmental dynamics cause simpler functions to evolve more readily than complex ones. By using conceptual tools derived from learning theory we show that this developmental bias can be interpreted as a learning bias in the acquisition of plasticity functions. Because of that bias, the evolution of plasticity enables cells, under some circumstances, to display appropriate plastic responses to environmental conditions that they have not experienced in their evolutionary past. This is possible when the selective environment mirrors the bias of the developmental dynamics favouring the acquisition of simple plasticity functions-an example of the necessary conditions for generalisation in learning systems. These results illustrate the functional parallelisms between learning in neural networks and the action of natural selection on environmentally sensitive gene regulatory networks. This offers a theoretical framework for the evolution of plastic responses that integrate information from multiple cues, a phenomenon that underpins the evolution of multicellularity and developmental robustness.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Adaptation, Physiological/*genetics
Animals
Biological Evolution
*Cell Differentiation
Computer Simulation
Developmental Biology/*methods
Environment
Gene Regulatory Networks
Genetic Variation
Learning
Models, Biological
Phenotype
Selection, Genetic
RevDate: 2020-10-06
CmpDate: 2020-07-27
Expanding the genetic code of the human hematopoietic system.
Proceedings of the National Academy of Sciences of the United States of America, 117(16):8845-8849.
The genetic incorporation of noncanonical amino acids (ncAAs) into proteins has been realized in bacteria, yeast, and mammalian cells, and recently, in multicellular organisms including plants and animals. However, the addition of new building blocks to the genetic code of tissues from human origin has not yet been achieved. To this end, we report a self-replicating Epstein-Barr virus-based episomal vector for the long-term encoding of ncAAs in human hematopoietic stem cells and reconstitution of this genetically engineered hematopoietic system in mice.
Additional Links: PMID-32253306
PubMed:
Citation:
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@article {pmid32253306,
year = {2020},
author = {Shao, S and Koh, M and Schultz, PG},
title = {Expanding the genetic code of the human hematopoietic system.},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {117},
number = {16},
pages = {8845-8849},
pmid = {32253306},
issn = {1091-6490},
support = {R01 GM132071/GM/NIGMS NIH HHS/United States ; },
mesh = {Amino Acids/*genetics ; Animals ; Cell Differentiation/*genetics ; Fetal Blood/cytology ; Gene Transfer Techniques ; Genetic Code ; Genetic Vectors/*genetics ; HEK293 Cells ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/*physiology ; Herpesvirus 4, Human/genetics ; Humans ; Mice ; Mice, Inbred NOD ; Plasmids/genetics ; Primary Cell Culture/methods ; Protein Engineering/*methods ; Transfection/methods ; Transplantation Chimera ; Transplantation, Heterologous/methods ; },
abstract = {The genetic incorporation of noncanonical amino acids (ncAAs) into proteins has been realized in bacteria, yeast, and mammalian cells, and recently, in multicellular organisms including plants and animals. However, the addition of new building blocks to the genetic code of tissues from human origin has not yet been achieved. To this end, we report a self-replicating Epstein-Barr virus-based episomal vector for the long-term encoding of ncAAs in human hematopoietic stem cells and reconstitution of this genetically engineered hematopoietic system in mice.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Amino Acids/*genetics
Animals
Cell Differentiation/*genetics
Fetal Blood/cytology
Gene Transfer Techniques
Genetic Code
Genetic Vectors/*genetics
HEK293 Cells
Hematopoietic Stem Cell Transplantation
Hematopoietic Stem Cells/*physiology
Herpesvirus 4, Human/genetics
Humans
Mice
Mice, Inbred NOD
Plasmids/genetics
Primary Cell Culture/methods
Protein Engineering/*methods
Transfection/methods
Transplantation Chimera
Transplantation, Heterologous/methods
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ESP Quick Facts
ESP Origins
In the early 1990's, Robert Robbins was a faculty member at Johns Hopkins, where he directed the informatics core of GDB — the human gene-mapping database of the international human genome project. To share papers with colleagues around the world, he set up a small paper-sharing section on his personal web page. This small project evolved into The Electronic Scholarly Publishing Project.
ESP Support
In 1995, Robbins became the VP/IT of the Fred Hutchinson Cancer Research Center in Seattle, WA. Soon after arriving in Seattle, Robbins secured funding, through the ELSI component of the US Human Genome Project, to create the original ESP.ORG web site, with the formal goal of providing free, world-wide access to the literature of classical genetics.
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Although the methods of molecular biology can seem almost magical to the uninitiated, the original techniques of classical genetics are readily appreciated by one and all: cross individuals that differ in some inherited trait, collect all of the progeny, score their attributes, and propose mechanisms to explain the patterns of inheritance observed.
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