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ESP: PubMed Auto Bibliography 12 Nov 2024 at 01:34 Created:
Origin of Multicellular Eukaryotes
Created with PubMed® Query: ( (origin OR evolution) AND (eukaryotes OR eukaryota) AND (multicelluarity OR multicellular) NOT 33634751[PMID] ) NOT pmcbook NOT ispreviousversion
Citations The Papers (from PubMed®)
RevDate: 2024-11-07
CmpDate: 2024-11-07
Plant ribosomes as a score to fathom the melody of 2'-O-methylation across evolution.
RNA biology, 21(1):70-81.
2'-O-ribose methylation (2'-O-Me) is one of the most common RNA modifications detected in ribosomal RNAs (rRNA) from bacteria to eukaryotic cells. 2'-O-Me favours a specific RNA conformation and protects RNA from hydrolysis. Moreover, rRNA 2'-O-Me might stabilize its interactions with messenger RNA (mRNA), transfer RNA (tRNA) or proteins. The extent of rRNA 2'-O-Me fluctuates between species from 3-4 sites in bacteria to tens of sites in archaea, yeast, algae, plants and human. Depending on the organism as well as the rRNA targeting site and position, the 2'-O-Me reaction can be carried out by several site-specific RNA methyltransferases (RMTase) or by a single RMTase associated to specific RNA guides. Here, we review current progresses in rRNA 2'-O-Me (sites/Nm and RMTases) in plants and compare the results with molecular clues from unicellular (bacteria, archaea, algae and yeast) as well as multicellular (human and plants) organisms.
Additional Links: PMID-39508203
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@article {pmid39508203,
year = {2024},
author = {Neumann, SA and Gaspin, C and Sáez-Vásquez, J},
title = {Plant ribosomes as a score to fathom the melody of 2'-O-methylation across evolution.},
journal = {RNA biology},
volume = {21},
number = {1},
pages = {70-81},
doi = {10.1080/15476286.2024.2417152},
pmid = {39508203},
issn = {1555-8584},
mesh = {Methylation ; *Ribosomes/metabolism ; *RNA, Ribosomal/metabolism/genetics/chemistry ; *Plants/metabolism/genetics ; Humans ; Evolution, Molecular ; Methyltransferases/metabolism/genetics/chemistry ; RNA, Plant/metabolism/genetics/chemistry ; Archaea/genetics/metabolism ; RNA, Transfer/metabolism/genetics/chemistry ; },
abstract = {2'-O-ribose methylation (2'-O-Me) is one of the most common RNA modifications detected in ribosomal RNAs (rRNA) from bacteria to eukaryotic cells. 2'-O-Me favours a specific RNA conformation and protects RNA from hydrolysis. Moreover, rRNA 2'-O-Me might stabilize its interactions with messenger RNA (mRNA), transfer RNA (tRNA) or proteins. The extent of rRNA 2'-O-Me fluctuates between species from 3-4 sites in bacteria to tens of sites in archaea, yeast, algae, plants and human. Depending on the organism as well as the rRNA targeting site and position, the 2'-O-Me reaction can be carried out by several site-specific RNA methyltransferases (RMTase) or by a single RMTase associated to specific RNA guides. Here, we review current progresses in rRNA 2'-O-Me (sites/Nm and RMTases) in plants and compare the results with molecular clues from unicellular (bacteria, archaea, algae and yeast) as well as multicellular (human and plants) organisms.},
}
MeSH Terms:
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Methylation
*Ribosomes/metabolism
*RNA, Ribosomal/metabolism/genetics/chemistry
*Plants/metabolism/genetics
Humans
Evolution, Molecular
Methyltransferases/metabolism/genetics/chemistry
RNA, Plant/metabolism/genetics/chemistry
Archaea/genetics/metabolism
RNA, Transfer/metabolism/genetics/chemistry
RevDate: 2024-11-04
CmpDate: 2024-11-04
Deciphering the topological landscape of glioma using a network theory framework.
Scientific reports, 14(1):26724.
Glioma stem cells have been recognized as key players in glioma recurrence and therapeutic resistance, presenting a promising target for novel treatments. However, the limited understanding of the role glioma stem cells play in the glioma hierarchy has drawn controversy and hindered research translation into therapies. Despite significant advances in our understanding of gene regulatory networks, the dynamics of these networks and their implications for glioma remain elusive. This study employs a systemic theoretical perspective to integrate experimental knowledge into a core endogenous network model for glioma, thereby elucidating its energy landscape through network dynamics computation. The model identifies two stable states corresponding to astrocytic-like and oligodendrocytic-like tumor cells, connected by a transition state with the feature of high stemness, which serves as one of the energy barriers between astrocytic-like and oligodendrocytic-like states, indicating the instability of glioma stem cells in vivo. We also obtained various stable states further supporting glioma's multicellular origins and uncovered a group of transition states that could potentially induce tumor heterogeneity and therapeutic resistance. This research proposes that the transition states linking both glioma stable states are central to glioma heterogeneity and therapy resistance. Our approach may contribute to the advancement of glioma therapy by offering a novel perspective on the complex landscape of glioma biology.
Additional Links: PMID-39496747
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@article {pmid39496747,
year = {2024},
author = {Yao, M and Su, Y and Xiong, R and Zhang, X and Zhu, X and Chen, YC and Ao, P},
title = {Deciphering the topological landscape of glioma using a network theory framework.},
journal = {Scientific reports},
volume = {14},
number = {1},
pages = {26724},
pmid = {39496747},
issn = {2045-2322},
support = {16Z103060007//National Natural Science Foundation of China/ ; 16Z103060007//National Natural Science Foundation of China/ ; 16Z103060007//National Natural Science Foundation of China/ ; 16Z103060007//National Natural Science Foundation of China/ ; 16Z103060007//National Natural Science Foundation of China/ ; 16Z103060007//National Natural Science Foundation of China/ ; 16Z103060007//National Natural Science Foundation of China/ ; },
mesh = {*Glioma/pathology/genetics/metabolism ; Humans ; *Gene Regulatory Networks ; *Neoplastic Stem Cells/metabolism/pathology ; *Brain Neoplasms/pathology/metabolism ; Gene Expression Regulation, Neoplastic ; Astrocytes/metabolism ; },
abstract = {Glioma stem cells have been recognized as key players in glioma recurrence and therapeutic resistance, presenting a promising target for novel treatments. However, the limited understanding of the role glioma stem cells play in the glioma hierarchy has drawn controversy and hindered research translation into therapies. Despite significant advances in our understanding of gene regulatory networks, the dynamics of these networks and their implications for glioma remain elusive. This study employs a systemic theoretical perspective to integrate experimental knowledge into a core endogenous network model for glioma, thereby elucidating its energy landscape through network dynamics computation. The model identifies two stable states corresponding to astrocytic-like and oligodendrocytic-like tumor cells, connected by a transition state with the feature of high stemness, which serves as one of the energy barriers between astrocytic-like and oligodendrocytic-like states, indicating the instability of glioma stem cells in vivo. We also obtained various stable states further supporting glioma's multicellular origins and uncovered a group of transition states that could potentially induce tumor heterogeneity and therapeutic resistance. This research proposes that the transition states linking both glioma stable states are central to glioma heterogeneity and therapy resistance. Our approach may contribute to the advancement of glioma therapy by offering a novel perspective on the complex landscape of glioma biology.},
}
MeSH Terms:
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*Glioma/pathology/genetics/metabolism
Humans
*Gene Regulatory Networks
*Neoplastic Stem Cells/metabolism/pathology
*Brain Neoplasms/pathology/metabolism
Gene Expression Regulation, Neoplastic
Astrocytes/metabolism
RevDate: 2024-10-31
CmpDate: 2024-10-31
The evolutionarily conserved PhLP3 is essential for sperm development in Drosophila melanogaster.
PloS one, 19(10):e0306676 pii:PONE-D-24-25002.
Phosducin-like proteins (PhLP) are thioredoxin domain-containing proteins that are highly conserved across unicellular and multicellular organisms. PhLP family proteins are hypothesized to function as co-chaperones in the folding of cytoskeletal proteins. Here, we present the initial molecular, biochemical, and functional characterization of CG4511 as Drosophila melanogaster PhLP3. We cloned the gene into a bacterial expression vector and produced enzymatically active recombinant PhLP3, which showed similar kinetics to previously characterized orthologues. A fly strain homozygous for a P-element insertion in the 5' UTR of the PhLP3 gene exhibited significant downregulation of PhLP3 expression. We found these male flies to be sterile. Microscopic analysis revealed altered testes morphology and impairment of spermiogenesis, leading to a lack of mature sperm. Among the most significant observations was the lack of actin cones during sperm maturation. Excision of the P-element insertion in PhLP3 restored male fertility, spermiogenesis, and seminal vesicle size. Given the high level of conservation of PhLP3, our data suggests PhLP3 may be an important regulator of sperm development across species.
Additional Links: PMID-39480878
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@article {pmid39480878,
year = {2024},
author = {Petit, C and Kojak, E and Webster, S and Marra, M and Sweeney, B and Chaikin, C and Jemc, JC and Kanzok, SM},
title = {The evolutionarily conserved PhLP3 is essential for sperm development in Drosophila melanogaster.},
journal = {PloS one},
volume = {19},
number = {10},
pages = {e0306676},
doi = {10.1371/journal.pone.0306676},
pmid = {39480878},
issn = {1932-6203},
mesh = {Animals ; *Drosophila melanogaster/genetics/metabolism/growth & development ; Male ; *Drosophila Proteins/genetics/metabolism ; *Spermatogenesis/genetics ; *Spermatozoa/metabolism ; Evolution, Molecular ; Testis/metabolism ; Conserved Sequence ; },
abstract = {Phosducin-like proteins (PhLP) are thioredoxin domain-containing proteins that are highly conserved across unicellular and multicellular organisms. PhLP family proteins are hypothesized to function as co-chaperones in the folding of cytoskeletal proteins. Here, we present the initial molecular, biochemical, and functional characterization of CG4511 as Drosophila melanogaster PhLP3. We cloned the gene into a bacterial expression vector and produced enzymatically active recombinant PhLP3, which showed similar kinetics to previously characterized orthologues. A fly strain homozygous for a P-element insertion in the 5' UTR of the PhLP3 gene exhibited significant downregulation of PhLP3 expression. We found these male flies to be sterile. Microscopic analysis revealed altered testes morphology and impairment of spermiogenesis, leading to a lack of mature sperm. Among the most significant observations was the lack of actin cones during sperm maturation. Excision of the P-element insertion in PhLP3 restored male fertility, spermiogenesis, and seminal vesicle size. Given the high level of conservation of PhLP3, our data suggests PhLP3 may be an important regulator of sperm development across species.},
}
MeSH Terms:
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Animals
*Drosophila melanogaster/genetics/metabolism/growth & development
Male
*Drosophila Proteins/genetics/metabolism
*Spermatogenesis/genetics
*Spermatozoa/metabolism
Evolution, Molecular
Testis/metabolism
Conserved Sequence
RevDate: 2024-10-30
CmpDate: 2024-10-30
Functional Optimization in Distinct Tissues and Conditions Constrains the Rate of Protein Evolution.
Molecular biology and evolution, 41(10):.
Understanding the main determinants of protein evolution is a fundamental challenge in biology. Despite many decades of active research, the molecular and cellular mechanisms underlying the substantial variability of evolutionary rates across cellular proteins are not currently well understood. It also remains unclear how protein molecular function is optimized in the context of multicellular species and why many proteins, such as enzymes, are only moderately efficient on average. Our analysis of genomics and functional datasets reveals in multiple organisms a strong inverse relationship between the optimality of protein molecular function and the rate of protein evolution. Furthermore, we find that highly expressed proteins tend to be substantially more functionally optimized. These results suggest that cellular expression costs lead to more pronounced functional optimization of abundant proteins and that the purifying selection to maintain high levels of functional optimality significantly slows protein evolution. We observe that in multicellular species both the rate of protein evolution and the degree of protein functional efficiency are primarily affected by expression in several distinct cell types and tissues, specifically, in developed neurons with upregulated synaptic processes in animals and in young and fast-growing tissues in plants. Overall, our analysis reveals how various constraints from the molecular, cellular, and species' levels of biological organization jointly affect the rate of protein evolution and the level of protein functional adaptation.
Additional Links: PMID-39431545
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@article {pmid39431545,
year = {2024},
author = {Usmanova, DR and Plata, G and Vitkup, D},
title = {Functional Optimization in Distinct Tissues and Conditions Constrains the Rate of Protein Evolution.},
journal = {Molecular biology and evolution},
volume = {41},
number = {10},
pages = {},
pmid = {39431545},
issn = {1537-1719},
support = {R35GM131884/GM/NIGMS NIH HHS/United States ; },
mesh = {*Evolution, Molecular ; Animals ; Proteins/genetics/metabolism ; Humans ; },
abstract = {Understanding the main determinants of protein evolution is a fundamental challenge in biology. Despite many decades of active research, the molecular and cellular mechanisms underlying the substantial variability of evolutionary rates across cellular proteins are not currently well understood. It also remains unclear how protein molecular function is optimized in the context of multicellular species and why many proteins, such as enzymes, are only moderately efficient on average. Our analysis of genomics and functional datasets reveals in multiple organisms a strong inverse relationship between the optimality of protein molecular function and the rate of protein evolution. Furthermore, we find that highly expressed proteins tend to be substantially more functionally optimized. These results suggest that cellular expression costs lead to more pronounced functional optimization of abundant proteins and that the purifying selection to maintain high levels of functional optimality significantly slows protein evolution. We observe that in multicellular species both the rate of protein evolution and the degree of protein functional efficiency are primarily affected by expression in several distinct cell types and tissues, specifically, in developed neurons with upregulated synaptic processes in animals and in young and fast-growing tissues in plants. Overall, our analysis reveals how various constraints from the molecular, cellular, and species' levels of biological organization jointly affect the rate of protein evolution and the level of protein functional adaptation.},
}
MeSH Terms:
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*Evolution, Molecular
Animals
Proteins/genetics/metabolism
Humans
RevDate: 2024-10-29
CmpDate: 2024-10-29
A novel 3D cardiac microtissue model for investigation of cardiovascular complications in rheumatoid arthritis.
Stem cell research & therapy, 15(1):382.
BACKGROUND: Rheumatoid arthritis (RA) is a chronic inflammatory disease that affects not only the joints but also has significant cardiovascular (CV) manifestations. The mechanistic interplay between RA and cardiovascular complications is not yet well understood due to the lack of relevant in vitro models. In this study, we established RA cardiac microtisses (cMTs) from iPSC-derived cardiomyocytes (CMs), endothelial cells (ECs) and cardiac fibroblasts (CFs) to investigate whether this fully human 3D multicellular system could serve as a platform to elucidate the connection between RA and CV disorders.
METHODS: PBMC and FLS from healthy and RA donors were reprogrammed to hiPSCs with Sendai vectors. hiPSCs pluripotency was assessed by IF, FACS, spontaneous embryoid bodies formation and teratoma assay. hiPSCs were differentiated to cardiac derivatives such as CMs, ECs and CFs, followed by cell markers characterizations (IF, FACS, qRT-PCR) and functional assessments. 3D cMTs were generated by aggregation of 70% CMs, 15% ECs and 15% CFs. After 21 days in culture, structural and metabolic properties of 3D cMTs were examined by IF, qRT-PCR and Seahorse bioanalyzer.
RESULTS: hiPSCs demonstrated typical colony-like morphology, normal karyotype, presence of pluripotency markers, and ability to differentiate into cells originating from all three germ layers. hiPSC-CMs showed spontaneous beating and expression of cardiac markers (cTnT, MYL7, NKX2.5, MYH7). hiPSC-ECs formed sprouting spheres and tubes and expressed CD31 and CD144. hiPSC-CFs presented spindle-shaped morphology and expression of vimentin, collagen 1 and DDR2. Self-aggregation of CMs/ECs/CFs allowed development of contracting 3D cMTs, demonstrating spherical organization of the cells, which partially resembled the cardiac muscle, both in structure and function. IF analysis confirmed the expression of cTnT, CD31, CD144 and DDR2 in generated 3D cMTs. RA cMTs exhibited significantly greater formation of capillary-like structures, mimicking enhanced vascularization-key RA feature-compared to control cMTs. Seahorse examination of cMTs revealed changes in mitochondrial and glycolytic rates in the presence of metabolic substrates and inhibitors.
CONCLUSIONS: The cMTs model may represent an advanced human stem cell-based platform for modeling CV complications in RA. The highly developed capillary-like structures observed within RA cMTs highlight a critical feature of inflammation-induced CV dysfunction in chronic inflammatory diseases.
Additional Links: PMID-39468575
PubMed:
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@article {pmid39468575,
year = {2024},
author = {Wolnik, J and Adamska, P and Oleksy, A and Sanetra, AM and Palus-Chramiec, K and Lewandowski, MH and Dulak, J and Biniecka, M},
title = {A novel 3D cardiac microtissue model for investigation of cardiovascular complications in rheumatoid arthritis.},
journal = {Stem cell research & therapy},
volume = {15},
number = {1},
pages = {382},
pmid = {39468575},
issn = {1757-6512},
support = {UMO-2017/25/B/NZ5/02243//Narodowe Centrum Nauki/ ; },
mesh = {Humans ; *Arthritis, Rheumatoid/metabolism/pathology ; *Induced Pluripotent Stem Cells/metabolism/cytology ; *Myocytes, Cardiac/metabolism/pathology/cytology ; *Cell Differentiation ; *Fibroblasts/metabolism/pathology ; Cardiovascular Diseases/pathology/metabolism ; Endothelial Cells/metabolism/pathology ; Cells, Cultured ; },
abstract = {BACKGROUND: Rheumatoid arthritis (RA) is a chronic inflammatory disease that affects not only the joints but also has significant cardiovascular (CV) manifestations. The mechanistic interplay between RA and cardiovascular complications is not yet well understood due to the lack of relevant in vitro models. In this study, we established RA cardiac microtisses (cMTs) from iPSC-derived cardiomyocytes (CMs), endothelial cells (ECs) and cardiac fibroblasts (CFs) to investigate whether this fully human 3D multicellular system could serve as a platform to elucidate the connection between RA and CV disorders.
METHODS: PBMC and FLS from healthy and RA donors were reprogrammed to hiPSCs with Sendai vectors. hiPSCs pluripotency was assessed by IF, FACS, spontaneous embryoid bodies formation and teratoma assay. hiPSCs were differentiated to cardiac derivatives such as CMs, ECs and CFs, followed by cell markers characterizations (IF, FACS, qRT-PCR) and functional assessments. 3D cMTs were generated by aggregation of 70% CMs, 15% ECs and 15% CFs. After 21 days in culture, structural and metabolic properties of 3D cMTs were examined by IF, qRT-PCR and Seahorse bioanalyzer.
RESULTS: hiPSCs demonstrated typical colony-like morphology, normal karyotype, presence of pluripotency markers, and ability to differentiate into cells originating from all three germ layers. hiPSC-CMs showed spontaneous beating and expression of cardiac markers (cTnT, MYL7, NKX2.5, MYH7). hiPSC-ECs formed sprouting spheres and tubes and expressed CD31 and CD144. hiPSC-CFs presented spindle-shaped morphology and expression of vimentin, collagen 1 and DDR2. Self-aggregation of CMs/ECs/CFs allowed development of contracting 3D cMTs, demonstrating spherical organization of the cells, which partially resembled the cardiac muscle, both in structure and function. IF analysis confirmed the expression of cTnT, CD31, CD144 and DDR2 in generated 3D cMTs. RA cMTs exhibited significantly greater formation of capillary-like structures, mimicking enhanced vascularization-key RA feature-compared to control cMTs. Seahorse examination of cMTs revealed changes in mitochondrial and glycolytic rates in the presence of metabolic substrates and inhibitors.
CONCLUSIONS: The cMTs model may represent an advanced human stem cell-based platform for modeling CV complications in RA. The highly developed capillary-like structures observed within RA cMTs highlight a critical feature of inflammation-induced CV dysfunction in chronic inflammatory diseases.},
}
MeSH Terms:
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Humans
*Arthritis, Rheumatoid/metabolism/pathology
*Induced Pluripotent Stem Cells/metabolism/cytology
*Myocytes, Cardiac/metabolism/pathology/cytology
*Cell Differentiation
*Fibroblasts/metabolism/pathology
Cardiovascular Diseases/pathology/metabolism
Endothelial Cells/metabolism/pathology
Cells, Cultured
RevDate: 2024-10-28
CmpDate: 2024-10-28
Back to the future - 20 years of progress and developments in photonic microscopy and biological imaging.
Journal of cell science, 137(20):.
In 2023, the ImaBio consortium (imabio-cnrs.fr), an interdisciplinary life microscopy research group at the Centre National de la Recherche Scientifique, celebrated its 20th anniversary. ImaBio contributes to the biological imaging community through organization of MiFoBio conferences, which are interdisciplinary conferences featuring lectures and hands-on workshops that attract specialists from around the world. MiFoBio conferences provide the community with an opportunity to reflect on the evolution of the field, and the 2023 event offered retrospective talks discussing the past 20 years of topics in microscopy, including imaging of multicellular assemblies, image analysis, quantification of molecular motions and interactions within cells, advancements in fluorescent labels, and laser technology for multiphoton and label-free imaging of thick biological samples. In this Perspective, we compile summaries of these presentations overviewing 20 years of advancements in a specific area of microscopy, each of which concludes with a brief look towards the future. The full presentations are available on the ImaBio YouTube channel (youtube.com/@gdrimabio5724).
Additional Links: PMID-39465534
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@article {pmid39465534,
year = {2024},
author = {Erard, M and Favard, C and Lavis, LD and Recher, G and Rigneault, H and Sage, D},
title = {Back to the future - 20 years of progress and developments in photonic microscopy and biological imaging.},
journal = {Journal of cell science},
volume = {137},
number = {20},
pages = {},
doi = {10.1242/jcs.262344},
pmid = {39465534},
issn = {1477-9137},
mesh = {Humans ; *Microscopy/methods/trends/instrumentation ; Animals ; Photons ; },
abstract = {In 2023, the ImaBio consortium (imabio-cnrs.fr), an interdisciplinary life microscopy research group at the Centre National de la Recherche Scientifique, celebrated its 20th anniversary. ImaBio contributes to the biological imaging community through organization of MiFoBio conferences, which are interdisciplinary conferences featuring lectures and hands-on workshops that attract specialists from around the world. MiFoBio conferences provide the community with an opportunity to reflect on the evolution of the field, and the 2023 event offered retrospective talks discussing the past 20 years of topics in microscopy, including imaging of multicellular assemblies, image analysis, quantification of molecular motions and interactions within cells, advancements in fluorescent labels, and laser technology for multiphoton and label-free imaging of thick biological samples. In this Perspective, we compile summaries of these presentations overviewing 20 years of advancements in a specific area of microscopy, each of which concludes with a brief look towards the future. The full presentations are available on the ImaBio YouTube channel (youtube.com/@gdrimabio5724).},
}
MeSH Terms:
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Humans
*Microscopy/methods/trends/instrumentation
Animals
Photons
RevDate: 2024-10-24
The Unknown within the Known: Nucleolus, Understudied Compartment in the Filamentous Fungi.
Mycobiology, 52(4):214-221.
Nucleolus is the most conspicuous sub-nuclear compartment that is well known as the site of RNA polymerase I-mediated rDNA transcription and assembly of ribosome subunits in eukaryotes. Recent studies on mammalian cells suggest that functions of nucleolus are not limited to ribosome biogenesis, and that nucleolus is involved in a diverse array of nuclear and cellular processes such as DNA repair, stress responses, and protein sequestration. In fungi, knowledge of nucleolus and its functions was primarily gleaned from the budding yeast. However, little is known about nucleolus of the filamentous fungi. Considering that the filamentous fungi are multi-cellular eukaryotes and thus distinct from the yeast in many aspects, researches on nucleoli of filamentous fungi would have the potential to uncover the evolution of nucleolus and its roles in the diverse cellular processes. Here we provide a brief up-to-date overview of nucleolus in general, and evidence suggesting their roles in fungal physiology and development.
Additional Links: PMID-39445133
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@article {pmid39445133,
year = {2024},
author = {Lee, SH and Dubey, N and Jeon, J},
title = {The Unknown within the Known: Nucleolus, Understudied Compartment in the Filamentous Fungi.},
journal = {Mycobiology},
volume = {52},
number = {4},
pages = {214-221},
pmid = {39445133},
issn = {1229-8093},
abstract = {Nucleolus is the most conspicuous sub-nuclear compartment that is well known as the site of RNA polymerase I-mediated rDNA transcription and assembly of ribosome subunits in eukaryotes. Recent studies on mammalian cells suggest that functions of nucleolus are not limited to ribosome biogenesis, and that nucleolus is involved in a diverse array of nuclear and cellular processes such as DNA repair, stress responses, and protein sequestration. In fungi, knowledge of nucleolus and its functions was primarily gleaned from the budding yeast. However, little is known about nucleolus of the filamentous fungi. Considering that the filamentous fungi are multi-cellular eukaryotes and thus distinct from the yeast in many aspects, researches on nucleoli of filamentous fungi would have the potential to uncover the evolution of nucleolus and its roles in the diverse cellular processes. Here we provide a brief up-to-date overview of nucleolus in general, and evidence suggesting their roles in fungal physiology and development.},
}
RevDate: 2024-10-24
A transcriptomic hourglass in brown algae.
Nature [Epub ahead of print].
Complex multicellularity has emerged independently across a few eukaryotic lineages and is often associated with the rise of elaborate, tightly coordinated developmental processes[1,2]. How multicellularity and development are interconnected in evolution is a major question in biology. The hourglass model of embryonic evolution depicts how developmental processes are conserved during evolution, and predicts morphological and molecular divergence in early and late embryogenesis, bridged by a conserved mid-embryonic (phylotypic) period linked to the formation of the basic body plan[3,4]. Initially found in animal embryos[5-8], molecular hourglass patterns have recently been proposed for land plants and fungi[9,10]. However, whether the hourglass pattern is an intrinsic feature of all complex multicellular eukaryotes remains unknown. Here we tested the presence of a molecular hourglass in the brown algae, a eukaryotic lineage that has evolved multicellularity independently from animals, fungi and plants[1,11,12]. By exploring transcriptome evolution patterns of brown algae with distinct morphological complexities, we uncovered an hourglass pattern during embryogenesis in morphologically complex species. Filamentous algae without canonical embryogenesis display transcriptome conservation in multicellular stages of the life cycle, whereas unicellular stages are more rapidly evolving. Our findings suggest that transcriptome conservation in brown algae is associated with cell differentiation stages, but is not necessarily linked to embryogenesis. Together with previous work in animals, plants and fungi, we provide further evidence for the generality of a developmental hourglass pattern across complex multicellular eukaryotes.
Additional Links: PMID-39443791
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@article {pmid39443791,
year = {2024},
author = {Lotharukpong, JS and Zheng, M and Luthringer, R and Liesner, D and Drost, HG and Coelho, SM},
title = {A transcriptomic hourglass in brown algae.},
journal = {Nature},
volume = {},
number = {},
pages = {},
pmid = {39443791},
issn = {1476-4687},
abstract = {Complex multicellularity has emerged independently across a few eukaryotic lineages and is often associated with the rise of elaborate, tightly coordinated developmental processes[1,2]. How multicellularity and development are interconnected in evolution is a major question in biology. The hourglass model of embryonic evolution depicts how developmental processes are conserved during evolution, and predicts morphological and molecular divergence in early and late embryogenesis, bridged by a conserved mid-embryonic (phylotypic) period linked to the formation of the basic body plan[3,4]. Initially found in animal embryos[5-8], molecular hourglass patterns have recently been proposed for land plants and fungi[9,10]. However, whether the hourglass pattern is an intrinsic feature of all complex multicellular eukaryotes remains unknown. Here we tested the presence of a molecular hourglass in the brown algae, a eukaryotic lineage that has evolved multicellularity independently from animals, fungi and plants[1,11,12]. By exploring transcriptome evolution patterns of brown algae with distinct morphological complexities, we uncovered an hourglass pattern during embryogenesis in morphologically complex species. Filamentous algae without canonical embryogenesis display transcriptome conservation in multicellular stages of the life cycle, whereas unicellular stages are more rapidly evolving. Our findings suggest that transcriptome conservation in brown algae is associated with cell differentiation stages, but is not necessarily linked to embryogenesis. Together with previous work in animals, plants and fungi, we provide further evidence for the generality of a developmental hourglass pattern across complex multicellular eukaryotes.},
}
RevDate: 2024-10-10
Candidate genes involved in biosynthesis and degradation of the main extracellular matrix polysaccharides of brown algae and their probable evolutionary history.
BMC genomics, 25(1):950.
BACKGROUND: Brown algae belong to the Stramenopiles phylum and are phylogenetically distant from plants and other multicellular organisms. This independent evolutionary history has shaped brown algae with numerous metabolic characteristics specific to this group, including the synthesis of peculiar polysaccharides contained in their extracellular matrix (ECM). Alginates and fucose-containing sulphated polysaccharides (FCSPs), the latter including fucans, are the main components of ECMs. However, the metabolic pathways of these polysaccharides remain poorly described due to a lack of genomic data.
RESULTS: An extensive genomic dataset has been recently released for brown algae and their close sister species, for which we previously performed an expert annotation of key genes involved in ECM-carbohydrate metabolisms. Here we provide a deeper analysis of this set of genes using comparative genomics, phylogenetics analyses, and protein modelling. Two key gene families involved in both the synthesis and degradation of alginate were suggested to have been acquired by the common ancestor of brown algae and their closest sister species Schizocladia ischiensis. Our analysis indicates that this assumption can be extended to additional metabolic steps, and thus to the whole alginate metabolic pathway. The pathway for the biosynthesis of fucans still remains biochemically unresolved and we also investigate putative fucosyltransferase genes that may harbour a fucan synthase activity in brown algae.
CONCLUSIONS: Our analysis is the first extensive survey of carbohydrate-related enzymes in brown algae, and provides a valuable resource for future research into the glycome and ECM of brown algae. The expansion of specific families related to alginate metabolism may have represented an important prerequisite for the evolution of developmental complexity in brown algae. Our analysis questions the possible occurrence of FCSPs outside brown algae, notably within their closest sister taxon and in other Stramenopiles such as diatoms. Filling this knowledge gap in the future will help determine the origin and evolutionary history of fucan synthesis in eukaryotes.
Additional Links: PMID-39390408
PubMed:
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@article {pmid39390408,
year = {2024},
author = {Mazéas, L and Bouguerba-Collin, A and Cock, JM and Denoeud, F and Godfroy, O and Brillet-Guéguen, L and Barbeyron, T and Lipinska, AP and Delage, L and Corre, E and Drula, E and Henrissat, B and Czjzek, M and Terrapon, N and Hervé, C},
title = {Candidate genes involved in biosynthesis and degradation of the main extracellular matrix polysaccharides of brown algae and their probable evolutionary history.},
journal = {BMC genomics},
volume = {25},
number = {1},
pages = {950},
pmid = {39390408},
issn = {1471-2164},
support = {ANR-20-CE44-0011//Agence Nationale de la Recherche/ ; ANR-20-CE44-0011//Agence Nationale de la Recherche/ ; ANR-10-INBS-09//Agence Nationale de la Recherche/ ; ANR-10-INBS-09//Agence Nationale de la Recherche/ ; ANR-11-INBS-0013//Agence Nationale de la Recherche/ ; ANR-11-INBS-0013//Agence Nationale de la Recherche/ ; ANR-20-CE44-0011//Agence Nationale de la Recherche/ ; ANR-20-CE44-0011//Agence Nationale de la Recherche/ ; ANR-11-INBS-0013//Agence Nationale de la Recherche/ ; ANR-20-CE44-0011//Agence Nationale de la Recherche/ ; ANR-20-CE44-0011//Agence Nationale de la Recherche/ ; ANR-20-CE44-0011//Agence Nationale de la Recherche/ ; ANR-20-CE44-0011//Agence Nationale de la Recherche/ ; ANR-20-CE44-0011//Agence Nationale de la Recherche/ ; 638240/ERC_/European Research Council/International ; },
abstract = {BACKGROUND: Brown algae belong to the Stramenopiles phylum and are phylogenetically distant from plants and other multicellular organisms. This independent evolutionary history has shaped brown algae with numerous metabolic characteristics specific to this group, including the synthesis of peculiar polysaccharides contained in their extracellular matrix (ECM). Alginates and fucose-containing sulphated polysaccharides (FCSPs), the latter including fucans, are the main components of ECMs. However, the metabolic pathways of these polysaccharides remain poorly described due to a lack of genomic data.
RESULTS: An extensive genomic dataset has been recently released for brown algae and their close sister species, for which we previously performed an expert annotation of key genes involved in ECM-carbohydrate metabolisms. Here we provide a deeper analysis of this set of genes using comparative genomics, phylogenetics analyses, and protein modelling. Two key gene families involved in both the synthesis and degradation of alginate were suggested to have been acquired by the common ancestor of brown algae and their closest sister species Schizocladia ischiensis. Our analysis indicates that this assumption can be extended to additional metabolic steps, and thus to the whole alginate metabolic pathway. The pathway for the biosynthesis of fucans still remains biochemically unresolved and we also investigate putative fucosyltransferase genes that may harbour a fucan synthase activity in brown algae.
CONCLUSIONS: Our analysis is the first extensive survey of carbohydrate-related enzymes in brown algae, and provides a valuable resource for future research into the glycome and ECM of brown algae. The expansion of specific families related to alginate metabolism may have represented an important prerequisite for the evolution of developmental complexity in brown algae. Our analysis questions the possible occurrence of FCSPs outside brown algae, notably within their closest sister taxon and in other Stramenopiles such as diatoms. Filling this knowledge gap in the future will help determine the origin and evolutionary history of fucan synthesis in eukaryotes.},
}
RevDate: 2024-10-09
CmpDate: 2024-10-09
Ecological principles for the evolution of communication in collective systems.
Proceedings. Biological sciences, 291(2032):20241562.
Communication allows members of a collective to share information about their environment. Advanced collective systems, such as multicellular organisms and social insect colonies, vary in whether they use communication at all and, if they do, in what types of signals they use, but the origins of these differences are poorly understood. Here, we develop a theoretical framework to investigate the evolution and diversity of communication strategies under collective-level selection. We find that whether communication can evolve depends on a collective's external environment: communication only evolves in sufficiently stable environments, where the costs of sensing are high enough to disfavour independent sensing but not so high that the optimal strategy is to ignore the environment altogether. Moreover, we find that the evolution of diverse signalling strategies-including those relying on prolonged signalling (e.g. honeybee waggle dance), persistence of signals in the environment (e.g. ant trail pheromones) and brief but frequent communicative interactions (e.g. ant antennal contacts)-can be explained theoretically in terms of the interplay between the demands of the environment and internal constraints on the signal. Altogether, we provide a general framework for comparing communication strategies found in nature and uncover simple ecological principles that may contribute to their diversity.
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@article {pmid39381908,
year = {2024},
author = {Staps, M and Tarnita, CE and Kawakatsu, M},
title = {Ecological principles for the evolution of communication in collective systems.},
journal = {Proceedings. Biological sciences},
volume = {291},
number = {2032},
pages = {20241562},
pmid = {39381908},
issn = {1471-2954},
support = {//James S. McDonnell Foundation/ ; },
mesh = {Animals ; *Animal Communication ; *Biological Evolution ; Bees/physiology ; Ants/physiology ; Models, Biological ; Social Behavior ; },
abstract = {Communication allows members of a collective to share information about their environment. Advanced collective systems, such as multicellular organisms and social insect colonies, vary in whether they use communication at all and, if they do, in what types of signals they use, but the origins of these differences are poorly understood. Here, we develop a theoretical framework to investigate the evolution and diversity of communication strategies under collective-level selection. We find that whether communication can evolve depends on a collective's external environment: communication only evolves in sufficiently stable environments, where the costs of sensing are high enough to disfavour independent sensing but not so high that the optimal strategy is to ignore the environment altogether. Moreover, we find that the evolution of diverse signalling strategies-including those relying on prolonged signalling (e.g. honeybee waggle dance), persistence of signals in the environment (e.g. ant trail pheromones) and brief but frequent communicative interactions (e.g. ant antennal contacts)-can be explained theoretically in terms of the interplay between the demands of the environment and internal constraints on the signal. Altogether, we provide a general framework for comparing communication strategies found in nature and uncover simple ecological principles that may contribute to their diversity.},
}
MeSH Terms:
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Animals
*Animal Communication
*Biological Evolution
Bees/physiology
Ants/physiology
Models, Biological
Social Behavior
RevDate: 2024-10-09
CmpDate: 2024-10-09
EnhancerNet: a predictive model of cell identity dynamics through enhancer selection.
Development (Cambridge, England), 151(19):.
Understanding how cell identity is encoded by the genome and acquired during differentiation is a central challenge in cell biology. I have developed a theoretical framework called EnhancerNet, which models the regulation of cell identity through the lens of transcription factor-enhancer interactions. I demonstrate that autoregulation in these interactions imposes a constraint on the model, resulting in simplified dynamics that can be parameterized from observed cell identities. Despite its simplicity, EnhancerNet recapitulates a broad range of experimental observations on cell identity dynamics, including enhancer selection, cell fate induction, hierarchical differentiation through multipotent progenitor states and direct reprogramming by transcription factor overexpression. The model makes specific quantitative predictions, reproducing known reprogramming recipes and the complex haematopoietic differentiation hierarchy without fitting unobserved parameters. EnhancerNet provides insights into how new cell types could evolve and highlights the functional importance of distal regulatory elements with dynamic chromatin in multicellular evolution.
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@article {pmid39289870,
year = {2024},
author = {Karin, O},
title = {EnhancerNet: a predictive model of cell identity dynamics through enhancer selection.},
journal = {Development (Cambridge, England)},
volume = {151},
number = {19},
pages = {},
doi = {10.1242/dev.202997},
pmid = {39289870},
issn = {1477-9129},
support = {//Imperial College London/ ; },
mesh = {*Enhancer Elements, Genetic/genetics ; *Cell Differentiation/genetics ; Animals ; *Transcription Factors/metabolism/genetics ; Chromatin/metabolism ; Cell Lineage/genetics ; Humans ; Models, Biological ; Models, Genetic ; },
abstract = {Understanding how cell identity is encoded by the genome and acquired during differentiation is a central challenge in cell biology. I have developed a theoretical framework called EnhancerNet, which models the regulation of cell identity through the lens of transcription factor-enhancer interactions. I demonstrate that autoregulation in these interactions imposes a constraint on the model, resulting in simplified dynamics that can be parameterized from observed cell identities. Despite its simplicity, EnhancerNet recapitulates a broad range of experimental observations on cell identity dynamics, including enhancer selection, cell fate induction, hierarchical differentiation through multipotent progenitor states and direct reprogramming by transcription factor overexpression. The model makes specific quantitative predictions, reproducing known reprogramming recipes and the complex haematopoietic differentiation hierarchy without fitting unobserved parameters. EnhancerNet provides insights into how new cell types could evolve and highlights the functional importance of distal regulatory elements with dynamic chromatin in multicellular evolution.},
}
MeSH Terms:
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*Enhancer Elements, Genetic/genetics
*Cell Differentiation/genetics
Animals
*Transcription Factors/metabolism/genetics
Chromatin/metabolism
Cell Lineage/genetics
Humans
Models, Biological
Models, Genetic
RevDate: 2024-10-08
CmpDate: 2024-10-08
Larger colony sizes favoured the evolution of more worker castes in ants.
Nature ecology & evolution, 8(10):1959-1971.
The size-complexity hypothesis is a leading explanation for the evolution of complex life on earth. It predicts that in lineages that have undergone a major transition in organismality, larger numbers of lower-level subunits select for increased division of labour. Current data from multicellular organisms and social insects support a positive correlation between the number of cells and number of cell types and between colony size and the number of castes. However, the implication of these results is unclear, because colony size and number of cells are correlated with other variables which may also influence selection for division of labour, and causality could be in either direction. Here, to resolve this problem, we tested multiple causal hypotheses using data from 794 ant species. We found that larger colony sizes favoured the evolution of increased division of labour, resulting in more worker castes and greater variation in worker size. By contrast, our results did not provide consistent support for alternative hypotheses regarding either queen mating frequency or number of queens per colony explaining variation in division of labour. Overall, our results provide strong support for the size-complexity hypothesis.
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@article {pmid39187609,
year = {2024},
author = {Bell-Roberts, L and Turner, JFR and Werner, GDA and Downing, PA and Ross, L and West, SA},
title = {Larger colony sizes favoured the evolution of more worker castes in ants.},
journal = {Nature ecology & evolution},
volume = {8},
number = {10},
pages = {1959-1971},
pmid = {39187609},
issn = {2397-334X},
support = {834164/ERC_/European Research Council/International ; 834164//EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 European Research Council (H2020 Excellent Science - European Research Council)/ ; BB/M011224/1//RCUK | Biotechnology and Biological Sciences Research Council (BBSRC)/ ; },
mesh = {*Ants/physiology ; Animals ; *Biological Evolution ; *Population Density ; Social Behavior ; },
abstract = {The size-complexity hypothesis is a leading explanation for the evolution of complex life on earth. It predicts that in lineages that have undergone a major transition in organismality, larger numbers of lower-level subunits select for increased division of labour. Current data from multicellular organisms and social insects support a positive correlation between the number of cells and number of cell types and between colony size and the number of castes. However, the implication of these results is unclear, because colony size and number of cells are correlated with other variables which may also influence selection for division of labour, and causality could be in either direction. Here, to resolve this problem, we tested multiple causal hypotheses using data from 794 ant species. We found that larger colony sizes favoured the evolution of increased division of labour, resulting in more worker castes and greater variation in worker size. By contrast, our results did not provide consistent support for alternative hypotheses regarding either queen mating frequency or number of queens per colony explaining variation in division of labour. Overall, our results provide strong support for the size-complexity hypothesis.},
}
MeSH Terms:
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*Ants/physiology
Animals
*Biological Evolution
*Population Density
Social Behavior
RevDate: 2024-10-08
Microtubule reorganization and quiescence: an intertwined relationship.
Physiology (Bethesda, Md.) [Epub ahead of print].
Quiescence is operationally defined as a reversible proliferation arrest. This cellular state is central for both organism development and homeostasis, its dysregulation causing many pathologies. The quiescent state encompasses very diverse cellular situations depending on the cell type and its environment. Further, quiescent cell properties evolve with time, a process that is thought to be at the origin of aging in multicellular organisms. Microtubules are found in all eukaryotes, and are essential for cell proliferation as they support chromosome segregation and intracellular trafficking. Upon proliferation cessation and quiescence establishment, the microtubule cytoskeleton was shown to undergo significant remodeling. The purpose of this review is to examine the literature in search of evidence to determine whether the observed microtubule reorganizations are merely a consequence of quiescence establishment or if they somehow participate in this cell fate decision.
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@article {pmid39378102,
year = {2024},
author = {Laporte, D and Sagot, I},
title = {Microtubule reorganization and quiescence: an intertwined relationship.},
journal = {Physiology (Bethesda, Md.)},
volume = {},
number = {},
pages = {},
doi = {10.1152/physiol.00036.2024},
pmid = {39378102},
issn = {1548-9221},
support = {ANR-21-CE13-0023-01//Agence Nationale de la Recherche (ANR)/ ; },
abstract = {Quiescence is operationally defined as a reversible proliferation arrest. This cellular state is central for both organism development and homeostasis, its dysregulation causing many pathologies. The quiescent state encompasses very diverse cellular situations depending on the cell type and its environment. Further, quiescent cell properties evolve with time, a process that is thought to be at the origin of aging in multicellular organisms. Microtubules are found in all eukaryotes, and are essential for cell proliferation as they support chromosome segregation and intracellular trafficking. Upon proliferation cessation and quiescence establishment, the microtubule cytoskeleton was shown to undergo significant remodeling. The purpose of this review is to examine the literature in search of evidence to determine whether the observed microtubule reorganizations are merely a consequence of quiescence establishment or if they somehow participate in this cell fate decision.},
}
RevDate: 2024-10-08
CmpDate: 2024-10-08
On the evolutionary developmental biology of the cell.
Trends in genetics : TIG, 40(10):822-833.
Organisms are complex assemblages of cells, cells that produce light, shoot harpoons, and secrete glue. Therefore, identifying the mechanisms that generate novelty at the level of the individual cell is essential for understanding how multicellular life evolves. For decades, the field of evolutionary developmental biology (Evo-Devo) has been developing a framework for connecting genetic variation that arises during embryonic development to the emergence of diverse adult forms. With increasing access to new single cell 'omics technologies and an array of techniques for manipulating gene expression, we can now extend these inquiries inward to the level of the individual cell. In this opinion, I argue that applying an Evo-Devo framework to single cells makes it possible to explore the natural history of cells, where this was once only possible at the organismal level.
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@article {pmid38971670,
year = {2024},
author = {Babonis, LS},
title = {On the evolutionary developmental biology of the cell.},
journal = {Trends in genetics : TIG},
volume = {40},
number = {10},
pages = {822-833},
doi = {10.1016/j.tig.2024.06.003},
pmid = {38971670},
issn = {0168-9525},
mesh = {*Developmental Biology ; *Biological Evolution ; Animals ; Humans ; Single-Cell Analysis/methods ; },
abstract = {Organisms are complex assemblages of cells, cells that produce light, shoot harpoons, and secrete glue. Therefore, identifying the mechanisms that generate novelty at the level of the individual cell is essential for understanding how multicellular life evolves. For decades, the field of evolutionary developmental biology (Evo-Devo) has been developing a framework for connecting genetic variation that arises during embryonic development to the emergence of diverse adult forms. With increasing access to new single cell 'omics technologies and an array of techniques for manipulating gene expression, we can now extend these inquiries inward to the level of the individual cell. In this opinion, I argue that applying an Evo-Devo framework to single cells makes it possible to explore the natural history of cells, where this was once only possible at the organismal level.},
}
MeSH Terms:
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*Developmental Biology
*Biological Evolution
Animals
Humans
Single-Cell Analysis/methods
RevDate: 2024-10-07
CmpDate: 2024-10-07
Molecular recording using DNA Typewriter.
Nature protocols, 19(10):2833-2862.
Recording molecular information to genomic DNA is a powerful means of investigating topics ranging from multicellular development to cancer evolution. With molecular recording based on genome editing, events such as cell divisions and signaling pathway activity drive specific alterations in a cell's DNA, marking the genome with information about a cell's history that can be read out after the fact. Although genome editing has been used for molecular recording, capturing the temporal relationships among recorded events in mammalian cells remains challenging. The DNA Typewriter system overcomes this limitation by leveraging prime editing to facilitate sequential insertions to an engineered genomic region. DNA Typewriter includes three distinct components: DNA Tape as the 'substrate' to which edits accrue in an ordered manner, the prime editor enzyme, and prime editing guide RNAs, which program insertional edits to DNA Tape. In this protocol, we describe general design considerations for DNA Typewriter, step-by-step instructions on how to perform recording experiments by using DNA Typewriter in HEK293T cells, and example scripts for analyzing DNA Typewriter data (https://doi.org/10.6084/m9.figshare.22728758). This protocol covers two main applications of DNA Typewriter: recording sequential transfection events with programmed barcode insertions by using prime editing and recording lineage information during the expansion of a single cell to many. Compared with other methods that are compatible with mammalian cells, DNA Typewriter enables the recording of temporal information with higher recording capacities and can be completed within 4-6 weeks with basic expertise in molecular cloning, mammalian cell culturing and DNA sequencing data analysis.
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@article {pmid38844553,
year = {2024},
author = {Liao, H and Choi, J and Shendure, J},
title = {Molecular recording using DNA Typewriter.},
journal = {Nature protocols},
volume = {19},
number = {10},
pages = {2833-2862},
pmid = {38844553},
issn = {1750-2799},
mesh = {Humans ; *DNA/genetics ; *Gene Editing/methods ; HEK293 Cells ; RNA, Guide, CRISPR-Cas Systems/genetics ; CRISPR-Cas Systems ; },
abstract = {Recording molecular information to genomic DNA is a powerful means of investigating topics ranging from multicellular development to cancer evolution. With molecular recording based on genome editing, events such as cell divisions and signaling pathway activity drive specific alterations in a cell's DNA, marking the genome with information about a cell's history that can be read out after the fact. Although genome editing has been used for molecular recording, capturing the temporal relationships among recorded events in mammalian cells remains challenging. The DNA Typewriter system overcomes this limitation by leveraging prime editing to facilitate sequential insertions to an engineered genomic region. DNA Typewriter includes three distinct components: DNA Tape as the 'substrate' to which edits accrue in an ordered manner, the prime editor enzyme, and prime editing guide RNAs, which program insertional edits to DNA Tape. In this protocol, we describe general design considerations for DNA Typewriter, step-by-step instructions on how to perform recording experiments by using DNA Typewriter in HEK293T cells, and example scripts for analyzing DNA Typewriter data (https://doi.org/10.6084/m9.figshare.22728758). This protocol covers two main applications of DNA Typewriter: recording sequential transfection events with programmed barcode insertions by using prime editing and recording lineage information during the expansion of a single cell to many. Compared with other methods that are compatible with mammalian cells, DNA Typewriter enables the recording of temporal information with higher recording capacities and can be completed within 4-6 weeks with basic expertise in molecular cloning, mammalian cell culturing and DNA sequencing data analysis.},
}
MeSH Terms:
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Humans
*DNA/genetics
*Gene Editing/methods
HEK293 Cells
RNA, Guide, CRISPR-Cas Systems/genetics
CRISPR-Cas Systems
RevDate: 2024-10-07
CmpDate: 2024-10-07
The evolution of multicellularity and cell differentiation symposium: bridging evolutionary cell biology and computational modelling using emerging model systems.
Biology open, 13(10):.
'The evolution of multicellularity and cell differentiation' symposium, organized as part of the EuroEvoDevo 2024 meeting on June 25-28th in Helsinki (Finland), addressed recent advances on the molecular and mechanistic basis for the evolution of multicellularity and cell differentiation in eukaryotes. The symposium involved over 100 participants and brought together 10 speakers at diverse career stages. Talks covered various topics at the interface of developmental biology, evolutionary cell biology, comparative genomics, computational biology, and ecology using animal, protist, algal and mathematical models. This symposium offered a unique opportunity for interdisciplinary dialog among researchers working on different systems, especially in promoting collaborations and aligning strategies for studying emerging model species. Moreover, it fostered opportunities to promote early career researchers in the field and opened discussions of ongoing work and unpublished results. In this Meeting Review, we aim to promote the research, capture the spirit of the meeting, and present key topics discussed within this dynamic, growing and open community.
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@article {pmid39373528,
year = {2024},
author = {Ros-Rocher, N},
title = {The evolution of multicellularity and cell differentiation symposium: bridging evolutionary cell biology and computational modelling using emerging model systems.},
journal = {Biology open},
volume = {13},
number = {10},
pages = {},
doi = {10.1242/bio.061720},
pmid = {39373528},
issn = {2046-6390},
support = {101106415//European Union's Horizon Europe research and innovation funding program/ ; //Institute Pasteur: Institut Pasteur; Baylor College of Medicine/ ; },
mesh = {*Cell Differentiation/genetics ; *Biological Evolution ; Animals ; Computational Biology/methods ; Humans ; Cell Biology ; Models, Biological ; Computer Simulation ; Genomics/methods ; },
abstract = {'The evolution of multicellularity and cell differentiation' symposium, organized as part of the EuroEvoDevo 2024 meeting on June 25-28th in Helsinki (Finland), addressed recent advances on the molecular and mechanistic basis for the evolution of multicellularity and cell differentiation in eukaryotes. The symposium involved over 100 participants and brought together 10 speakers at diverse career stages. Talks covered various topics at the interface of developmental biology, evolutionary cell biology, comparative genomics, computational biology, and ecology using animal, protist, algal and mathematical models. This symposium offered a unique opportunity for interdisciplinary dialog among researchers working on different systems, especially in promoting collaborations and aligning strategies for studying emerging model species. Moreover, it fostered opportunities to promote early career researchers in the field and opened discussions of ongoing work and unpublished results. In this Meeting Review, we aim to promote the research, capture the spirit of the meeting, and present key topics discussed within this dynamic, growing and open community.},
}
MeSH Terms:
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*Cell Differentiation/genetics
*Biological Evolution
Animals
Computational Biology/methods
Humans
Cell Biology
Models, Biological
Computer Simulation
Genomics/methods
RevDate: 2024-10-03
CmpDate: 2024-09-20
Genome of Halimeda opuntia reveals differentiation of subgenomes and molecular bases of multinucleation and calcification in algae.
Proceedings of the National Academy of Sciences of the United States of America, 121(39):e2403222121.
Algae mostly occur either as unicellular (microalgae) or multicellular (macroalgae) species, both being uninucleate. There are important exceptions, however, as some unicellular algae are multinucleate and macroscopic, some of which inhabit tropical seas and contribute to biocalcification and coral reef robustness. The evolutionary mechanisms and ecological significance of multinucleation and associated traits (e.g., rapid wound healing) are poorly understood. Here, we report the genome of Halimeda opuntia, a giant multinucleate unicellular chlorophyte characterized by interutricular calcification. We achieve a high-quality genome assembly that shows segregation into four subgenomes, with evidence for polyploidization concomitant with historical sea level and climate changes. We further find myosin VIII missing in H. opuntia and three other unicellular multinucleate chlorophytes, suggesting a potential mechanism that may underpin multinucleation. Genome analysis provides clues about how the unicellular alga could survive fragmentation and regenerate, as well as potential signatures for extracellular calcification and the coupling of calcification with photosynthesis. In addition, proteomic alkalinity shifts were found to potentially confer plasticity of H. opuntia to ocean acidification (OA). Our study provides crucial genetic information necessary for understanding multinucleation, cell regeneration, plasticity to OA, and different modes of calcification in algae and other organisms, which has important implications in reef conservation and bioengineering.
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@article {pmid39302967,
year = {2024},
author = {Zhang, H and Wang, X and Qu, M and Yu, H and Yin, J and Liu, X and Liu, Y and Zhang, B and Zhang, Y and Wei, Z and Yang, F and Wang, J and Shi, C and Fan, G and Sun, J and Long, L and Hutchins, DA and Bowler, C and Lin, S and Wang, D and Lin, Q},
title = {Genome of Halimeda opuntia reveals differentiation of subgenomes and molecular bases of multinucleation and calcification in algae.},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {121},
number = {39},
pages = {e2403222121},
pmid = {39302967},
issn = {1091-6490},
support = {2022YFC3102403//the National Key Research and Development Programm of China/ ; 42230409//the National Natural Science Foundation of China/ ; 4980.01//the Gordon and Betty Moore Foundation/ ; 42030404//the National Natural Science Foundation of China/ ; 42076155//the National Natural Science Foundation of China/ ; 42425004//the National Natural Science Foundation of China/ ; },
mesh = {*Calcification, Physiologic/genetics ; Chlorophyta/genetics/metabolism ; Phylogeny ; Genome, Plant ; Photosynthesis/genetics ; },
abstract = {Algae mostly occur either as unicellular (microalgae) or multicellular (macroalgae) species, both being uninucleate. There are important exceptions, however, as some unicellular algae are multinucleate and macroscopic, some of which inhabit tropical seas and contribute to biocalcification and coral reef robustness. The evolutionary mechanisms and ecological significance of multinucleation and associated traits (e.g., rapid wound healing) are poorly understood. Here, we report the genome of Halimeda opuntia, a giant multinucleate unicellular chlorophyte characterized by interutricular calcification. We achieve a high-quality genome assembly that shows segregation into four subgenomes, with evidence for polyploidization concomitant with historical sea level and climate changes. We further find myosin VIII missing in H. opuntia and three other unicellular multinucleate chlorophytes, suggesting a potential mechanism that may underpin multinucleation. Genome analysis provides clues about how the unicellular alga could survive fragmentation and regenerate, as well as potential signatures for extracellular calcification and the coupling of calcification with photosynthesis. In addition, proteomic alkalinity shifts were found to potentially confer plasticity of H. opuntia to ocean acidification (OA). Our study provides crucial genetic information necessary for understanding multinucleation, cell regeneration, plasticity to OA, and different modes of calcification in algae and other organisms, which has important implications in reef conservation and bioengineering.},
}
MeSH Terms:
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*Calcification, Physiologic/genetics
Chlorophyta/genetics/metabolism
Phylogeny
Genome, Plant
Photosynthesis/genetics
RevDate: 2024-09-21
CmpDate: 2024-09-14
Multicellularity and increasing Reynolds number impact on the evolutionary shift in flash-induced ciliary response in Volvocales.
BMC ecology and evolution, 24(1):119.
BACKGROUND: Volvocales in green algae have evolved by multicellularity of Chlamydomonas-like unicellular ancestor. Those with various cell numbers exist, such as unicellular Chlamydomonas, four-celled Tetrabaena, and Volvox species with different cell numbers (~1,000, ~5,000, and ~10,000). Each cell of these organisms shares two cilia and an eyespot, which are used for swimming and photosensing. They are all freshwater microalgae but inhabit different fluid environments: unicellular species live in low Reynolds-number (Re) environments where viscous forces dominate, whereas multicellular species live in relatively higher Re where inertial forces become non-negligible. Despite significant changes in the physical environment, during the evolution of multicellularity, they maintained photobehaviors (i.e., photoshock and phototactic responses), which allows them to survive under changing light conditions.
RESULTS: In this study, we utilized high-speed imaging to observe flash-induced changes in the ciliary beating manner of 27 Volvocales strains. We classified flash-induced ciliary responses in Volvocales into four patterns: "1: temporal waveform conversion", "2: no obvious response", "3: pause in ciliary beating", and "4: temporal changes in ciliary beating directions". We found that which species exhibit which pattern depends on Re, which is associated with the individual size of each species rather than phylogenetic relationships.
CONCLUSIONS: These results suggest that only organisms that acquired different patterns of ciliary responses survived the evolutionary transition to multicellularity with a greater number of cells while maintaining photobehaviors. This study highlights the significance of the Re as a selection pressure in evolution and offers insights for designing propulsion systems in biomimetic micromachines.
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@article {pmid39277710,
year = {2024},
author = {Ueki, N and Wakabayashi, KI},
title = {Multicellularity and increasing Reynolds number impact on the evolutionary shift in flash-induced ciliary response in Volvocales.},
journal = {BMC ecology and evolution},
volume = {24},
number = {1},
pages = {119},
pmid = {39277710},
issn = {2730-7182},
mesh = {*Cilia/physiology ; *Biological Evolution ; Chlorophyta/physiology/genetics ; Volvox/genetics/physiology ; Light ; },
abstract = {BACKGROUND: Volvocales in green algae have evolved by multicellularity of Chlamydomonas-like unicellular ancestor. Those with various cell numbers exist, such as unicellular Chlamydomonas, four-celled Tetrabaena, and Volvox species with different cell numbers (~1,000, ~5,000, and ~10,000). Each cell of these organisms shares two cilia and an eyespot, which are used for swimming and photosensing. They are all freshwater microalgae but inhabit different fluid environments: unicellular species live in low Reynolds-number (Re) environments where viscous forces dominate, whereas multicellular species live in relatively higher Re where inertial forces become non-negligible. Despite significant changes in the physical environment, during the evolution of multicellularity, they maintained photobehaviors (i.e., photoshock and phototactic responses), which allows them to survive under changing light conditions.
RESULTS: In this study, we utilized high-speed imaging to observe flash-induced changes in the ciliary beating manner of 27 Volvocales strains. We classified flash-induced ciliary responses in Volvocales into four patterns: "1: temporal waveform conversion", "2: no obvious response", "3: pause in ciliary beating", and "4: temporal changes in ciliary beating directions". We found that which species exhibit which pattern depends on Re, which is associated with the individual size of each species rather than phylogenetic relationships.
CONCLUSIONS: These results suggest that only organisms that acquired different patterns of ciliary responses survived the evolutionary transition to multicellularity with a greater number of cells while maintaining photobehaviors. This study highlights the significance of the Re as a selection pressure in evolution and offers insights for designing propulsion systems in biomimetic micromachines.},
}
MeSH Terms:
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*Cilia/physiology
*Biological Evolution
Chlorophyta/physiology/genetics
Volvox/genetics/physiology
Light
RevDate: 2024-09-16
CmpDate: 2024-09-14
The Spiral Model of Evolution: Stable Life Forms of Organisms and Unstable Life Forms of Cancers.
International journal of molecular sciences, 25(17):.
If one must prioritize among the vast array of contributing factors to cancer evolution, environmental-stress-mediated chromosome instability (CIN) should easily surpass individual gene mutations. CIN leads to the emergence of genomically unstable life forms, enabling them to grow dominantly within the stable life form of the host. In contrast, stochastic gene mutations play a role in aiding the growth of the cancer population, with their importance depending on the initial emergence of the new system. Furthermore, many specific gene mutations among the many available can perform this function, decreasing the clinical value of any specific gene mutation. Since these unstable life forms can respond to treatment differently than stable ones, cancer often escapes from drug treatment by forming new systems, which leads to problems during the treatment for patients. To understand how diverse factors impact CIN-mediated macroevolution and genome integrity-ensured microevolution, the concept of two-phased cancer evolution is used to reconcile some major characteristics of cancer, such as bioenergetic, unicellular, and multicellular evolution. Specifically, the spiral of life function model is proposed, which integrates major historical evolutionary innovations and conservation with information management. Unlike normal organismal evolution in the microevolutionary phase, where a given species occupies a specific location within the spiral, cancer populations are highly heterogenous at multiple levels, including epigenetic levels. Individual cells occupy different levels and positions within the spiral, leading to supersystems of mixed cellular populations that exhibit both macro and microevolution. This analysis, utilizing karyotype to define the genetic networks of the cellular system and CIN to determine the instability of the system, as well as considering gene mutation and epigenetics as modifiers of the system for information amplification and usage, explores the high evolutionary potential of cancer. It provides a new, unified understanding of cancer as a supersystem, encouraging efforts to leverage the dynamics of CIN to develop improved treatment options. Moreover, it offers a historically contingent model for organismal evolution that reconciles the roles of both evolutionary innovation and conservation through macroevolution and microevolution, respectively.
Additional Links: PMID-39273111
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@article {pmid39273111,
year = {2024},
author = {Kasperski, A and Heng, HH},
title = {The Spiral Model of Evolution: Stable Life Forms of Organisms and Unstable Life Forms of Cancers.},
journal = {International journal of molecular sciences},
volume = {25},
number = {17},
pages = {},
pmid = {39273111},
issn = {1422-0067},
mesh = {*Neoplasms/genetics ; Humans ; *Chromosomal Instability ; Biological Evolution ; Animals ; Mutation ; Evolution, Molecular ; Epigenesis, Genetic ; Genomic Instability ; },
abstract = {If one must prioritize among the vast array of contributing factors to cancer evolution, environmental-stress-mediated chromosome instability (CIN) should easily surpass individual gene mutations. CIN leads to the emergence of genomically unstable life forms, enabling them to grow dominantly within the stable life form of the host. In contrast, stochastic gene mutations play a role in aiding the growth of the cancer population, with their importance depending on the initial emergence of the new system. Furthermore, many specific gene mutations among the many available can perform this function, decreasing the clinical value of any specific gene mutation. Since these unstable life forms can respond to treatment differently than stable ones, cancer often escapes from drug treatment by forming new systems, which leads to problems during the treatment for patients. To understand how diverse factors impact CIN-mediated macroevolution and genome integrity-ensured microevolution, the concept of two-phased cancer evolution is used to reconcile some major characteristics of cancer, such as bioenergetic, unicellular, and multicellular evolution. Specifically, the spiral of life function model is proposed, which integrates major historical evolutionary innovations and conservation with information management. Unlike normal organismal evolution in the microevolutionary phase, where a given species occupies a specific location within the spiral, cancer populations are highly heterogenous at multiple levels, including epigenetic levels. Individual cells occupy different levels and positions within the spiral, leading to supersystems of mixed cellular populations that exhibit both macro and microevolution. This analysis, utilizing karyotype to define the genetic networks of the cellular system and CIN to determine the instability of the system, as well as considering gene mutation and epigenetics as modifiers of the system for information amplification and usage, explores the high evolutionary potential of cancer. It provides a new, unified understanding of cancer as a supersystem, encouraging efforts to leverage the dynamics of CIN to develop improved treatment options. Moreover, it offers a historically contingent model for organismal evolution that reconciles the roles of both evolutionary innovation and conservation through macroevolution and microevolution, respectively.},
}
MeSH Terms:
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*Neoplasms/genetics
Humans
*Chromosomal Instability
Biological Evolution
Animals
Mutation
Evolution, Molecular
Epigenesis, Genetic
Genomic Instability
RevDate: 2024-09-13
CmpDate: 2024-09-13
Current computational methods for spatial transcriptomics in cancer biology.
Advances in cancer research, 163:71-106.
Cells in multicellular organisms constitute a self-organizing society by interacting with their neighbors. Cancer originates from malfunction of cellular behavior in the context of such a self-organizing system. The identities or characteristics of individual tumor cells can be represented by the hallmark of gene expression or transcriptome, which can be addressed using single-cell dissociation followed by RNA sequencing. However, the dissociation process of single cells results in losing the cellular address in tissue or neighbor information of each tumor cell, which is critical to understanding the malfunctioning cellular behavior in the microenvironment. Spatial transcriptomics technology enables measuring the transcriptome which is tagged by the address within a tissue. However, to understand cellular behavior in a self-organizing society, we need to apply mathematical or statistical methods. Here, we provide a review on current computational methods for spatial transcriptomics in cancer biology.
Additional Links: PMID-39271268
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PubMed:
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@article {pmid39271268,
year = {2024},
author = {Mo, J and Bae, J and Saqib, J and Hwang, D and Jin, Y and Park, B and Park, J and Kim, J},
title = {Current computational methods for spatial transcriptomics in cancer biology.},
journal = {Advances in cancer research},
volume = {163},
number = {},
pages = {71-106},
doi = {10.1016/bs.acr.2024.06.006},
pmid = {39271268},
issn = {2162-5557},
mesh = {Humans ; *Neoplasms/genetics/pathology ; *Transcriptome/genetics ; *Computational Biology/methods ; Gene Expression Profiling/methods ; Tumor Microenvironment/genetics ; Animals ; },
abstract = {Cells in multicellular organisms constitute a self-organizing society by interacting with their neighbors. Cancer originates from malfunction of cellular behavior in the context of such a self-organizing system. The identities or characteristics of individual tumor cells can be represented by the hallmark of gene expression or transcriptome, which can be addressed using single-cell dissociation followed by RNA sequencing. However, the dissociation process of single cells results in losing the cellular address in tissue or neighbor information of each tumor cell, which is critical to understanding the malfunctioning cellular behavior in the microenvironment. Spatial transcriptomics technology enables measuring the transcriptome which is tagged by the address within a tissue. However, to understand cellular behavior in a self-organizing society, we need to apply mathematical or statistical methods. Here, we provide a review on current computational methods for spatial transcriptomics in cancer biology.},
}
MeSH Terms:
show MeSH Terms
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Humans
*Neoplasms/genetics/pathology
*Transcriptome/genetics
*Computational Biology/methods
Gene Expression Profiling/methods
Tumor Microenvironment/genetics
Animals
RevDate: 2024-09-20
CmpDate: 2024-09-20
Algorithms for Autonomous Formation of Multicellular Shapes from Single Cells.
ACS synthetic biology, 13(9):2753-2763.
Multicellular organisms originate from a single cell, ultimately giving rise to mature organisms of heterogeneous cell type composition in complex structures. Recent work in the areas of stem cell biology and tissue engineering has laid major groundwork in the ability to convert certain types of cells into other types, but there has been limited progress in the ability to control the morphology of cellular masses as they grow. Contemporary approaches to this problem have included the use of artificial scaffolds, 3D bioprinting, and complex media formulations; however, there are no existing approaches to controlling this process purely through genetics and from a single-cell starting point. Here we describe a computer-aided design approach, called CellArchitect, for designing recombinase-based genetic circuits for controlling the formation of multicellular masses into arbitrary shapes in human cells.
Additional Links: PMID-39194023
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PubMed:
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@article {pmid39194023,
year = {2024},
author = {Appleton, E and Mehdipour, N and Daifuku, T and Briers, D and Haghighi, I and Moret, M and Chao, G and Wannier, T and Chiappino-Pepe, A and Huang, J and Belta, C and Church, GM},
title = {Algorithms for Autonomous Formation of Multicellular Shapes from Single Cells.},
journal = {ACS synthetic biology},
volume = {13},
number = {9},
pages = {2753-2763},
doi = {10.1021/acssynbio.4c00037},
pmid = {39194023},
issn = {2161-5063},
mesh = {Humans ; *Algorithms ; Gene Regulatory Networks ; Single-Cell Analysis/methods ; Tissue Engineering/methods ; Computer-Aided Design ; Cell Shape ; },
abstract = {Multicellular organisms originate from a single cell, ultimately giving rise to mature organisms of heterogeneous cell type composition in complex structures. Recent work in the areas of stem cell biology and tissue engineering has laid major groundwork in the ability to convert certain types of cells into other types, but there has been limited progress in the ability to control the morphology of cellular masses as they grow. Contemporary approaches to this problem have included the use of artificial scaffolds, 3D bioprinting, and complex media formulations; however, there are no existing approaches to controlling this process purely through genetics and from a single-cell starting point. Here we describe a computer-aided design approach, called CellArchitect, for designing recombinase-based genetic circuits for controlling the formation of multicellular masses into arbitrary shapes in human cells.},
}
MeSH Terms:
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Humans
*Algorithms
Gene Regulatory Networks
Single-Cell Analysis/methods
Tissue Engineering/methods
Computer-Aided Design
Cell Shape
RevDate: 2024-08-25
CmpDate: 2024-08-23
TF-High-Evolutionary: In Vivo Mutagenesis of Gene Regulatory Networks for the Study of the Genetics and Evolution of the Drosophila Regulatory Genome.
Molecular biology and evolution, 41(8):.
Understanding the evolutionary potential of mutations in gene regulatory networks is essential to furthering the study of evolution and development. However, in multicellular systems, genetic manipulation of regulatory networks in a targeted and high-throughput way remains challenging. In this study, we designed TF-High-Evolutionary (HighEvo), a transcription factor (TF) fused with a base editor (activation-induced deaminase), to continuously induce germline mutations at TF-binding sites across regulatory networks in Drosophila. Populations of flies expressing TF-HighEvo in their germlines accumulated mutations at rates an order of magnitude higher than natural populations. Importantly, these mutations accumulated around the targeted TF-binding sites across the genome, leading to distinct morphological phenotypes consistent with the developmental roles of the tagged TFs. As such, this TF-HighEvo method allows the interrogation of the mutational space of gene regulatory networks at scale and can serve as a powerful reagent for experimental evolution and genetic screens focused on the regulatory genome.
Additional Links: PMID-39117360
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@article {pmid39117360,
year = {2024},
author = {Li, XC and Srinivasan, V and Laiker, I and Misunou, N and Frankel, N and Pallares, LF and Crocker, J},
title = {TF-High-Evolutionary: In Vivo Mutagenesis of Gene Regulatory Networks for the Study of the Genetics and Evolution of the Drosophila Regulatory Genome.},
journal = {Molecular biology and evolution},
volume = {41},
number = {8},
pages = {},
pmid = {39117360},
issn = {1537-1719},
support = {//European Molecular Biology Laboratory Interdisciplinary Postdoc Programme/ ; //European Molecular Biology Laboratory/ ; //Max Planck Society/ ; },
mesh = {Animals ; *Gene Regulatory Networks ; *Transcription Factors/genetics/metabolism ; Genome, Insect ; Mutagenesis ; Drosophila/genetics ; Evolution, Molecular ; Drosophila melanogaster/genetics ; },
abstract = {Understanding the evolutionary potential of mutations in gene regulatory networks is essential to furthering the study of evolution and development. However, in multicellular systems, genetic manipulation of regulatory networks in a targeted and high-throughput way remains challenging. In this study, we designed TF-High-Evolutionary (HighEvo), a transcription factor (TF) fused with a base editor (activation-induced deaminase), to continuously induce germline mutations at TF-binding sites across regulatory networks in Drosophila. Populations of flies expressing TF-HighEvo in their germlines accumulated mutations at rates an order of magnitude higher than natural populations. Importantly, these mutations accumulated around the targeted TF-binding sites across the genome, leading to distinct morphological phenotypes consistent with the developmental roles of the tagged TFs. As such, this TF-HighEvo method allows the interrogation of the mutational space of gene regulatory networks at scale and can serve as a powerful reagent for experimental evolution and genetic screens focused on the regulatory genome.},
}
MeSH Terms:
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hide MeSH Terms
Animals
*Gene Regulatory Networks
*Transcription Factors/genetics/metabolism
Genome, Insect
Mutagenesis
Drosophila/genetics
Evolution, Molecular
Drosophila melanogaster/genetics
RevDate: 2024-07-27
CmpDate: 2024-07-28
Exploring the Function of Gene Promoter Regulatory Elements Using CRISPR Tools.
Methods in molecular biology (Clifton, N.J.), 2844:145-156.
Gene promoters serve as pivotal regulators of transcription, orchestrating the initiation, rate, and specificity of gene expression, resulting in cellular diversity found among distinct cell types within multicellular organisms. Identification of the sequence and function of promoters' regulatory elements and their complex interaction with transcription factors, enhancers, silencers, and insulators is fundamental to coordinated transcriptional processes within cells. Identifying these regulatory elements and scrutinizing their functions and interactions through the use of synthetic promoters can pave the way for researchers in various fields ranging from uncovering the origins of diseases associated with promoter mutations to harnessing these regulatory components in biotechnological applications.In this chapter, we describe the manipulation of regulatory elements within promoters, with a specific focus on the use of CRISPR technology on enhancers and silencer elements of the Ovalbumin gene promoter. We explain and discuss processes for the deletion of/interference with regulatory elements within the promoter, employing CRISPR-based approaches. Furthermore, we demonstrate that a CRISPR/Cas-manipulated promoter can activate gene transcription in cell types where it is normally inactive. This confirms that CRISPR technology can be effectively used to engineer synthetic promoters with desired characteristics, such as inducibility, tissue-specificity, or enhanced transcriptional strength. Such an approach provides valuable insights into the mechanisms and dynamics of gene expression, thereby offering new opportunities in the fields of biotechnology and medicine.
Additional Links: PMID-39068338
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@article {pmid39068338,
year = {2024},
author = {Yousefi Taemeh, S and Dehdilani, N and Goshayeshi, L and Dehghani, H},
title = {Exploring the Function of Gene Promoter Regulatory Elements Using CRISPR Tools.},
journal = {Methods in molecular biology (Clifton, N.J.)},
volume = {2844},
number = {},
pages = {145-156},
pmid = {39068338},
issn = {1940-6029},
mesh = {*Promoter Regions, Genetic ; *CRISPR-Cas Systems ; Animals ; Humans ; Gene Expression Regulation ; Enhancer Elements, Genetic ; Ovalbumin/genetics ; Clustered Regularly Interspaced Short Palindromic Repeats/genetics ; },
abstract = {Gene promoters serve as pivotal regulators of transcription, orchestrating the initiation, rate, and specificity of gene expression, resulting in cellular diversity found among distinct cell types within multicellular organisms. Identification of the sequence and function of promoters' regulatory elements and their complex interaction with transcription factors, enhancers, silencers, and insulators is fundamental to coordinated transcriptional processes within cells. Identifying these regulatory elements and scrutinizing their functions and interactions through the use of synthetic promoters can pave the way for researchers in various fields ranging from uncovering the origins of diseases associated with promoter mutations to harnessing these regulatory components in biotechnological applications.In this chapter, we describe the manipulation of regulatory elements within promoters, with a specific focus on the use of CRISPR technology on enhancers and silencer elements of the Ovalbumin gene promoter. We explain and discuss processes for the deletion of/interference with regulatory elements within the promoter, employing CRISPR-based approaches. Furthermore, we demonstrate that a CRISPR/Cas-manipulated promoter can activate gene transcription in cell types where it is normally inactive. This confirms that CRISPR technology can be effectively used to engineer synthetic promoters with desired characteristics, such as inducibility, tissue-specificity, or enhanced transcriptional strength. Such an approach provides valuable insights into the mechanisms and dynamics of gene expression, thereby offering new opportunities in the fields of biotechnology and medicine.},
}
MeSH Terms:
show MeSH Terms
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*Promoter Regions, Genetic
*CRISPR-Cas Systems
Animals
Humans
Gene Expression Regulation
Enhancer Elements, Genetic
Ovalbumin/genetics
Clustered Regularly Interspaced Short Palindromic Repeats/genetics
RevDate: 2024-10-02
CmpDate: 2024-10-02
Adaptive Cellular Radiations and the Genetic Mechanisms Underlying Animal Nervous System Diversification.
Annual review of cell and developmental biology, 40(1):407-425.
In animals, the nervous system evolved as the primary interface between multicellular organisms and the environment. As organisms became larger and more complex, the primary functions of the nervous system expanded to include the modulation and coordination of individual responsive cells via paracrine and synaptic functions as well as to monitor and maintain the organism's own internal environment. This was initially accomplished via paracrine signaling and eventually through the assembly of multicell circuits in some lineages. Cells with similar functions and centralized nervous systems have independently arisen in several lineages. We highlight the molecular mechanisms that underlie parallel diversifications of the nervous system.
Additional Links: PMID-39052757
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@article {pmid39052757,
year = {2024},
author = {Hehmeyer, J and Plessier, F and Marlow, H},
title = {Adaptive Cellular Radiations and the Genetic Mechanisms Underlying Animal Nervous System Diversification.},
journal = {Annual review of cell and developmental biology},
volume = {40},
number = {1},
pages = {407-425},
doi = {10.1146/annurev-cellbio-111822-124041},
pmid = {39052757},
issn = {1530-8995},
mesh = {Animals ; *Nervous System/metabolism ; Biological Evolution ; Humans ; Signal Transduction/genetics ; },
abstract = {In animals, the nervous system evolved as the primary interface between multicellular organisms and the environment. As organisms became larger and more complex, the primary functions of the nervous system expanded to include the modulation and coordination of individual responsive cells via paracrine and synaptic functions as well as to monitor and maintain the organism's own internal environment. This was initially accomplished via paracrine signaling and eventually through the assembly of multicell circuits in some lineages. Cells with similar functions and centralized nervous systems have independently arisen in several lineages. We highlight the molecular mechanisms that underlie parallel diversifications of the nervous system.},
}
MeSH Terms:
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Animals
*Nervous System/metabolism
Biological Evolution
Humans
Signal Transduction/genetics
RevDate: 2024-07-16
CmpDate: 2024-07-15
Adaptation of SIVmac to baboon primary cells results in complete absence of in vivo baboon infectivity.
Frontiers in cellular and infection microbiology, 14:1408245.
While simian immunodeficiency virus (SIV) infection is non-pathogenic in naturally infected African nonhuman primate hosts, experimental or accidental infection in rhesus macaques often leads to AIDS. Baboons, widely distributed throughout Africa, do not naturally harbor SIV, and experimental infection of baboons with SIVmac results in transient low-level viral replication. Elucidation of mechanisms of natural immunity in baboons could uncover new targets of antiviral intervention. We tested the hypothesis that an SIVmac adapted to replicate in baboon primary cells will gain the capacity to establish chronic infections in vivo. Here, we generated SIVmac variants in baboon cells through serial passage in PBMC from different donors (SIVbn-PBMC s1), in PBMC from the same donors (SIVbn-PBMC s2), or in isolated CD4 cells from the same donors used for series 2 (SIVbn-CD4). While SIVbn-PBMC s1 and SIVbn-CD4 demonstrated increased replication capacity, SIVbn-PBMC s2 did not. Pharmacological blockade of CCR5 revealed SIVbn-PBMC s1 could more efficiently use available CCR5 than SIVmac, a trait we hypothesize arose to circumvent receptor occupation by chemokines. Sequencing analysis showed that all three viruses accumulated different types of mutations, and that more non-synonymous mutations became fixed in SIVbn-PBMC s1 than SIVbn-PBMC s2 and SIVbn-CD4, supporting the notion of stronger fitness pressure in PBMC from different genetic backgrounds. Testing the individual contribution of several newly fixed SIV mutations suggested that is the additive effect of these mutations in SIVbn-PBMC s1 that contributed to its enhanced fitness, as recombinant single mutant viruses showed no difference in replication capacity over the parental SIVmac239 strain. The replicative capacity of SIVbn-PBMC passage 4 (P4) s1 was tested in vivo by infecting baboons intravenously with SIVbn-PBMC P4 s1 or SIVmac251. While animals infected with SIVmac251 showed the known pattern of transient low-level viremia, animals infected with SIVbn-PBMC P4 s1 had undetectable viremia or viral DNA in lymphoid tissue. These studies suggest that adaptation of SIV to grow in baboon primary cells results in mutations that confer increased replicative capacity in the artificial environment of cell culture but make the virus unable to avoid the restrictive factors generated by a complex multicellular organism.
Additional Links: PMID-39006742
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@article {pmid39006742,
year = {2024},
author = {Obregon-Perko, V and Mannino, A and Ladner, JT and Hodara, V and Ebrahimi, D and Parodi, L and Callery, J and Palacios, G and Giavedoni, LD},
title = {Adaptation of SIVmac to baboon primary cells results in complete absence of in vivo baboon infectivity.},
journal = {Frontiers in cellular and infection microbiology},
volume = {14},
number = {},
pages = {1408245},
pmid = {39006742},
issn = {2235-2988},
mesh = {Animals ; *Simian Immunodeficiency Virus/genetics/physiology ; *Virus Replication ; *Simian Acquired Immunodeficiency Syndrome/virology/immunology ; *Papio ; Leukocytes, Mononuclear/virology/immunology ; Receptors, CCR5/metabolism/genetics ; CD4-Positive T-Lymphocytes/virology/immunology ; Cells, Cultured ; Serial Passage ; },
abstract = {While simian immunodeficiency virus (SIV) infection is non-pathogenic in naturally infected African nonhuman primate hosts, experimental or accidental infection in rhesus macaques often leads to AIDS. Baboons, widely distributed throughout Africa, do not naturally harbor SIV, and experimental infection of baboons with SIVmac results in transient low-level viral replication. Elucidation of mechanisms of natural immunity in baboons could uncover new targets of antiviral intervention. We tested the hypothesis that an SIVmac adapted to replicate in baboon primary cells will gain the capacity to establish chronic infections in vivo. Here, we generated SIVmac variants in baboon cells through serial passage in PBMC from different donors (SIVbn-PBMC s1), in PBMC from the same donors (SIVbn-PBMC s2), or in isolated CD4 cells from the same donors used for series 2 (SIVbn-CD4). While SIVbn-PBMC s1 and SIVbn-CD4 demonstrated increased replication capacity, SIVbn-PBMC s2 did not. Pharmacological blockade of CCR5 revealed SIVbn-PBMC s1 could more efficiently use available CCR5 than SIVmac, a trait we hypothesize arose to circumvent receptor occupation by chemokines. Sequencing analysis showed that all three viruses accumulated different types of mutations, and that more non-synonymous mutations became fixed in SIVbn-PBMC s1 than SIVbn-PBMC s2 and SIVbn-CD4, supporting the notion of stronger fitness pressure in PBMC from different genetic backgrounds. Testing the individual contribution of several newly fixed SIV mutations suggested that is the additive effect of these mutations in SIVbn-PBMC s1 that contributed to its enhanced fitness, as recombinant single mutant viruses showed no difference in replication capacity over the parental SIVmac239 strain. The replicative capacity of SIVbn-PBMC passage 4 (P4) s1 was tested in vivo by infecting baboons intravenously with SIVbn-PBMC P4 s1 or SIVmac251. While animals infected with SIVmac251 showed the known pattern of transient low-level viremia, animals infected with SIVbn-PBMC P4 s1 had undetectable viremia or viral DNA in lymphoid tissue. These studies suggest that adaptation of SIV to grow in baboon primary cells results in mutations that confer increased replicative capacity in the artificial environment of cell culture but make the virus unable to avoid the restrictive factors generated by a complex multicellular organism.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Simian Immunodeficiency Virus/genetics/physiology
*Virus Replication
*Simian Acquired Immunodeficiency Syndrome/virology/immunology
*Papio
Leukocytes, Mononuclear/virology/immunology
Receptors, CCR5/metabolism/genetics
CD4-Positive T-Lymphocytes/virology/immunology
Cells, Cultured
Serial Passage
RevDate: 2024-09-18
CmpDate: 2024-09-12
Molecular mechanism of TRIM32 in antiviral immunity in rainbow trout (Oncorhynchus mykiss).
Fish & shellfish immunology, 153:109765.
TRIM family proteins are widely found in multicellular organisms and are involved in a wide range of life activities, and also act as crucial regulators in the antiviral natural immune response. This study aimed to reveal the molecular mechanism of rainbow trout TRIM protein in the anti-IHNV process. The results demonstrated that 99.1 % homology between the rainbow trout and the chinook salmon (Oncorhynchus tshawytscha) TRIM32. When rainbow trout were infected with IHNV, the TRIM32 was highly expressed in the gill, spleen, kidney and blood. Meanwhile, rainbow trout TRIM32 has E3 ubiquitin ligase activity and undergoes K29-linked polyubiquitination modifications dependent on the RING structural domain was determined by immunoprecipitation. TRIM32 could interact with the NV protein of IHNV and degrade NV protein through the ubiquitin-proteasome pathway, and was also able to activate NF-κB transcription, thereby inhibiting the replication of IHNV. Moreover, the results of the animal studies showed that the survival rate of rainbow trout overexpressing TRIM32 was 70.2 % which was significantly higher than that of the control group, and stimulating the body to produce high levels of IgM when the host was infected with the virus. In addition, TRIM32 can activate the NF-κB signalling pathway and participate in the antiviral natural immune response. The results of this study will help us to understand the molecular mechanism of TRIM protein resistance in rainbow trout, and provide new ideas for disease resistance breeding, vaccine development and immune formulation development in rainbow trout.
Additional Links: PMID-39004296
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PubMed:
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@article {pmid39004296,
year = {2024},
author = {Zhang, M and Sun, J and Zhang, F and Zhang, Y and Wu, M and Kong, W and Guan, X and Liu, M},
title = {Molecular mechanism of TRIM32 in antiviral immunity in rainbow trout (Oncorhynchus mykiss).},
journal = {Fish & shellfish immunology},
volume = {153},
number = {},
pages = {109765},
doi = {10.1016/j.fsi.2024.109765},
pmid = {39004296},
issn = {1095-9947},
mesh = {Animals ; *Oncorhynchus mykiss/immunology ; *Fish Diseases/immunology ; *Fish Proteins/genetics/immunology ; *Rhabdoviridae Infections/immunology/veterinary ; *Immunity, Innate/genetics ; *Tripartite Motif Proteins/genetics/immunology ; Ubiquitin-Protein Ligases/genetics/immunology ; Gene Expression Regulation/immunology ; Gene Expression Profiling/veterinary ; Infectious hematopoietic necrosis virus/immunology/physiology ; Sequence Alignment/veterinary ; Phylogeny ; },
abstract = {TRIM family proteins are widely found in multicellular organisms and are involved in a wide range of life activities, and also act as crucial regulators in the antiviral natural immune response. This study aimed to reveal the molecular mechanism of rainbow trout TRIM protein in the anti-IHNV process. The results demonstrated that 99.1 % homology between the rainbow trout and the chinook salmon (Oncorhynchus tshawytscha) TRIM32. When rainbow trout were infected with IHNV, the TRIM32 was highly expressed in the gill, spleen, kidney and blood. Meanwhile, rainbow trout TRIM32 has E3 ubiquitin ligase activity and undergoes K29-linked polyubiquitination modifications dependent on the RING structural domain was determined by immunoprecipitation. TRIM32 could interact with the NV protein of IHNV and degrade NV protein through the ubiquitin-proteasome pathway, and was also able to activate NF-κB transcription, thereby inhibiting the replication of IHNV. Moreover, the results of the animal studies showed that the survival rate of rainbow trout overexpressing TRIM32 was 70.2 % which was significantly higher than that of the control group, and stimulating the body to produce high levels of IgM when the host was infected with the virus. In addition, TRIM32 can activate the NF-κB signalling pathway and participate in the antiviral natural immune response. The results of this study will help us to understand the molecular mechanism of TRIM protein resistance in rainbow trout, and provide new ideas for disease resistance breeding, vaccine development and immune formulation development in rainbow trout.},
}
MeSH Terms:
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hide MeSH Terms
Animals
*Oncorhynchus mykiss/immunology
*Fish Diseases/immunology
*Fish Proteins/genetics/immunology
*Rhabdoviridae Infections/immunology/veterinary
*Immunity, Innate/genetics
*Tripartite Motif Proteins/genetics/immunology
Ubiquitin-Protein Ligases/genetics/immunology
Gene Expression Regulation/immunology
Gene Expression Profiling/veterinary
Infectious hematopoietic necrosis virus/immunology/physiology
Sequence Alignment/veterinary
Phylogeny
RevDate: 2024-07-12
CmpDate: 2024-07-11
Natural selection drives emergent genetic homogeneity in a century-scale experiment with barley.
Science (New York, N.Y.), 385(6705):eadl0038.
Direct observation is central to our understanding of adaptation, but evolution is rarely documented in a large, multicellular organism for more than a few generations. In this study, we observed evolution across a century-scale competition experiment, barley composite cross II (CCII). CCII was founded in 1929 in Davis, California, with thousands of genotypes, but we found that natural selection has massively reduced genetic diversity, leading to a single lineage constituting most of the population by generation 50. Selection favored alleles originating from climates similar to that of Davis and targeted loci contributing to reproductive development, including the barley diversification loci Vrs1, HvCEN, Ppd-H1, and Vrn-H2. Our findings point to selection as the predominant force shaping genomic variation in one of the world's oldest biological experiments.
Additional Links: PMID-38991084
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PubMed:
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@article {pmid38991084,
year = {2024},
author = {Landis, JB and Guercio, AM and Brown, KE and Fiscus, CJ and Morrell, PL and Koenig, D},
title = {Natural selection drives emergent genetic homogeneity in a century-scale experiment with barley.},
journal = {Science (New York, N.Y.)},
volume = {385},
number = {6705},
pages = {eadl0038},
doi = {10.1126/science.adl0038},
pmid = {38991084},
issn = {1095-9203},
mesh = {*Hordeum/genetics ; *Selection, Genetic ; *Genetic Variation ; *Alleles ; Genotype ; Crosses, Genetic ; Genome, Plant ; },
abstract = {Direct observation is central to our understanding of adaptation, but evolution is rarely documented in a large, multicellular organism for more than a few generations. In this study, we observed evolution across a century-scale competition experiment, barley composite cross II (CCII). CCII was founded in 1929 in Davis, California, with thousands of genotypes, but we found that natural selection has massively reduced genetic diversity, leading to a single lineage constituting most of the population by generation 50. Selection favored alleles originating from climates similar to that of Davis and targeted loci contributing to reproductive development, including the barley diversification loci Vrs1, HvCEN, Ppd-H1, and Vrn-H2. Our findings point to selection as the predominant force shaping genomic variation in one of the world's oldest biological experiments.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Hordeum/genetics
*Selection, Genetic
*Genetic Variation
*Alleles
Genotype
Crosses, Genetic
Genome, Plant
RevDate: 2024-07-09
CmpDate: 2024-07-09
Irreducible Complexity of Hox Gene: Path to the Canonical Function of the Hox Cluster.
Biochemistry. Biokhimiia, 89(6):987-1001.
The evolution of major taxa is often associated with the emergence of new gene families. In all multicellular animals except sponges and comb jellies, the genomes contain Hox genes, which are crucial regulators of development. The canonical function of Hox genes involves colinear patterning of body parts in bilateral animals. This general function is implemented through complex, precisely coordinated mechanisms, not all of which are evolutionarily conserved and fully understood. We suggest that the emergence of this regulatory complexity was preceded by a stage of cooperation between more ancient morphogenetic programs or their individual elements. Footprints of these programs may be present in modern animals to execute non-canonical Hox functions. Non-canonical functions of Hox genes are involved in maintaining terminal nerve cell specificity, autophagy, oogenesis, pre-gastrulation embryogenesis, vertical signaling, and a number of general biological processes. These functions are realized by the basic properties of homeodomain protein and could have triggered the evolution of ParaHoxozoa and Nephrozoa subsequently. Some of these non-canonical Hox functions are discussed in our review.
Additional Links: PMID-38981695
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@article {pmid38981695,
year = {2024},
author = {Kulakova, MA and Maslakov, GP and Poliushkevich, LO},
title = {Irreducible Complexity of Hox Gene: Path to the Canonical Function of the Hox Cluster.},
journal = {Biochemistry. Biokhimiia},
volume = {89},
number = {6},
pages = {987-1001},
doi = {10.1134/S0006297924060014},
pmid = {38981695},
issn = {1608-3040},
mesh = {Animals ; *Genes, Homeobox ; Homeodomain Proteins/genetics/metabolism ; Multigene Family ; Humans ; Evolution, Molecular ; Gene Expression Regulation, Developmental ; },
abstract = {The evolution of major taxa is often associated with the emergence of new gene families. In all multicellular animals except sponges and comb jellies, the genomes contain Hox genes, which are crucial regulators of development. The canonical function of Hox genes involves colinear patterning of body parts in bilateral animals. This general function is implemented through complex, precisely coordinated mechanisms, not all of which are evolutionarily conserved and fully understood. We suggest that the emergence of this regulatory complexity was preceded by a stage of cooperation between more ancient morphogenetic programs or their individual elements. Footprints of these programs may be present in modern animals to execute non-canonical Hox functions. Non-canonical functions of Hox genes are involved in maintaining terminal nerve cell specificity, autophagy, oogenesis, pre-gastrulation embryogenesis, vertical signaling, and a number of general biological processes. These functions are realized by the basic properties of homeodomain protein and could have triggered the evolution of ParaHoxozoa and Nephrozoa subsequently. Some of these non-canonical Hox functions are discussed in our review.},
}
MeSH Terms:
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hide MeSH Terms
Animals
*Genes, Homeobox
Homeodomain Proteins/genetics/metabolism
Multigene Family
Humans
Evolution, Molecular
Gene Expression Regulation, Developmental
RevDate: 2024-07-09
CmpDate: 2024-07-06
Genomic sequencing reveals convergent adaptation during experimental evolution in two budding yeast species.
Communications biology, 7(1):825.
Convergent evolution is central in the origins of multicellularity. Identifying the basis for convergent multicellular evolution is challenging because of the diverse evolutionary origins and environments involved. Haploid Kluyveromyces lactis populations evolve multicellularity during selection for increased settling in liquid media. Strong genomic and phenotypic convergence is observed between K. lactis and previously selected S. cerevisiae populations under similar selection, despite their >100-million-year divergence. We find K. lactis multicellularity is conferred by mutations in genes ACE2 or AIM44, with ACE2 being predominant. They are a subset of the six genes involved in the S. cerevisiae multicellularity. Both ACE2 and AIM44 regulate cell division, indicating that the genetic convergence is likely due to conserved cellular replication mechanisms. Complex population dynamics involving multiple ACE2/AIM44 genotypes are found in most K. lactis lineages. The results show common ancestry and natural selection shape convergence while chance and contingency determine the degree of divergence.
Additional Links: PMID-38971878
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@article {pmid38971878,
year = {2024},
author = {Wang, P and Driscoll, WW and Travisano, M},
title = {Genomic sequencing reveals convergent adaptation during experimental evolution in two budding yeast species.},
journal = {Communications biology},
volume = {7},
number = {1},
pages = {825},
pmid = {38971878},
issn = {2399-3642},
support = {1724011//Center for Hierarchical Manufacturing, National Science Foundation (Center for Hierarchical Manufacturing)/ ; 16-IDEAS16-0002//National Aeronautics and Space Administration (NASA)/ ; },
mesh = {*Kluyveromyces/genetics/physiology ; Saccharomyces cerevisiae/genetics ; Genome, Fungal ; Mutation ; Evolution, Molecular ; Adaptation, Physiological/genetics ; Selection, Genetic ; Biological Evolution ; Saccharomyces cerevisiae Proteins/genetics/metabolism ; Genomics/methods ; },
abstract = {Convergent evolution is central in the origins of multicellularity. Identifying the basis for convergent multicellular evolution is challenging because of the diverse evolutionary origins and environments involved. Haploid Kluyveromyces lactis populations evolve multicellularity during selection for increased settling in liquid media. Strong genomic and phenotypic convergence is observed between K. lactis and previously selected S. cerevisiae populations under similar selection, despite their >100-million-year divergence. We find K. lactis multicellularity is conferred by mutations in genes ACE2 or AIM44, with ACE2 being predominant. They are a subset of the six genes involved in the S. cerevisiae multicellularity. Both ACE2 and AIM44 regulate cell division, indicating that the genetic convergence is likely due to conserved cellular replication mechanisms. Complex population dynamics involving multiple ACE2/AIM44 genotypes are found in most K. lactis lineages. The results show common ancestry and natural selection shape convergence while chance and contingency determine the degree of divergence.},
}
MeSH Terms:
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hide MeSH Terms
*Kluyveromyces/genetics/physiology
Saccharomyces cerevisiae/genetics
Genome, Fungal
Mutation
Evolution, Molecular
Adaptation, Physiological/genetics
Selection, Genetic
Biological Evolution
Saccharomyces cerevisiae Proteins/genetics/metabolism
Genomics/methods
RevDate: 2024-08-19
CmpDate: 2024-07-20
A gene for all seasons: The evolutionary consequences of HIF-1 in carcinogenesis, tumor growth and metastasis.
Seminars in cancer biology, 102-103:17-24.
Oxygen played a pivotal role in the evolution of multicellularity during the Cambrian Explosion. Not surprisingly, responses to fluctuating oxygen concentrations are integral to the evolution of cancer-a disease characterized by the breakdown of multicellularity. Poorly organized tumor vasculature results in chaotic patterns of blood flow characterized by large spatial and temporal variations in intra-tumoral oxygen concentrations. Hypoxia-inducible growth factor (HIF-1) plays a pivotal role in enabling cells to adapt, metabolize, and proliferate in low oxygen conditions. HIF-1 is often constitutively activated in cancers, underscoring its importance in cancer progression. Here, we argue that the phenotypic changes mediated by HIF-1, in addition to adapting the cancer cells to their local environment, also "pre-adapt" them for proliferation at distant, metastatic sites. HIF-1-mediated adaptations include a metabolic shift towards anaerobic respiration or glycolysis, activation of cell survival mechanisms like phenotypic plasticity and epigenetic reprogramming, and formation of tumor vasculature through angiogenesis. Hypoxia induced epigenetic reprogramming can trigger epithelial to mesenchymal transition in cancer cells-the first step in the metastatic cascade. Highly glycolytic cells facilitate local invasion by acidifying the tumor microenvironment. New blood vessels, formed due to angiogenesis, provide cancer cells a conduit to the circulatory system. Moreover, survival mechanisms acquired by cancer cells in the primary site allow them to remodel tissue at the metastatic site generating tumor promoting microenvironment. Thus, hypoxia in the primary tumor promoted adaptations conducive to all stages of the metastatic cascade from the initial escape entry into a blood vessel, intravascular survival, extravasation into distant tissues, and establishment of secondary tumors.
Additional Links: PMID-38969311
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PubMed:
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@article {pmid38969311,
year = {2024},
author = {Bhattacharya, R and Brown, JS and Gatenby, RA and Ibrahim-Hashim, A},
title = {A gene for all seasons: The evolutionary consequences of HIF-1 in carcinogenesis, tumor growth and metastasis.},
journal = {Seminars in cancer biology},
volume = {102-103},
number = {},
pages = {17-24},
doi = {10.1016/j.semcancer.2024.06.003},
pmid = {38969311},
issn = {1096-3650},
mesh = {Humans ; *Neoplasms/pathology/genetics/metabolism ; Animals ; *Neoplasm Metastasis ; *Carcinogenesis/genetics/pathology ; Hypoxia-Inducible Factor 1/metabolism/genetics ; Neovascularization, Pathologic/genetics/pathology/metabolism ; Epithelial-Mesenchymal Transition/genetics ; Tumor Microenvironment/genetics ; Epigenesis, Genetic ; Gene Expression Regulation, Neoplastic ; },
abstract = {Oxygen played a pivotal role in the evolution of multicellularity during the Cambrian Explosion. Not surprisingly, responses to fluctuating oxygen concentrations are integral to the evolution of cancer-a disease characterized by the breakdown of multicellularity. Poorly organized tumor vasculature results in chaotic patterns of blood flow characterized by large spatial and temporal variations in intra-tumoral oxygen concentrations. Hypoxia-inducible growth factor (HIF-1) plays a pivotal role in enabling cells to adapt, metabolize, and proliferate in low oxygen conditions. HIF-1 is often constitutively activated in cancers, underscoring its importance in cancer progression. Here, we argue that the phenotypic changes mediated by HIF-1, in addition to adapting the cancer cells to their local environment, also "pre-adapt" them for proliferation at distant, metastatic sites. HIF-1-mediated adaptations include a metabolic shift towards anaerobic respiration or glycolysis, activation of cell survival mechanisms like phenotypic plasticity and epigenetic reprogramming, and formation of tumor vasculature through angiogenesis. Hypoxia induced epigenetic reprogramming can trigger epithelial to mesenchymal transition in cancer cells-the first step in the metastatic cascade. Highly glycolytic cells facilitate local invasion by acidifying the tumor microenvironment. New blood vessels, formed due to angiogenesis, provide cancer cells a conduit to the circulatory system. Moreover, survival mechanisms acquired by cancer cells in the primary site allow them to remodel tissue at the metastatic site generating tumor promoting microenvironment. Thus, hypoxia in the primary tumor promoted adaptations conducive to all stages of the metastatic cascade from the initial escape entry into a blood vessel, intravascular survival, extravasation into distant tissues, and establishment of secondary tumors.},
}
MeSH Terms:
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hide MeSH Terms
Humans
*Neoplasms/pathology/genetics/metabolism
Animals
*Neoplasm Metastasis
*Carcinogenesis/genetics/pathology
Hypoxia-Inducible Factor 1/metabolism/genetics
Neovascularization, Pathologic/genetics/pathology/metabolism
Epithelial-Mesenchymal Transition/genetics
Tumor Microenvironment/genetics
Epigenesis, Genetic
Gene Expression Regulation, Neoplastic
RevDate: 2024-09-05
CmpDate: 2024-09-03
Charting the evolutionary path of the SUMO modification system in plants reveals molecular hardwiring of development to stress adaptation.
The Plant cell, 36(9):3131-3144.
SUMO modification is part of the spectrum of Ubiquitin-like (UBL) systems that give rise to proteoform complexity through post-translational modifications (PTMs). Proteoforms are essential modifiers of cell signaling for plant adaptation to changing environments. Exploration of the evolutionary emergence of Ubiquitin-like (UBL) systems unveils their origin from prokaryotes, where it is linked to the mechanisms that enable sulfur uptake into biomolecules. We explore the emergence of the SUMO machinery across the plant lineage from single-cell to land plants. We reveal the evolutionary point at which plants acquired the ability to form SUMO chains through the emergence of SUMO E4 ligases, hinting at its role in facilitating multicellularity. Additionally, we explore the possible mechanism for the neofunctionalization of SUMO proteases through the fusion of conserved catalytic domains with divergent sequences. We highlight the pivotal role of SUMO proteases in plant development and adaptation, offering new insights into target specificity mechanisms of SUMO modification during plant evolution. Correlating the emergence of adaptive traits in the plant lineage with established experimental evidence for SUMO in developmental processes, we propose that SUMO modification has evolved to link developmental processes to adaptive functions in land plants.
Additional Links: PMID-38923935
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Citation:
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@article {pmid38923935,
year = {2024},
author = {Ghosh, S and Mellado Sanchez, M and Sue-Ob, K and Roy, D and Jones, A and Blazquez, MA and Sadanandom, A},
title = {Charting the evolutionary path of the SUMO modification system in plants reveals molecular hardwiring of development to stress adaptation.},
journal = {The Plant cell},
volume = {36},
number = {9},
pages = {3131-3144},
pmid = {38923935},
issn = {1532-298X},
support = {BB/V003534/1//BBSRC/ ; },
mesh = {*Sumoylation ; *Plants/metabolism/genetics ; Plant Proteins/metabolism/genetics ; Small Ubiquitin-Related Modifier Proteins/metabolism/genetics ; Stress, Physiological ; Adaptation, Physiological/genetics ; Evolution, Molecular ; Protein Processing, Post-Translational ; Plant Development/genetics ; },
abstract = {SUMO modification is part of the spectrum of Ubiquitin-like (UBL) systems that give rise to proteoform complexity through post-translational modifications (PTMs). Proteoforms are essential modifiers of cell signaling for plant adaptation to changing environments. Exploration of the evolutionary emergence of Ubiquitin-like (UBL) systems unveils their origin from prokaryotes, where it is linked to the mechanisms that enable sulfur uptake into biomolecules. We explore the emergence of the SUMO machinery across the plant lineage from single-cell to land plants. We reveal the evolutionary point at which plants acquired the ability to form SUMO chains through the emergence of SUMO E4 ligases, hinting at its role in facilitating multicellularity. Additionally, we explore the possible mechanism for the neofunctionalization of SUMO proteases through the fusion of conserved catalytic domains with divergent sequences. We highlight the pivotal role of SUMO proteases in plant development and adaptation, offering new insights into target specificity mechanisms of SUMO modification during plant evolution. Correlating the emergence of adaptive traits in the plant lineage with established experimental evidence for SUMO in developmental processes, we propose that SUMO modification has evolved to link developmental processes to adaptive functions in land plants.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Sumoylation
*Plants/metabolism/genetics
Plant Proteins/metabolism/genetics
Small Ubiquitin-Related Modifier Proteins/metabolism/genetics
Stress, Physiological
Adaptation, Physiological/genetics
Evolution, Molecular
Protein Processing, Post-Translational
Plant Development/genetics
RevDate: 2024-08-12
CmpDate: 2024-08-12
Innate immune responses and monocyte-derived phagocyte recruitment in protective immunity to pathogenic bacteria: insights from Legionella pneumophila.
Current opinion in microbiology, 80:102495.
Legionella species are Gram-negative intracellular bacteria that evolved in soil and freshwater environments, where they infect and replicate within various unicellular protozoa. The primary virulence factor of Legionella is the expression of a type IV secretion system (T4SS), which contributes to the translocation of effector proteins that subvert biological processes of the host cells. Because of its evolution in unicellular organisms, T4SS effector proteins are not adapted to subvert specific mammalian signaling pathways and immunity. Consequently, Legionella pneumophila has emerged as an interesting infection model for investigating immune responses against pathogenic bacteria in multicellular organisms. This review highlights recent advances in our understanding of mammalian innate immunity derived from studies involving L. pneumophila. This includes recent insights into inflammasome-mediated mechanisms restricting bacterial replication in macrophages, mechanisms inducing cell death in response to infection, induction of effector-triggered immunity, activation of specific pulmonary cell types in mammalian lungs, and the protective role of recruiting monocyte-derived cells to infected lungs.
Additional Links: PMID-38908045
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PubMed:
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@article {pmid38908045,
year = {2024},
author = {Mascarenhas, DP and Zamboni, DS},
title = {Innate immune responses and monocyte-derived phagocyte recruitment in protective immunity to pathogenic bacteria: insights from Legionella pneumophila.},
journal = {Current opinion in microbiology},
volume = {80},
number = {},
pages = {102495},
doi = {10.1016/j.mib.2024.102495},
pmid = {38908045},
issn = {1879-0364},
mesh = {*Legionella pneumophila/immunology/pathogenicity ; *Immunity, Innate ; Humans ; Animals ; *Legionnaires' Disease/immunology/microbiology ; Phagocytes/immunology/microbiology ; Type IV Secretion Systems/immunology/genetics/metabolism ; Inflammasomes/immunology/metabolism ; Monocytes/immunology/microbiology ; Virulence Factors/immunology/metabolism ; Macrophages/immunology/microbiology ; Host-Pathogen Interactions/immunology ; },
abstract = {Legionella species are Gram-negative intracellular bacteria that evolved in soil and freshwater environments, where they infect and replicate within various unicellular protozoa. The primary virulence factor of Legionella is the expression of a type IV secretion system (T4SS), which contributes to the translocation of effector proteins that subvert biological processes of the host cells. Because of its evolution in unicellular organisms, T4SS effector proteins are not adapted to subvert specific mammalian signaling pathways and immunity. Consequently, Legionella pneumophila has emerged as an interesting infection model for investigating immune responses against pathogenic bacteria in multicellular organisms. This review highlights recent advances in our understanding of mammalian innate immunity derived from studies involving L. pneumophila. This includes recent insights into inflammasome-mediated mechanisms restricting bacterial replication in macrophages, mechanisms inducing cell death in response to infection, induction of effector-triggered immunity, activation of specific pulmonary cell types in mammalian lungs, and the protective role of recruiting monocyte-derived cells to infected lungs.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Legionella pneumophila/immunology/pathogenicity
*Immunity, Innate
Humans
Animals
*Legionnaires' Disease/immunology/microbiology
Phagocytes/immunology/microbiology
Type IV Secretion Systems/immunology/genetics/metabolism
Inflammasomes/immunology/metabolism
Monocytes/immunology/microbiology
Virulence Factors/immunology/metabolism
Macrophages/immunology/microbiology
Host-Pathogen Interactions/immunology
RevDate: 2024-09-11
CmpDate: 2024-09-11
Global and local genomic features together modulate the spontaneous single nucleotide mutation rate.
Computational biology and chemistry, 112:108107.
Spontaneous mutations are evolutionary engines as they generate variants for the evolutionary downstream processes that give rise to speciation and adaptation. Single nucleotide mutations (SNM) are the most abundant type of mutations among them. Here, we perform a meta-analysis to quantify the influence of selected global genomic parameters (genome size, genomic GC content, genomic repeat fraction, number of coding genes, gene count, and strand bias in prokaryotes) and local genomic features (local GC content, repeat content, CpG content and the number of SNM at CpG islands) on spontaneous SNM rates across the tree of life (prokaryotes, unicellular eukaryotes, multicellular eukaryotes) using wild-type sequence data in two different taxon classification systems. We find that the spontaneous SNM rates in our data are correlated with many genomic features in prokaryotes and unicellular eukaryotes irrespective of their sample sizes. On the other hand, only the number of coding genes was correlated with the spontaneous SNM rates in multicellular eukaryotes primarily contributed by vertebrates data. Considering local features, we notice that local GC content and CpG content significantly were correlated with the spontaneous SNM rates in the unicellular eukaryotes, while local repeat fraction is an important feature in prokaryotes and certain specific uni- and multi-cellular eukaryotes. Such predictive features of the spontaneous SNM rates often support non-linear models as the best fit compared to the linear model. We also observe that the strand asymmetry in prokaryotes plays an important role in determining the spontaneous SNM rates but the SNM spectrum does not.
Additional Links: PMID-38875896
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PubMed:
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@article {pmid38875896,
year = {2024},
author = {Ajay, A and Begum, T and Arya, A and Kumar, K and Ahmad, S},
title = {Global and local genomic features together modulate the spontaneous single nucleotide mutation rate.},
journal = {Computational biology and chemistry},
volume = {112},
number = {},
pages = {108107},
doi = {10.1016/j.compbiolchem.2024.108107},
pmid = {38875896},
issn = {1476-928X},
mesh = {*Base Composition ; Mutation Rate ; Genomics ; Genome/genetics ; Nucleotides/genetics ; Prokaryotic Cells/metabolism ; CpG Islands/genetics ; Animals ; },
abstract = {Spontaneous mutations are evolutionary engines as they generate variants for the evolutionary downstream processes that give rise to speciation and adaptation. Single nucleotide mutations (SNM) are the most abundant type of mutations among them. Here, we perform a meta-analysis to quantify the influence of selected global genomic parameters (genome size, genomic GC content, genomic repeat fraction, number of coding genes, gene count, and strand bias in prokaryotes) and local genomic features (local GC content, repeat content, CpG content and the number of SNM at CpG islands) on spontaneous SNM rates across the tree of life (prokaryotes, unicellular eukaryotes, multicellular eukaryotes) using wild-type sequence data in two different taxon classification systems. We find that the spontaneous SNM rates in our data are correlated with many genomic features in prokaryotes and unicellular eukaryotes irrespective of their sample sizes. On the other hand, only the number of coding genes was correlated with the spontaneous SNM rates in multicellular eukaryotes primarily contributed by vertebrates data. Considering local features, we notice that local GC content and CpG content significantly were correlated with the spontaneous SNM rates in the unicellular eukaryotes, while local repeat fraction is an important feature in prokaryotes and certain specific uni- and multi-cellular eukaryotes. Such predictive features of the spontaneous SNM rates often support non-linear models as the best fit compared to the linear model. We also observe that the strand asymmetry in prokaryotes plays an important role in determining the spontaneous SNM rates but the SNM spectrum does not.},
}
MeSH Terms:
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hide MeSH Terms
*Base Composition
Mutation Rate
Genomics
Genome/genetics
Nucleotides/genetics
Prokaryotic Cells/metabolism
CpG Islands/genetics
Animals
RevDate: 2024-07-19
CmpDate: 2024-06-07
A developmental constraint model of cancer cell states and tumor heterogeneity.
Cell, 187(12):2907-2918.
Cancer is a disease that stems from a fundamental liability inherent to multicellular life forms in which an individual cell is capable of reneging on the interests of the collective organism. Although cancer is commonly described as an evolutionary process, a less appreciated aspect of tumorigenesis may be the constraints imposed by the organism's developmental programs. Recent work from single-cell transcriptomic analyses across a range of cancer types has revealed the recurrence, plasticity, and co-option of distinct cellular states among cancer cell populations. Here, we note that across diverse cancer types, the observed cell states are proximate within the developmental hierarchy of the cell of origin. We thus posit a model by which cancer cell states are directly constrained by the organism's "developmental map." According to this model, a population of cancer cells traverses the developmental map, thereby generating a heterogeneous set of states whose interactions underpin emergent tumor behavior.
Additional Links: PMID-38848676
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@article {pmid38848676,
year = {2024},
author = {Patel, AS and Yanai, I},
title = {A developmental constraint model of cancer cell states and tumor heterogeneity.},
journal = {Cell},
volume = {187},
number = {12},
pages = {2907-2918},
pmid = {38848676},
issn = {1097-4172},
support = {R01 LM013522/LM/NLM NIH HHS/United States ; R21 CA264361/CA/NCI NIH HHS/United States ; U01 CA260432/CA/NCI NIH HHS/United States ; U54 CA263001/CA/NCI NIH HHS/United States ; },
mesh = {Animals ; Humans ; Carcinogenesis/pathology/genetics ; *Models, Biological ; *Neoplasms/pathology/genetics/metabolism ; Single-Cell Analysis ; Transcriptome/genetics ; Neoplastic Stem Cells/pathology ; },
abstract = {Cancer is a disease that stems from a fundamental liability inherent to multicellular life forms in which an individual cell is capable of reneging on the interests of the collective organism. Although cancer is commonly described as an evolutionary process, a less appreciated aspect of tumorigenesis may be the constraints imposed by the organism's developmental programs. Recent work from single-cell transcriptomic analyses across a range of cancer types has revealed the recurrence, plasticity, and co-option of distinct cellular states among cancer cell populations. Here, we note that across diverse cancer types, the observed cell states are proximate within the developmental hierarchy of the cell of origin. We thus posit a model by which cancer cell states are directly constrained by the organism's "developmental map." According to this model, a population of cancer cells traverses the developmental map, thereby generating a heterogeneous set of states whose interactions underpin emergent tumor behavior.},
}
MeSH Terms:
show MeSH Terms
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Animals
Humans
Carcinogenesis/pathology/genetics
*Models, Biological
*Neoplasms/pathology/genetics/metabolism
Single-Cell Analysis
Transcriptome/genetics
Neoplastic Stem Cells/pathology
RevDate: 2024-08-03
CmpDate: 2024-07-23
Causes and consequences of a complex recombinational landscape in the ant Cardiocondyla obscurior.
Genome research, 34(6):863-876.
Eusocial Hymenoptera have the highest recombination rates among all multicellular animals studied so far, but it is unclear why this is and how this affects the biology of individual species. A high-resolution linkage map for the ant Cardiocondyla obscurior corroborates genome-wide high recombination rates reported for ants (8.1 cM/Mb). However, recombination is locally suppressed in regions that are enriched with TEs, that have strong haplotype divergence, or that show signatures of epistatic selection in C. obscurior The results do not support the hypotheses that high recombination rates are linked to phenotypic plasticity or to modulating selection efficiency. Instead, genetic diversity and the frequency of structural variants correlate positively with local recombination rates, potentially compensating for the low levels of genetic variation expected in haplodiploid social Hymenoptera with low effective population size. Ultimately, the data show that recombination contributes to within-population polymorphism and to the divergence of the lineages within C. obscurior.
Additional Links: PMID-38839375
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@article {pmid38839375,
year = {2024},
author = {Errbii, M and Gadau, J and Becker, K and Schrader, L and Oettler, J},
title = {Causes and consequences of a complex recombinational landscape in the ant Cardiocondyla obscurior.},
journal = {Genome research},
volume = {34},
number = {6},
pages = {863-876},
pmid = {38839375},
issn = {1549-5469},
mesh = {Animals ; *Ants/genetics ; *Recombination, Genetic ; Chromosome Mapping ; Haplotypes ; Genetic Variation ; Genome, Insect ; Selection, Genetic ; Evolution, Molecular ; },
abstract = {Eusocial Hymenoptera have the highest recombination rates among all multicellular animals studied so far, but it is unclear why this is and how this affects the biology of individual species. A high-resolution linkage map for the ant Cardiocondyla obscurior corroborates genome-wide high recombination rates reported for ants (8.1 cM/Mb). However, recombination is locally suppressed in regions that are enriched with TEs, that have strong haplotype divergence, or that show signatures of epistatic selection in C. obscurior The results do not support the hypotheses that high recombination rates are linked to phenotypic plasticity or to modulating selection efficiency. Instead, genetic diversity and the frequency of structural variants correlate positively with local recombination rates, potentially compensating for the low levels of genetic variation expected in haplodiploid social Hymenoptera with low effective population size. Ultimately, the data show that recombination contributes to within-population polymorphism and to the divergence of the lineages within C. obscurior.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Ants/genetics
*Recombination, Genetic
Chromosome Mapping
Haplotypes
Genetic Variation
Genome, Insect
Selection, Genetic
Evolution, Molecular
RevDate: 2024-08-25
CmpDate: 2024-08-23
Phylogeny and evolution of streptophyte algae.
Annals of botany, 134(3):385-400.
The Streptophyta emerged about a billion years ago. Nowadays, this branch of the green lineage is most famous for one of its clades, the land plants (Embryophyta). Although Embryophyta make up the major share of species numbers in Streptophyta, there is a diversity of probably >5000 species of streptophyte algae that form a paraphyletic grade next to land plants. Here, we focus on the deep divergences that gave rise to the diversity of streptophytes, hence particularly on the streptophyte algae. Phylogenomic efforts have not only clarified the position of streptophyte algae relative to land plants, but recent efforts have also begun to unravel the relationships and major radiations within streptophyte algal diversity. We illustrate how new phylogenomic perspectives have changed our view on the evolutionary emergence of key traits, such as intricate signalling networks that are intertwined with multicellular growth and the chemodiverse hotbed from which they emerged. These traits are key for the biology of land plants but were bequeathed from their algal progenitors.
Additional Links: PMID-38832756
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@article {pmid38832756,
year = {2024},
author = {Bierenbroodspot, MJ and Pröschold, T and Fürst-Jansen, JMR and de Vries, S and Irisarri, I and Darienko, T and de Vries, J},
title = {Phylogeny and evolution of streptophyte algae.},
journal = {Annals of botany},
volume = {134},
number = {3},
pages = {385-400},
pmid = {38832756},
issn = {1095-8290},
support = {509535047//German Research Foundation/ ; 852725//European Union's Horizon 2020 research and innovation/ ; },
mesh = {*Phylogeny ; *Streptophyta/genetics/physiology ; *Biological Evolution ; },
abstract = {The Streptophyta emerged about a billion years ago. Nowadays, this branch of the green lineage is most famous for one of its clades, the land plants (Embryophyta). Although Embryophyta make up the major share of species numbers in Streptophyta, there is a diversity of probably >5000 species of streptophyte algae that form a paraphyletic grade next to land plants. Here, we focus on the deep divergences that gave rise to the diversity of streptophytes, hence particularly on the streptophyte algae. Phylogenomic efforts have not only clarified the position of streptophyte algae relative to land plants, but recent efforts have also begun to unravel the relationships and major radiations within streptophyte algal diversity. We illustrate how new phylogenomic perspectives have changed our view on the evolutionary emergence of key traits, such as intricate signalling networks that are intertwined with multicellular growth and the chemodiverse hotbed from which they emerged. These traits are key for the biology of land plants but were bequeathed from their algal progenitors.},
}
MeSH Terms:
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*Phylogeny
*Streptophyta/genetics/physiology
*Biological Evolution
RevDate: 2024-06-03
CmpDate: 2024-05-31
Ribonuclease inhibitor and angiogenin system regulates cell type-specific global translation.
Science advances, 10(22):eadl0320.
Translation of mRNAs is a fundamental process that occurs in all cell types of multicellular organisms. Conventionally, it has been considered a default step in gene expression, lacking specific regulation. However, recent studies have documented that certain mRNAs exhibit cell type-specific translation. Despite this, it remains unclear whether global translation is controlled in a cell type-specific manner. By using human cell lines and mouse models, we found that deletion of the ribosome-associated protein ribonuclease inhibitor 1 (RNH1) decreases global translation selectively in hematopoietic-origin cells but not in the non-hematopoietic-origin cells. RNH1-mediated cell type-specific translation is mechanistically linked to angiogenin-induced ribosomal biogenesis. Collectively, this study unravels the existence of cell type-specific global translation regulators and highlights the complex translation regulation in vertebrates.
Additional Links: PMID-38820160
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@article {pmid38820160,
year = {2024},
author = {Stillinovic, M and Sarangdhar, MA and Andina, N and Tardivel, A and Greub, F and Bombaci, G and Ansermet, C and Zatti, M and Saha, D and Xiong, J and Sagae, T and Yokogawa, M and Osawa, M and Heller, M and Keogh, A and Keller, I and Angelillo-Scherrer, A and Allam, R},
title = {Ribonuclease inhibitor and angiogenin system regulates cell type-specific global translation.},
journal = {Science advances},
volume = {10},
number = {22},
pages = {eadl0320},
pmid = {38820160},
issn = {2375-2548},
mesh = {*Ribonuclease, Pancreatic/metabolism/genetics ; Humans ; *Protein Biosynthesis ; Animals ; Mice ; *Ribosomes/metabolism ; RNA, Messenger/genetics/metabolism ; Gene Expression Regulation ; Cell Line ; Organ Specificity ; Carrier Proteins ; },
abstract = {Translation of mRNAs is a fundamental process that occurs in all cell types of multicellular organisms. Conventionally, it has been considered a default step in gene expression, lacking specific regulation. However, recent studies have documented that certain mRNAs exhibit cell type-specific translation. Despite this, it remains unclear whether global translation is controlled in a cell type-specific manner. By using human cell lines and mouse models, we found that deletion of the ribosome-associated protein ribonuclease inhibitor 1 (RNH1) decreases global translation selectively in hematopoietic-origin cells but not in the non-hematopoietic-origin cells. RNH1-mediated cell type-specific translation is mechanistically linked to angiogenin-induced ribosomal biogenesis. Collectively, this study unravels the existence of cell type-specific global translation regulators and highlights the complex translation regulation in vertebrates.},
}
MeSH Terms:
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*Ribonuclease, Pancreatic/metabolism/genetics
Humans
*Protein Biosynthesis
Animals
Mice
*Ribosomes/metabolism
RNA, Messenger/genetics/metabolism
Gene Expression Regulation
Cell Line
Organ Specificity
Carrier Proteins
RevDate: 2024-06-01
CmpDate: 2024-05-29
Rapid response of fly populations to gene dosage across development and generations.
Nature communications, 15(1):4551.
Although the effects of genetic and environmental perturbations on multicellular organisms are rarely restricted to single phenotypic layers, our current understanding of how developmental programs react to these challenges remains limited. Here, we have examined the phenotypic consequences of disturbing the bicoid regulatory network in early Drosophila embryos. We generated flies with two extra copies of bicoid, which causes a posterior shift of the network's regulatory outputs and a decrease in fitness. We subjected these flies to EMS mutagenesis, followed by experimental evolution. After only 8-15 generations, experimental populations have normalized patterns of gene expression and increased survival. Using a phenomics approach, we find that populations were normalized through rapid increases in embryo size driven by maternal changes in metabolism and ovariole development. We extend our results to additional populations of flies, demonstrating predictability. Together, our results necessitate a broader view of regulatory network evolution at the systems level.
Additional Links: PMID-38811562
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@article {pmid38811562,
year = {2024},
author = {Li, XC and Gandara, L and Ekelöf, M and Richter, K and Alexandrov, T and Crocker, J},
title = {Rapid response of fly populations to gene dosage across development and generations.},
journal = {Nature communications},
volume = {15},
number = {1},
pages = {4551},
pmid = {38811562},
issn = {2041-1723},
mesh = {Animals ; *Drosophila Proteins/genetics/metabolism ; *Gene Expression Regulation, Developmental ; *Gene Regulatory Networks ; Female ; *Drosophila melanogaster/genetics/growth & development/embryology ; *Gene Dosage ; Homeodomain Proteins/genetics/metabolism ; Phenotype ; Male ; Embryo, Nonmammalian/metabolism ; Drosophila/genetics/embryology/metabolism ; Mutagenesis ; Trans-Activators ; },
abstract = {Although the effects of genetic and environmental perturbations on multicellular organisms are rarely restricted to single phenotypic layers, our current understanding of how developmental programs react to these challenges remains limited. Here, we have examined the phenotypic consequences of disturbing the bicoid regulatory network in early Drosophila embryos. We generated flies with two extra copies of bicoid, which causes a posterior shift of the network's regulatory outputs and a decrease in fitness. We subjected these flies to EMS mutagenesis, followed by experimental evolution. After only 8-15 generations, experimental populations have normalized patterns of gene expression and increased survival. Using a phenomics approach, we find that populations were normalized through rapid increases in embryo size driven by maternal changes in metabolism and ovariole development. We extend our results to additional populations of flies, demonstrating predictability. Together, our results necessitate a broader view of regulatory network evolution at the systems level.},
}
MeSH Terms:
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Animals
*Drosophila Proteins/genetics/metabolism
*Gene Expression Regulation, Developmental
*Gene Regulatory Networks
Female
*Drosophila melanogaster/genetics/growth & development/embryology
*Gene Dosage
Homeodomain Proteins/genetics/metabolism
Phenotype
Male
Embryo, Nonmammalian/metabolism
Drosophila/genetics/embryology/metabolism
Mutagenesis
Trans-Activators
RevDate: 2024-09-02
CmpDate: 2024-07-02
Origins of cancer: ain't it just mature cells misbehaving?.
The EMBO journal, 43(13):2530-2551.
A pervasive view is that undifferentiated stem cells are alone responsible for generating all other cells and are the origins of cancer. However, emerging evidence demonstrates fully differentiated cells are plastic, can be coaxed to proliferate, and also play essential roles in tissue maintenance, regeneration, and tumorigenesis. Here, we review the mechanisms governing how differentiated cells become cancer cells. First, we examine the unique characteristics of differentiated cell division, focusing on why differentiated cells are more susceptible than stem cells to accumulating mutations. Next, we investigate why the evolution of multicellularity in animals likely required plastic differentiated cells that maintain the capacity to return to the cell cycle and required the tumor suppressor p53. Finally, we examine an example of an evolutionarily conserved program for the plasticity of differentiated cells, paligenosis, which helps explain the origins of cancers that arise in adults. Altogether, we highlight new perspectives for understanding the development of cancer and new strategies for preventing carcinogenic cellular transformations from occurring.
Additional Links: PMID-38773319
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@article {pmid38773319,
year = {2024},
author = {Cho, CJ and Brown, JW and Mills, JC},
title = {Origins of cancer: ain't it just mature cells misbehaving?.},
journal = {The EMBO journal},
volume = {43},
number = {13},
pages = {2530-2551},
pmid = {38773319},
issn = {1460-2075},
support = {R01 CA239645/CA/NCI NIH HHS/United States ; P30 CA125123/CA/NCI NIH HHS/United States ; P30 DK056338/DK/NIDDK NIH HHS/United States ; R21 AI156236/AI/NIAID NIH HHS/United States ; W81XWH2210327//DOD | USA | MEDCOM | CDMRP | DOD Peer Reviewed Cancer Research Program (PRCRP)/ ; P30 DK052574/DK/NIDDK NIH HHS/United States ; K08 DK132496/DK/NIDDK NIH HHS/United States ; R01 DK105129/DK/NIDDK NIH HHS/United States ; R01DK105129//HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)/ ; R01 DK134531/DK/NIDDK NIH HHS/United States ; W81XWH-20-1-0630//DOD | USA | MEDCOM | CDMRP | DOD Peer Reviewed Cancer Research Program (PRCRP)/ ; R01DK134531//HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)/ ; },
mesh = {Humans ; Animals ; *Neoplasms/pathology/genetics ; *Cell Differentiation ; Tumor Suppressor Protein p53/metabolism/genetics ; Cell Transformation, Neoplastic/genetics/pathology ; Stem Cells ; Carcinogenesis/pathology ; },
abstract = {A pervasive view is that undifferentiated stem cells are alone responsible for generating all other cells and are the origins of cancer. However, emerging evidence demonstrates fully differentiated cells are plastic, can be coaxed to proliferate, and also play essential roles in tissue maintenance, regeneration, and tumorigenesis. Here, we review the mechanisms governing how differentiated cells become cancer cells. First, we examine the unique characteristics of differentiated cell division, focusing on why differentiated cells are more susceptible than stem cells to accumulating mutations. Next, we investigate why the evolution of multicellularity in animals likely required plastic differentiated cells that maintain the capacity to return to the cell cycle and required the tumor suppressor p53. Finally, we examine an example of an evolutionarily conserved program for the plasticity of differentiated cells, paligenosis, which helps explain the origins of cancers that arise in adults. Altogether, we highlight new perspectives for understanding the development of cancer and new strategies for preventing carcinogenic cellular transformations from occurring.},
}
MeSH Terms:
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Humans
Animals
*Neoplasms/pathology/genetics
*Cell Differentiation
Tumor Suppressor Protein p53/metabolism/genetics
Cell Transformation, Neoplastic/genetics/pathology
Stem Cells
Carcinogenesis/pathology
RevDate: 2024-05-24
CmpDate: 2024-05-21
The molecular evolution of cancer associated genes in mammals.
Scientific reports, 14(1):11650.
Cancer is a disease that many multicellular organisms have faced for millions of years, and species have evolved various tumour suppression mechanisms to control oncogenesis. Although cancer occurs across the tree of life, cancer related mortality risks vary across mammalian orders, with Carnivorans particularly affected. Evolutionary theory predicts different selection pressures on genes associated with cancer progression and suppression, including oncogenes, tumour suppressor genes and immune genes. Therefore, we investigated the evolutionary history of cancer associated gene sequences across 384 mammalian taxa, to detect signatures of selection across categories of oncogenes (GRB2, FGL2 and CDC42), tumour suppressors (LITAF, Casp8 and BRCA2) and immune genes (IL2, CD274 and B2M). This approach allowed us to conduct a fine scale analysis of gene wide and site-specific signatures of selection across mammalian lineages under the lens of cancer susceptibility. Phylogenetic analyses revealed that for most species the evolution of cancer associated genes follows the species' evolution. The gene wide selection analyses revealed oncogenes being the most conserved, tumour suppressor and immune genes having similar amounts of episodic diversifying selection. Despite BRCA2's status as a key caretaker gene, episodic diversifying selection was detected across mammals. The site-specific selection analyses revealed that the two apoptosis associated domains of the Casp8 gene of bats (Chiroptera) are under opposing forces of selection (positive and negative respectively), highlighting the importance of site-specific selection analyses to understand the evolution of highly complex gene families. Our results highlighted the need to critically assess different types of selection pressure on cancer associated genes when investigating evolutionary adaptations to cancer across the tree of life. This study provides an extensive assessment of cancer associated genes in mammals with highly representative, and substantially large sample size for a comparative genomic analysis in the field and identifies various avenues for future research into the mechanisms of cancer resistance and susceptibility in mammals.
Additional Links: PMID-38773187
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Citation:
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@article {pmid38773187,
year = {2024},
author = {MacDonald, N and Raven, N and Diep, W and Evans, S and Pannipitiya, S and Bramwell, G and Vanbeek, C and Thomas, F and Russell, T and Dujon, AM and Telonis-Scott, M and Ujvari, B},
title = {The molecular evolution of cancer associated genes in mammals.},
journal = {Scientific reports},
volume = {14},
number = {1},
pages = {11650},
pmid = {38773187},
issn = {2045-2322},
mesh = {Animals ; *Evolution, Molecular ; *Mammals/genetics ; *Neoplasms/genetics ; *Phylogeny ; Humans ; Selection, Genetic ; Oncogenes/genetics ; Genes, Tumor Suppressor ; Genetic Predisposition to Disease ; },
abstract = {Cancer is a disease that many multicellular organisms have faced for millions of years, and species have evolved various tumour suppression mechanisms to control oncogenesis. Although cancer occurs across the tree of life, cancer related mortality risks vary across mammalian orders, with Carnivorans particularly affected. Evolutionary theory predicts different selection pressures on genes associated with cancer progression and suppression, including oncogenes, tumour suppressor genes and immune genes. Therefore, we investigated the evolutionary history of cancer associated gene sequences across 384 mammalian taxa, to detect signatures of selection across categories of oncogenes (GRB2, FGL2 and CDC42), tumour suppressors (LITAF, Casp8 and BRCA2) and immune genes (IL2, CD274 and B2M). This approach allowed us to conduct a fine scale analysis of gene wide and site-specific signatures of selection across mammalian lineages under the lens of cancer susceptibility. Phylogenetic analyses revealed that for most species the evolution of cancer associated genes follows the species' evolution. The gene wide selection analyses revealed oncogenes being the most conserved, tumour suppressor and immune genes having similar amounts of episodic diversifying selection. Despite BRCA2's status as a key caretaker gene, episodic diversifying selection was detected across mammals. The site-specific selection analyses revealed that the two apoptosis associated domains of the Casp8 gene of bats (Chiroptera) are under opposing forces of selection (positive and negative respectively), highlighting the importance of site-specific selection analyses to understand the evolution of highly complex gene families. Our results highlighted the need to critically assess different types of selection pressure on cancer associated genes when investigating evolutionary adaptations to cancer across the tree of life. This study provides an extensive assessment of cancer associated genes in mammals with highly representative, and substantially large sample size for a comparative genomic analysis in the field and identifies various avenues for future research into the mechanisms of cancer resistance and susceptibility in mammals.},
}
MeSH Terms:
show MeSH Terms
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Animals
*Evolution, Molecular
*Mammals/genetics
*Neoplasms/genetics
*Phylogeny
Humans
Selection, Genetic
Oncogenes/genetics
Genes, Tumor Suppressor
Genetic Predisposition to Disease
RevDate: 2024-09-10
CmpDate: 2024-05-21
Heterogeneity generating capacity in tumorigenesis and cancer therapeutics.
Biochimica et biophysica acta. Molecular basis of disease, 1870(5):167226.
Cells of multicellular organisms generate heterogeneity in a controlled and transient fashion during embryogenesis, which can be reactivated in pathologies such as cancer. Although genomic heterogeneity is an important part of tumorigenesis, continuous generation of phenotypic heterogeneity is central for the adaptation of cancer cells to the challenges of tumorigenesis and response to therapy. Here I discuss the capacity of generating heterogeneity, hereafter called cell hetness, in cancer cells both as the activation of hetness oncogenes and inactivation of hetness tumor suppressor genes, which increase the generation of heterogeneity, ultimately producing an increase in adaptability and cell fitness. Transcriptomic high hetness states in therapy-tolerant cell states denote its importance in cancer resistance to therapy. The definition of the concept of hetness will allow the understanding of its origins, its control during embryogenesis, its loss of control in tumorigenesis and cancer therapeutics and its active targeting.
Additional Links: PMID-38734320
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@article {pmid38734320,
year = {2024},
author = {Lenz, G},
title = {Heterogeneity generating capacity in tumorigenesis and cancer therapeutics.},
journal = {Biochimica et biophysica acta. Molecular basis of disease},
volume = {1870},
number = {5},
pages = {167226},
doi = {10.1016/j.bbadis.2024.167226},
pmid = {38734320},
issn = {1879-260X},
mesh = {Humans ; *Neoplasms/genetics/pathology/therapy/metabolism ; *Carcinogenesis/genetics/pathology ; Genetic Heterogeneity ; Oncogenes/genetics ; Animals ; Cell Transformation, Neoplastic/genetics/metabolism ; Genes, Tumor Suppressor ; Gene Expression Regulation, Neoplastic ; },
abstract = {Cells of multicellular organisms generate heterogeneity in a controlled and transient fashion during embryogenesis, which can be reactivated in pathologies such as cancer. Although genomic heterogeneity is an important part of tumorigenesis, continuous generation of phenotypic heterogeneity is central for the adaptation of cancer cells to the challenges of tumorigenesis and response to therapy. Here I discuss the capacity of generating heterogeneity, hereafter called cell hetness, in cancer cells both as the activation of hetness oncogenes and inactivation of hetness tumor suppressor genes, which increase the generation of heterogeneity, ultimately producing an increase in adaptability and cell fitness. Transcriptomic high hetness states in therapy-tolerant cell states denote its importance in cancer resistance to therapy. The definition of the concept of hetness will allow the understanding of its origins, its control during embryogenesis, its loss of control in tumorigenesis and cancer therapeutics and its active targeting.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Neoplasms/genetics/pathology/therapy/metabolism
*Carcinogenesis/genetics/pathology
Genetic Heterogeneity
Oncogenes/genetics
Animals
Cell Transformation, Neoplastic/genetics/metabolism
Genes, Tumor Suppressor
Gene Expression Regulation, Neoplastic
RevDate: 2024-05-19
CmpDate: 2024-05-17
Group-selection via aggregative propagule-formation enables cooperative multicellularity in an individual based, spatial model.
PLoS computational biology, 20(5):e1012107.
The emergence of multicellularity is one of the major transitions in evolution that happened multiple times independently. During aggregative multicellularity, genetically potentially unrelated lineages cooperate to form transient multicellular groups. Unlike clonal multicellularity, aggregative multicellular organisms do not rely on kin selection instead other mechanisms maintain cooperation against cheater phenotypes that benefit from cooperators but do not contribute to groups. Spatiality with limited diffusion can facilitate group selection, as interactions among individuals are restricted to local neighbourhoods only. Selection for larger size (e.g. avoiding predation) may facilitate the emergence of aggregation, though it is unknown, whether and how much role such selection played during the evolution of aggregative multicellularity. We have investigated the effect of spatiality and the necessity of predation on the stability of aggregative multicellularity via individual-based modelling on the ecological timescale. We have examined whether aggregation facilitates the survival of cooperators in a temporally heterogeneous environment against cheaters, where only a subset of the population is allowed to periodically colonize a new, resource-rich habitat. Cooperators constitutively produce adhesive molecules to promote aggregation and propagule-formation while cheaters spare this expense to grow faster but cannot aggregate on their own, hence depending on cooperators for long-term survival. We have compared different population-level reproduction modes with and without individual selection (predation) to evaluate the different hypotheses. In a temporally homogeneous environment without propagule-based colonization, cheaters always win. Predation can benefit cooperators, but it is not enough to maintain the necessary cooperator amount in successive dispersals, either randomly or by fragmentation. Aggregation-based propagation however can ensure the adequate ratio of cooperators-to-cheaters in the propagule and is sufficient to do so even without predation. Spatiality combined with temporal heterogeneity helps cooperators via group selection, thus facilitating aggregative multicellularity. External stress selecting for larger size (e.g. predation) may facilitate aggregation, however, according to our results, it is neither necessary nor sufficient for aggregative multicellularity to be maintained when there is effective group-selection.
Additional Links: PMID-38713735
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@article {pmid38713735,
year = {2024},
author = {Oszoli, I and Zachar, I},
title = {Group-selection via aggregative propagule-formation enables cooperative multicellularity in an individual based, spatial model.},
journal = {PLoS computational biology},
volume = {20},
number = {5},
pages = {e1012107},
pmid = {38713735},
issn = {1553-7358},
mesh = {*Models, Biological ; *Biological Evolution ; Computational Biology ; Ecosystem ; Animals ; Predatory Behavior/physiology ; Selection, Genetic ; Computer Simulation ; },
abstract = {The emergence of multicellularity is one of the major transitions in evolution that happened multiple times independently. During aggregative multicellularity, genetically potentially unrelated lineages cooperate to form transient multicellular groups. Unlike clonal multicellularity, aggregative multicellular organisms do not rely on kin selection instead other mechanisms maintain cooperation against cheater phenotypes that benefit from cooperators but do not contribute to groups. Spatiality with limited diffusion can facilitate group selection, as interactions among individuals are restricted to local neighbourhoods only. Selection for larger size (e.g. avoiding predation) may facilitate the emergence of aggregation, though it is unknown, whether and how much role such selection played during the evolution of aggregative multicellularity. We have investigated the effect of spatiality and the necessity of predation on the stability of aggregative multicellularity via individual-based modelling on the ecological timescale. We have examined whether aggregation facilitates the survival of cooperators in a temporally heterogeneous environment against cheaters, where only a subset of the population is allowed to periodically colonize a new, resource-rich habitat. Cooperators constitutively produce adhesive molecules to promote aggregation and propagule-formation while cheaters spare this expense to grow faster but cannot aggregate on their own, hence depending on cooperators for long-term survival. We have compared different population-level reproduction modes with and without individual selection (predation) to evaluate the different hypotheses. In a temporally homogeneous environment without propagule-based colonization, cheaters always win. Predation can benefit cooperators, but it is not enough to maintain the necessary cooperator amount in successive dispersals, either randomly or by fragmentation. Aggregation-based propagation however can ensure the adequate ratio of cooperators-to-cheaters in the propagule and is sufficient to do so even without predation. Spatiality combined with temporal heterogeneity helps cooperators via group selection, thus facilitating aggregative multicellularity. External stress selecting for larger size (e.g. predation) may facilitate aggregation, however, according to our results, it is neither necessary nor sufficient for aggregative multicellularity to be maintained when there is effective group-selection.},
}
MeSH Terms:
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*Models, Biological
*Biological Evolution
Computational Biology
Ecosystem
Animals
Predatory Behavior/physiology
Selection, Genetic
Computer Simulation
RevDate: 2024-06-13
CmpDate: 2024-06-05
HMG-B transcription factors of unicellular opisthokonts and their relatedness to the Sox-Tcf/Lef-Mata proteins of Metazoa and fungi.
Gene, 921:148520.
A phylogenetic analysis of transcription factors of the Sox-Tcf/Lef-Mata (STM) family of the HMG-B superfamily was carried out in order to clarify the evolutionary roots of the Wnt signaling pathway in unicellular organisms. The data set for analysis included protein sequences of metazoans, fungi, unicellular opisthokonts, apusomonads and amoebozoans. The topology of the phylogenetic tree suggests that STM-related proteins arose in the common ancestor of Opisthokonta and Amoebozoa, two of amoebozoan STM proteins are sister-related to opisthokont ones and the three known lineages of STM transcription factors (STM family in narrow sence) are found in Opisthokonta only. Of these, the holozoan Sox protein branch is the result of either the first or second branching, that originated in the common ancestor of Opisthokonta. The lineage containing Tcf/Lef proteins (holozoan) and the lineage containing Mata proteins (holomycotan) are sister. They derived either at the time of the Holozoa and Holomycota divergence or originate from two paralogs of the common ancestor of Opisthokonta, which arose after the separation of the Sox lineage. Interaction with Armadillo-like proteins may be an original feature of the STM protein family and existed in the unicellular ancestors of multicellular animals; a connection is possible between the presence of Mata-related proteins in Aphelidium protococcorum and specific genome feature of this species.
Additional Links: PMID-38702020
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@article {pmid38702020,
year = {2024},
author = {Pozdnyakov, IR and Selyuk, AO and Kalashnikova, VA and Karpov, SA},
title = {HMG-B transcription factors of unicellular opisthokonts and their relatedness to the Sox-Tcf/Lef-Mata proteins of Metazoa and fungi.},
journal = {Gene},
volume = {921},
number = {},
pages = {148520},
doi = {10.1016/j.gene.2024.148520},
pmid = {38702020},
issn = {1879-0038},
mesh = {*Phylogeny ; Animals ; *Evolution, Molecular ; Fungi/genetics/metabolism ; HMGB Proteins/genetics/metabolism ; SOX Transcription Factors/genetics/metabolism ; Transcription Factors/genetics/metabolism ; Fungal Proteins/genetics/metabolism ; Wnt Signaling Pathway ; },
abstract = {A phylogenetic analysis of transcription factors of the Sox-Tcf/Lef-Mata (STM) family of the HMG-B superfamily was carried out in order to clarify the evolutionary roots of the Wnt signaling pathway in unicellular organisms. The data set for analysis included protein sequences of metazoans, fungi, unicellular opisthokonts, apusomonads and amoebozoans. The topology of the phylogenetic tree suggests that STM-related proteins arose in the common ancestor of Opisthokonta and Amoebozoa, two of amoebozoan STM proteins are sister-related to opisthokont ones and the three known lineages of STM transcription factors (STM family in narrow sence) are found in Opisthokonta only. Of these, the holozoan Sox protein branch is the result of either the first or second branching, that originated in the common ancestor of Opisthokonta. The lineage containing Tcf/Lef proteins (holozoan) and the lineage containing Mata proteins (holomycotan) are sister. They derived either at the time of the Holozoa and Holomycota divergence or originate from two paralogs of the common ancestor of Opisthokonta, which arose after the separation of the Sox lineage. Interaction with Armadillo-like proteins may be an original feature of the STM protein family and existed in the unicellular ancestors of multicellular animals; a connection is possible between the presence of Mata-related proteins in Aphelidium protococcorum and specific genome feature of this species.},
}
MeSH Terms:
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hide MeSH Terms
*Phylogeny
Animals
*Evolution, Molecular
Fungi/genetics/metabolism
HMGB Proteins/genetics/metabolism
SOX Transcription Factors/genetics/metabolism
Transcription Factors/genetics/metabolism
Fungal Proteins/genetics/metabolism
Wnt Signaling Pathway
RevDate: 2024-10-02
CmpDate: 2024-05-15
Genomes of multicellular algal sisters to land plants illuminate signaling network evolution.
Nature genetics, 56(5):1018-1031.
Zygnematophyceae are the algal sisters of land plants. Here we sequenced four genomes of filamentous Zygnematophyceae, including chromosome-scale assemblies for three strains of Zygnema circumcarinatum. We inferred traits in the ancestor of Zygnematophyceae and land plants that might have ushered in the conquest of land by plants: expanded genes for signaling cascades, environmental response, and multicellular growth. Zygnematophyceae and land plants share all the major enzymes for cell wall synthesis and remodifications, and gene gains shaped this toolkit. Co-expression network analyses uncover gene cohorts that unite environmental signaling with multicellular developmental programs. Our data shed light on a molecular chassis that balances environmental response and growth modulation across more than 600 million years of streptophyte evolution.
Additional Links: PMID-38693345
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@article {pmid38693345,
year = {2024},
author = {Feng, X and Zheng, J and Irisarri, I and Yu, H and Zheng, B and Ali, Z and de Vries, S and Keller, J and Fürst-Jansen, JMR and Dadras, A and Zegers, JMS and Rieseberg, TP and Dhabalia Ashok, A and Darienko, T and Bierenbroodspot, MJ and Gramzow, L and Petroll, R and Haas, FB and Fernandez-Pozo, N and Nousias, O and Li, T and Fitzek, E and Grayburn, WS and Rittmeier, N and Permann, C and Rümpler, F and Archibald, JM and Theißen, G and Mower, JP and Lorenz, M and Buschmann, H and von Schwartzenberg, K and Boston, L and Hayes, RD and Daum, C and Barry, K and Grigoriev, IV and Wang, X and Li, FW and Rensing, SA and Ben Ari, J and Keren, N and Mosquna, A and Holzinger, A and Delaux, PM and Zhang, C and Huang, J and Mutwil, M and de Vries, J and Yin, Y},
title = {Genomes of multicellular algal sisters to land plants illuminate signaling network evolution.},
journal = {Nature genetics},
volume = {56},
number = {5},
pages = {1018-1031},
pmid = {38693345},
issn = {1546-1718},
support = {R01GM140370//Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.)/ ; RE 1697/16-1//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; RE 1697/18-1//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 1933521//National Science Foundation (NSF)/ ; R21AI171952//Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.)/ ; DE-AC02-05CH11231//U.S. Department of Energy (DOE)/ ; 852725//EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 European Research Council (H2020 Excellent Science - European Research Council)/ ; R01 GM140370/GM/NIGMS NIH HHS/United States ; R21 AI171952/AI/NIAID NIH HHS/United States ; P34181-B//Austrian Science Fund (Fonds zur Förderung der Wissenschaftlichen Forschung)/ ; 58-8042-9-089//United States Department of Agriculture | Agricultural Research Service (USDA Agricultural Research Service)/ ; ANR-10-LABX-41//LABoratoires d'EXcellence ARCANE (Labex ARCANE)/ ; 410739858//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; TH417/12-1//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 440231723//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; OPP1172165//Bill and Melinda Gates Foundation (Bill & Melinda Gates Foundation)/ ; 101001675//EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 European Research Council (H2020 Excellent Science - European Research Council)/ ; 440540015//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; },
mesh = {*Signal Transduction/genetics ; *Embryophyta/genetics ; *Evolution, Molecular ; *Phylogeny ; Gene Regulatory Networks ; Genome/genetics ; Genome, Plant ; },
abstract = {Zygnematophyceae are the algal sisters of land plants. Here we sequenced four genomes of filamentous Zygnematophyceae, including chromosome-scale assemblies for three strains of Zygnema circumcarinatum. We inferred traits in the ancestor of Zygnematophyceae and land plants that might have ushered in the conquest of land by plants: expanded genes for signaling cascades, environmental response, and multicellular growth. Zygnematophyceae and land plants share all the major enzymes for cell wall synthesis and remodifications, and gene gains shaped this toolkit. Co-expression network analyses uncover gene cohorts that unite environmental signaling with multicellular developmental programs. Our data shed light on a molecular chassis that balances environmental response and growth modulation across more than 600 million years of streptophyte evolution.},
}
MeSH Terms:
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*Signal Transduction/genetics
*Embryophyta/genetics
*Evolution, Molecular
*Phylogeny
Gene Regulatory Networks
Genome/genetics
Genome, Plant
RevDate: 2024-07-02
CmpDate: 2024-04-30
Disruption of metazoan gene regulatory networks in cancer alters the balance of co-expression between genes of unicellular and multicellular origins.
Genome biology, 25(1):110.
BACKGROUND: Metazoans inherited genes from unicellular ancestors that perform essential biological processes such as cell division, metabolism, and protein translation. Multicellularity requires careful control and coordination of these unicellular genes to maintain tissue integrity and homeostasis. Gene regulatory networks (GRNs) that arose during metazoan evolution are frequently altered in cancer, resulting in over-expression of unicellular genes. We propose that an imbalance in co-expression of unicellular (UC) and multicellular (MC) genes is a driving force in cancer.
RESULTS: We combine gene co-expression analysis to infer changes to GRNs in cancer with protein sequence conservation data to distinguish genes with UC and MC origins. Co-expression networks created using RNA sequencing data from 31 tumor types and normal tissue samples are divided into modules enriched for UC genes, MC genes, or mixed UC-MC modules. The greatest differences between tumor and normal tissue co-expression networks occur within mixed UC-MC modules. MC and UC genes not commonly co-expressed in normal tissues form distinct co-expression modules seen only in tumors. The degree of rewiring of genes within mixed UC-MC modules increases with tumor grade and stage. Mixed UC-MC modules are enriched for somatic mutations in cancer genes, particularly amplifications, suggesting an important driver of the rewiring observed in tumors is copy number changes.
CONCLUSIONS: Our study shows the greatest changes to gene co-expression patterns during tumor progression occur between genes of MC and UC origins, implicating the breakdown and rewiring of metazoan gene regulatory networks in cancer development and progression.
Additional Links: PMID-38685127
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@article {pmid38685127,
year = {2024},
author = {Trigos, AS and Bongiovanni, F and Zhang, Y and Zethoven, M and Tothill, R and Pearson, R and Papenfuss, AT and Goode, DL},
title = {Disruption of metazoan gene regulatory networks in cancer alters the balance of co-expression between genes of unicellular and multicellular origins.},
journal = {Genome biology},
volume = {25},
number = {1},
pages = {110},
pmid = {38685127},
issn = {1474-760X},
support = {MCRF17005//Victorian Cancer Agency/ ; 2003115//National Health and Medical Research Council/ ; 2003887//National Health and Medical Research Council/ ; },
mesh = {*Gene Regulatory Networks ; *Neoplasms/genetics ; Humans ; Animals ; Gene Expression Regulation, Neoplastic ; Evolution, Molecular ; },
abstract = {BACKGROUND: Metazoans inherited genes from unicellular ancestors that perform essential biological processes such as cell division, metabolism, and protein translation. Multicellularity requires careful control and coordination of these unicellular genes to maintain tissue integrity and homeostasis. Gene regulatory networks (GRNs) that arose during metazoan evolution are frequently altered in cancer, resulting in over-expression of unicellular genes. We propose that an imbalance in co-expression of unicellular (UC) and multicellular (MC) genes is a driving force in cancer.
RESULTS: We combine gene co-expression analysis to infer changes to GRNs in cancer with protein sequence conservation data to distinguish genes with UC and MC origins. Co-expression networks created using RNA sequencing data from 31 tumor types and normal tissue samples are divided into modules enriched for UC genes, MC genes, or mixed UC-MC modules. The greatest differences between tumor and normal tissue co-expression networks occur within mixed UC-MC modules. MC and UC genes not commonly co-expressed in normal tissues form distinct co-expression modules seen only in tumors. The degree of rewiring of genes within mixed UC-MC modules increases with tumor grade and stage. Mixed UC-MC modules are enriched for somatic mutations in cancer genes, particularly amplifications, suggesting an important driver of the rewiring observed in tumors is copy number changes.
CONCLUSIONS: Our study shows the greatest changes to gene co-expression patterns during tumor progression occur between genes of MC and UC origins, implicating the breakdown and rewiring of metazoan gene regulatory networks in cancer development and progression.},
}
MeSH Terms:
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*Gene Regulatory Networks
*Neoplasms/genetics
Humans
Animals
Gene Expression Regulation, Neoplastic
Evolution, Molecular
RevDate: 2024-06-11
CmpDate: 2024-06-11
Diversity of genome size and chromosome number in homothallic and heterothallic strains of the Closterium peracerosum-strigosum-littorale complex (Desmidiales, Zygnematophyceae, Streptophyta).
Journal of phycology, 60(3):654-667.
The evolutionary transitions of mating systems between outcrossing and self-fertilization are often suggested to associate with the cytological and genomic changes, but the empirical reports are limited in multicellular organisms. Here we used the unicellular zygnematophycean algae, the Closterium peracerosum-strigosum-littorale (C. psl.) complex, to address whether genomic properties such as genome sizes and chromosome numbers are associated with mating system transitions between homothallism (self-fertility) and heterothallism (self-sterility). Phylogenetic analysis revealed the polyphyly of homothallic strains, suggesting multiple transitions between homothallism and heterothallism in the C. psl. complex. Flow cytometry analysis identified a more than 2-fold genome size variation, ranging from 0.53 to 1.42 Gbp, which was positively correlated with chromosome number variation between strains. Although we did not find consistent trends in genome size change and mating system transitions, the mean chromosome sizes tend to be smaller in homothallic strains than in their relative heterothallic strains. This result suggests that homothallic strains possibly have more fragmented chromosomes, which is consistent with the argument that self-fertilizing populations may tolerate more chromosomal rearrangements.
Additional Links: PMID-38678594
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@article {pmid38678594,
year = {2024},
author = {Tsuchikane, Y and Watanabe, M and Kawaguchi, YW and Uehara, K and Nishiyama, T and Sekimoto, H and Tsuchimatsu, T},
title = {Diversity of genome size and chromosome number in homothallic and heterothallic strains of the Closterium peracerosum-strigosum-littorale complex (Desmidiales, Zygnematophyceae, Streptophyta).},
journal = {Journal of phycology},
volume = {60},
number = {3},
pages = {654-667},
doi = {10.1111/jpy.13457},
pmid = {38678594},
issn = {1529-8817},
support = {25304012//Japan Society for the Promotion of Science/ ; 26650147//Japan Society for the Promotion of Science/ ; 18K06367//Japan Society for the Promotion of Science/ ; 19K22446//Japan Society for the Promotion of Science/ ; 19K22448//Japan Society for the Promotion of Science/ ; 15H05237//Japan Society for the Promotion of Science/ ; 16H04836//Japan Society for the Promotion of Science/ ; 16K02518//Japan Society for the Promotion of Science/ ; 18K19365//Japan Society for the Promotion of Science/ ; 20K21451//Japan Society for the Promotion of Science/ ; 21H02549//Japan Society for the Promotion of Science/ ; 22H05177//Japan Society for the Promotion of Science/ ; 19K06827//Japan Society for the Promotion of Science/ ; 24K09588//Japan Society for the Promotion of Science/ ; 15K18583//Japan Society for the Promotion of Science/ ; 17K15165//Japan Society for the Promotion of Science/ ; 22K21352//Japan Society for the Promotion of Science/ ; },
mesh = {*Genome Size ; *Phylogeny ; Closterium/genetics ; },
abstract = {The evolutionary transitions of mating systems between outcrossing and self-fertilization are often suggested to associate with the cytological and genomic changes, but the empirical reports are limited in multicellular organisms. Here we used the unicellular zygnematophycean algae, the Closterium peracerosum-strigosum-littorale (C. psl.) complex, to address whether genomic properties such as genome sizes and chromosome numbers are associated with mating system transitions between homothallism (self-fertility) and heterothallism (self-sterility). Phylogenetic analysis revealed the polyphyly of homothallic strains, suggesting multiple transitions between homothallism and heterothallism in the C. psl. complex. Flow cytometry analysis identified a more than 2-fold genome size variation, ranging from 0.53 to 1.42 Gbp, which was positively correlated with chromosome number variation between strains. Although we did not find consistent trends in genome size change and mating system transitions, the mean chromosome sizes tend to be smaller in homothallic strains than in their relative heterothallic strains. This result suggests that homothallic strains possibly have more fragmented chromosomes, which is consistent with the argument that self-fertilizing populations may tolerate more chromosomal rearrangements.},
}
MeSH Terms:
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*Genome Size
*Phylogeny
Closterium/genetics
RevDate: 2024-06-13
CmpDate: 2024-06-13
Prenatal acetaminophen exposure and the developing ovary: Time, dose, and course consequences for fetal mice.
Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association, 189:114679.
Acetaminophen is an emerging endocrine disrupting chemical and has been detected in various natural matrices. Numerous studies have documented developmental toxicity associated with prenatal acetaminophen exposure (PAcE). In this study, we established a PAcE Kunming mouse model at different time (middle pregnancy and third trimester), doses (low, middle, high) and courses (single or multi-) to systematically investigate their effects on fetal ovarian development. The findings indicated PAcE affected ovarian development, reduced fetal ovarian oocyte number and inhibited cell proliferation. A reduction in mRNA expression was observed for genes associated with oocyte markers (NOBOX and Figlα), follicular development markers (BMP15 and GDF9), and pre-granulosa cell steroid synthase (SF1 and StAR). Notably, exposure in middle pregnancy, high dose, multi-course resulted in the most pronounced inhibition of oocyte development; exposure in third trimester, high dose and multi-course led to the most pronounced inhibition of follicular development; and in third trimester, low dose and single course, the inhibition of pre-granulosa cell function was most pronounced. Mechanistic investigations revealed that PAcE had the most pronounced suppression of the ovarian Notch signaling pathway. Overall, PAcE caused fetal ovarian multicellular toxicity and inhibited follicular development with time, dose and course differences.
Additional Links: PMID-38657942
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@article {pmid38657942,
year = {2024},
author = {Wu, T and Huang, J and Li, Y and Guo, Y and Wang, H and Zhang, Y},
title = {Prenatal acetaminophen exposure and the developing ovary: Time, dose, and course consequences for fetal mice.},
journal = {Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association},
volume = {189},
number = {},
pages = {114679},
doi = {10.1016/j.fct.2024.114679},
pmid = {38657942},
issn = {1873-6351},
mesh = {Female ; Animals ; Pregnancy ; Mice ; *Acetaminophen/toxicity ; *Ovary/drug effects/metabolism ; Dose-Response Relationship, Drug ; Oocytes/drug effects ; Prenatal Exposure Delayed Effects/chemically induced ; Bone Morphogenetic Protein 15/genetics ; Growth Differentiation Factor 9/genetics/metabolism ; Cell Proliferation/drug effects ; },
abstract = {Acetaminophen is an emerging endocrine disrupting chemical and has been detected in various natural matrices. Numerous studies have documented developmental toxicity associated with prenatal acetaminophen exposure (PAcE). In this study, we established a PAcE Kunming mouse model at different time (middle pregnancy and third trimester), doses (low, middle, high) and courses (single or multi-) to systematically investigate their effects on fetal ovarian development. The findings indicated PAcE affected ovarian development, reduced fetal ovarian oocyte number and inhibited cell proliferation. A reduction in mRNA expression was observed for genes associated with oocyte markers (NOBOX and Figlα), follicular development markers (BMP15 and GDF9), and pre-granulosa cell steroid synthase (SF1 and StAR). Notably, exposure in middle pregnancy, high dose, multi-course resulted in the most pronounced inhibition of oocyte development; exposure in third trimester, high dose and multi-course led to the most pronounced inhibition of follicular development; and in third trimester, low dose and single course, the inhibition of pre-granulosa cell function was most pronounced. Mechanistic investigations revealed that PAcE had the most pronounced suppression of the ovarian Notch signaling pathway. Overall, PAcE caused fetal ovarian multicellular toxicity and inhibited follicular development with time, dose and course differences.},
}
MeSH Terms:
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Female
Animals
Pregnancy
Mice
*Acetaminophen/toxicity
*Ovary/drug effects/metabolism
Dose-Response Relationship, Drug
Oocytes/drug effects
Prenatal Exposure Delayed Effects/chemically induced
Bone Morphogenetic Protein 15/genetics
Growth Differentiation Factor 9/genetics/metabolism
Cell Proliferation/drug effects
RevDate: 2024-04-25
CmpDate: 2024-04-24
[Evolution of cancer resistance in the animal kingdom].
Medecine sciences : M/S, 40(4):343-350.
Cancer is an inevitable collateral problem inherent in the evolution of multicellular organisms, which appeared at the end of the Precambrian. Faced to this constraint, a range of diverse anticancer defenses has evolved across the animal kingdom. Today, investigating how animal organisms, especially those of large size and long lifespan, manage cancer-related issues has both fundamental and applied outcomes, as it could inspire strategies for preventing or treating human cancers. In this article, we begin by presenting the conceptual framework for understanding evolutionary theories regarding the development of anti-cancer defenses. We then present a number of examples that have been extensively studied in recent years, including naked mole rats, elephants, whales, placozoa, xenarthras (such as sloths, armadillos and anteaters) and bats. The contributions of comparative genomics to understanding evolutionary convergences are also discussed. Finally, we emphasize that natural selection has also favored anti-cancer adaptations aimed at avoiding mutagenic environments, for example by maximizing immediate reproductive efforts in the event of cancer. Exploring these adaptive solutions holds promise for identifying novel approaches to improve human health.
Additional Links: PMID-38651959
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@article {pmid38651959,
year = {2024},
author = {Thomas, F and Ujvari, B and Dujon, AM},
title = {[Evolution of cancer resistance in the animal kingdom].},
journal = {Medecine sciences : M/S},
volume = {40},
number = {4},
pages = {343-350},
doi = {10.1051/medsci/2024038},
pmid = {38651959},
issn = {1958-5381},
mesh = {Animals ; *Neoplasms/genetics/pathology ; Humans ; *Biological Evolution ; Disease Resistance/genetics/physiology ; Selection, Genetic ; Mole Rats/physiology/genetics ; Elephants/genetics ; },
abstract = {Cancer is an inevitable collateral problem inherent in the evolution of multicellular organisms, which appeared at the end of the Precambrian. Faced to this constraint, a range of diverse anticancer defenses has evolved across the animal kingdom. Today, investigating how animal organisms, especially those of large size and long lifespan, manage cancer-related issues has both fundamental and applied outcomes, as it could inspire strategies for preventing or treating human cancers. In this article, we begin by presenting the conceptual framework for understanding evolutionary theories regarding the development of anti-cancer defenses. We then present a number of examples that have been extensively studied in recent years, including naked mole rats, elephants, whales, placozoa, xenarthras (such as sloths, armadillos and anteaters) and bats. The contributions of comparative genomics to understanding evolutionary convergences are also discussed. Finally, we emphasize that natural selection has also favored anti-cancer adaptations aimed at avoiding mutagenic environments, for example by maximizing immediate reproductive efforts in the event of cancer. Exploring these adaptive solutions holds promise for identifying novel approaches to improve human health.},
}
MeSH Terms:
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Animals
*Neoplasms/genetics/pathology
Humans
*Biological Evolution
Disease Resistance/genetics/physiology
Selection, Genetic
Mole Rats/physiology/genetics
Elephants/genetics
RevDate: 2024-05-31
CmpDate: 2024-05-27
Critically assessing atavism, an evolution-centered and deterministic hypothesis on cancer.
BioEssays : news and reviews in molecular, cellular and developmental biology, 46(6):e2300221.
Cancer is most commonly viewed as resulting from somatic mutations enhancing proliferation and invasion. Some hypotheses further propose that these new capacities reveal a breakdown of multicellularity allowing cancer cells to escape proliferation and cooperation control mechanisms that were implemented during evolution of multicellularity. Here we critically review one such hypothesis, named "atavism," which puts forward the idea that cancer results from the re-expression of normally repressed genes forming a program, or toolbox, inherited from unicellular or simple multicellular ancestors. This hypothesis places cancer in an interesting evolutionary perspective that has not been widely explored and deserves attention. Thinking about cancer within an evolutionary framework, especially the major transitions to multicellularity, offers particularly promising perspectives. It is therefore of the utmost important to analyze why one approach that tries to achieve this aim, the atavism hypothesis, has not so far emerged as a major theory on cancer. We outline the features of the atavism hypothesis that, would benefit from clarification and, if possible, unification.
Additional Links: PMID-38644621
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@article {pmid38644621,
year = {2024},
author = {Daignan-Fornier, B and Pradeu, T},
title = {Critically assessing atavism, an evolution-centered and deterministic hypothesis on cancer.},
journal = {BioEssays : news and reviews in molecular, cellular and developmental biology},
volume = {46},
number = {6},
pages = {e2300221},
doi = {10.1002/bies.202300221},
pmid = {38644621},
issn = {1521-1878},
support = {//NewMoon research program of the University of Bordeaux/ ; GBMF9021//Gordon and Betty Moore Foundation/ ; },
mesh = {*Neoplasms/genetics/pathology ; Humans ; Animals ; Biological Evolution ; Mutation ; Cell Proliferation/genetics ; },
abstract = {Cancer is most commonly viewed as resulting from somatic mutations enhancing proliferation and invasion. Some hypotheses further propose that these new capacities reveal a breakdown of multicellularity allowing cancer cells to escape proliferation and cooperation control mechanisms that were implemented during evolution of multicellularity. Here we critically review one such hypothesis, named "atavism," which puts forward the idea that cancer results from the re-expression of normally repressed genes forming a program, or toolbox, inherited from unicellular or simple multicellular ancestors. This hypothesis places cancer in an interesting evolutionary perspective that has not been widely explored and deserves attention. Thinking about cancer within an evolutionary framework, especially the major transitions to multicellularity, offers particularly promising perspectives. It is therefore of the utmost important to analyze why one approach that tries to achieve this aim, the atavism hypothesis, has not so far emerged as a major theory on cancer. We outline the features of the atavism hypothesis that, would benefit from clarification and, if possible, unification.},
}
MeSH Terms:
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*Neoplasms/genetics/pathology
Humans
Animals
Biological Evolution
Mutation
Cell Proliferation/genetics
RevDate: 2024-04-25
CmpDate: 2024-04-12
Fossil-calibrated molecular clock data enable reconstruction of steps leading to differentiated multicellularity and anisogamy in the Volvocine algae.
BMC biology, 22(1):79.
BACKGROUND: Throughout its nearly four-billion-year history, life has undergone evolutionary transitions in which simpler subunits have become integrated to form a more complex whole. Many of these transitions opened the door to innovations that resulted in increased biodiversity and/or organismal efficiency. The evolution of multicellularity from unicellular forms represents one such transition, one that paved the way for cellular differentiation, including differentiation of male and female gametes. A useful model for studying the evolution of multicellularity and cellular differentiation is the volvocine algae, a clade of freshwater green algae whose members range from unicellular to colonial, from undifferentiated to completely differentiated, and whose gamete types can be isogamous, anisogamous, or oogamous. To better understand how multicellularity, differentiation, and gametes evolved in this group, we used comparative genomics and fossil data to establish a geologically calibrated roadmap of when these innovations occurred.
RESULTS: Our ancestral-state reconstructions, show that multicellularity arose independently twice in the volvocine algae. Our chronograms indicate multicellularity evolved during the Carboniferous-Triassic periods in Goniaceae + Volvocaceae, and possibly as early as the Cretaceous in Tetrabaenaceae. Using divergence time estimates we inferred when, and in what order, specific developmental changes occurred that led to differentiated multicellularity and oogamy. We find that in the volvocine algae the temporal sequence of developmental changes leading to differentiated multicellularity is much as proposed by David Kirk, and that multicellularity is correlated with the acquisition of anisogamy and oogamy. Lastly, morphological, molecular, and divergence time data suggest the possibility of cryptic species in Tetrabaenaceae.
CONCLUSIONS: Large molecular datasets and robust phylogenetic methods are bringing the evolutionary history of the volvocine algae more sharply into focus. Mounting evidence suggests that extant species in this group are the result of two independent origins of multicellularity and multiple independent origins of cell differentiation. Also, the origin of the Tetrabaenaceae-Goniaceae-Volvocaceae clade may be much older than previously thought. Finally, the possibility of cryptic species in the Tetrabaenaceae provides an exciting opportunity to study the recent divergence of lineages adapted to live in very different thermal environments.
Additional Links: PMID-38600528
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@article {pmid38600528,
year = {2024},
author = {Lindsey, CR and Knoll, AH and Herron, MD and Rosenzweig, F},
title = {Fossil-calibrated molecular clock data enable reconstruction of steps leading to differentiated multicellularity and anisogamy in the Volvocine algae.},
journal = {BMC biology},
volume = {22},
number = {1},
pages = {79},
pmid = {38600528},
issn = {1741-7007},
support = {80NSSC20K0621//Ames Research Center/ ; 80NSSC23K1357//Ames Research Center/ ; OAC-1828187//National Science Foundation/ ; },
mesh = {Phylogeny ; Biological Evolution ; *Volvox/genetics ; Fossils ; Plants ; *Chlorophyceae ; Cell Differentiation ; },
abstract = {BACKGROUND: Throughout its nearly four-billion-year history, life has undergone evolutionary transitions in which simpler subunits have become integrated to form a more complex whole. Many of these transitions opened the door to innovations that resulted in increased biodiversity and/or organismal efficiency. The evolution of multicellularity from unicellular forms represents one such transition, one that paved the way for cellular differentiation, including differentiation of male and female gametes. A useful model for studying the evolution of multicellularity and cellular differentiation is the volvocine algae, a clade of freshwater green algae whose members range from unicellular to colonial, from undifferentiated to completely differentiated, and whose gamete types can be isogamous, anisogamous, or oogamous. To better understand how multicellularity, differentiation, and gametes evolved in this group, we used comparative genomics and fossil data to establish a geologically calibrated roadmap of when these innovations occurred.
RESULTS: Our ancestral-state reconstructions, show that multicellularity arose independently twice in the volvocine algae. Our chronograms indicate multicellularity evolved during the Carboniferous-Triassic periods in Goniaceae + Volvocaceae, and possibly as early as the Cretaceous in Tetrabaenaceae. Using divergence time estimates we inferred when, and in what order, specific developmental changes occurred that led to differentiated multicellularity and oogamy. We find that in the volvocine algae the temporal sequence of developmental changes leading to differentiated multicellularity is much as proposed by David Kirk, and that multicellularity is correlated with the acquisition of anisogamy and oogamy. Lastly, morphological, molecular, and divergence time data suggest the possibility of cryptic species in Tetrabaenaceae.
CONCLUSIONS: Large molecular datasets and robust phylogenetic methods are bringing the evolutionary history of the volvocine algae more sharply into focus. Mounting evidence suggests that extant species in this group are the result of two independent origins of multicellularity and multiple independent origins of cell differentiation. Also, the origin of the Tetrabaenaceae-Goniaceae-Volvocaceae clade may be much older than previously thought. Finally, the possibility of cryptic species in the Tetrabaenaceae provides an exciting opportunity to study the recent divergence of lineages adapted to live in very different thermal environments.},
}
MeSH Terms:
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Phylogeny
Biological Evolution
*Volvox/genetics
Fossils
Plants
*Chlorophyceae
Cell Differentiation
RevDate: 2024-05-11
CmpDate: 2024-05-09
High-resolution comparative atomic structures of two Giardiavirus prototypes infecting G. duodenalis parasite.
PLoS pathogens, 20(4):e1012140.
The Giardia lamblia virus (GLV) is a non-enveloped icosahedral dsRNA and endosymbiont virus that infects the zoonotic protozoan parasite Giardia duodenalis (syn. G. lamblia, G. intestinalis), which is a pathogen of mammals, including humans. Elucidating the transmission mechanism of GLV is crucial for gaining an in-depth understanding of the virulence of the virus in G. duodenalis. GLV belongs to the family Totiviridae, which infects yeast and protozoa intracellularly; however, it also transmits extracellularly, similar to the phylogenetically, distantly related toti-like viruses that infect multicellular hosts. The GLV capsid structure is extensively involved in the longstanding discussion concerning extracellular transmission in Totiviridae and toti-like viruses. Hence, this study constructed the first high-resolution comparative atomic models of two GLV strains, namely GLV-HP and GLV-CAT, which showed different intracellular localization and virulence phenotypes, using cryogenic electron microscopy single-particle analysis. The atomic models of the GLV capsids presented swapped C-terminal extensions, extra surface loops, and a lack of cap-snatching pockets, similar to those of toti-like viruses. However, their open pores and absence of the extra crown protein resemble those of other yeast and protozoan Totiviridae viruses, demonstrating the essential structures for extracellular cell-to-cell transmission. The structural comparison between GLV-HP and GLV-CAT indicates the first evidence of critical structural motifs for the transmission and virulence of GLV in G. duodenalis.
Additional Links: PMID-38598600
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@article {pmid38598600,
year = {2024},
author = {Wang, H and Marucci, G and Munke, A and Hassan, MM and Lalle, M and Okamoto, K},
title = {High-resolution comparative atomic structures of two Giardiavirus prototypes infecting G. duodenalis parasite.},
journal = {PLoS pathogens},
volume = {20},
number = {4},
pages = {e1012140},
pmid = {38598600},
issn = {1553-7374},
mesh = {*Giardia lamblia/ultrastructure/pathogenicity ; *Giardiavirus/genetics ; Cryoelectron Microscopy ; Animals ; Capsid/ultrastructure/metabolism ; Humans ; Phylogeny ; },
abstract = {The Giardia lamblia virus (GLV) is a non-enveloped icosahedral dsRNA and endosymbiont virus that infects the zoonotic protozoan parasite Giardia duodenalis (syn. G. lamblia, G. intestinalis), which is a pathogen of mammals, including humans. Elucidating the transmission mechanism of GLV is crucial for gaining an in-depth understanding of the virulence of the virus in G. duodenalis. GLV belongs to the family Totiviridae, which infects yeast and protozoa intracellularly; however, it also transmits extracellularly, similar to the phylogenetically, distantly related toti-like viruses that infect multicellular hosts. The GLV capsid structure is extensively involved in the longstanding discussion concerning extracellular transmission in Totiviridae and toti-like viruses. Hence, this study constructed the first high-resolution comparative atomic models of two GLV strains, namely GLV-HP and GLV-CAT, which showed different intracellular localization and virulence phenotypes, using cryogenic electron microscopy single-particle analysis. The atomic models of the GLV capsids presented swapped C-terminal extensions, extra surface loops, and a lack of cap-snatching pockets, similar to those of toti-like viruses. However, their open pores and absence of the extra crown protein resemble those of other yeast and protozoan Totiviridae viruses, demonstrating the essential structures for extracellular cell-to-cell transmission. The structural comparison between GLV-HP and GLV-CAT indicates the first evidence of critical structural motifs for the transmission and virulence of GLV in G. duodenalis.},
}
MeSH Terms:
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*Giardia lamblia/ultrastructure/pathogenicity
*Giardiavirus/genetics
Cryoelectron Microscopy
Animals
Capsid/ultrastructure/metabolism
Humans
Phylogeny
RevDate: 2024-04-09
CmpDate: 2024-04-08
Single-cell RNA sequencing explores the evolution of the ecosystem from leukoplakia to head and neck squamous cell carcinoma.
Scientific reports, 14(1):8097.
It has been found that progression from leukoplakia to head and neck squamous cell carcinoma (HNSCC) is a long-term process that may involve changes in the multicellular ecosystem. We acquired scRNA-seq samples information from gene expression omnibus and UCSC Xena database. The BEAM function was used to construct the pseudotime trajectory and analyze the differentially expressed genes in different branches. We used the ssGSEA method to explore the correlation between each cell subgroup and survival time, and obtained the cell subgroup related to prognosis. During the progression from leukoplakia to HNSCC, we found several prognostic cell subgroups, such as AURKB + epithelial cells, SFRP1 + fibroblasts, SLC7A8 + macrophages, FCER1A + CD1C + dendritic cells, and TRGC2 + NK/T cells. All cell subgroups had two different fates, one tending to cell proliferation, migration, and enhancement of angiogenesis capacity, and the other tending to inflammatory immune response, leukocyte chemotaxis, and T cell activation. Tumor-promoting genes such as CD163 and CD209 were highly expressed in the myeloid cells, and depletion marker genes such as TIGIT, LAG3 were highly expressed in NK/T cells. Our study may provide a reference for the molecular mechanism of HNSCC and theoretical basis for the development of new therapeutic strategies.
Additional Links: PMID-38582791
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@article {pmid38582791,
year = {2024},
author = {Wang, H and Guan, Z and Zheng, L},
title = {Single-cell RNA sequencing explores the evolution of the ecosystem from leukoplakia to head and neck squamous cell carcinoma.},
journal = {Scientific reports},
volume = {14},
number = {1},
pages = {8097},
pmid = {38582791},
issn = {2045-2322},
support = {SBGJ202102175//the Henan Provincial Medical Science and Technology Research Plan/ ; },
mesh = {Humans ; Squamous Cell Carcinoma of Head and Neck/genetics ; *Ecosystem ; Leukoplakia ; *Head and Neck Neoplasms/genetics ; Sequence Analysis, RNA ; Prognosis ; Tumor Microenvironment/genetics ; },
abstract = {It has been found that progression from leukoplakia to head and neck squamous cell carcinoma (HNSCC) is a long-term process that may involve changes in the multicellular ecosystem. We acquired scRNA-seq samples information from gene expression omnibus and UCSC Xena database. The BEAM function was used to construct the pseudotime trajectory and analyze the differentially expressed genes in different branches. We used the ssGSEA method to explore the correlation between each cell subgroup and survival time, and obtained the cell subgroup related to prognosis. During the progression from leukoplakia to HNSCC, we found several prognostic cell subgroups, such as AURKB + epithelial cells, SFRP1 + fibroblasts, SLC7A8 + macrophages, FCER1A + CD1C + dendritic cells, and TRGC2 + NK/T cells. All cell subgroups had two different fates, one tending to cell proliferation, migration, and enhancement of angiogenesis capacity, and the other tending to inflammatory immune response, leukocyte chemotaxis, and T cell activation. Tumor-promoting genes such as CD163 and CD209 were highly expressed in the myeloid cells, and depletion marker genes such as TIGIT, LAG3 were highly expressed in NK/T cells. Our study may provide a reference for the molecular mechanism of HNSCC and theoretical basis for the development of new therapeutic strategies.},
}
MeSH Terms:
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Humans
Squamous Cell Carcinoma of Head and Neck/genetics
*Ecosystem
Leukoplakia
*Head and Neck Neoplasms/genetics
Sequence Analysis, RNA
Prognosis
Tumor Microenvironment/genetics
RevDate: 2024-04-26
CmpDate: 2024-04-19
Multicellular ecotypes shape progression of lung adenocarcinoma from ground-glass opacity toward advanced stages.
Cell reports. Medicine, 5(4):101489.
Lung adenocarcinoma is a type of cancer that exhibits a wide range of clinical radiological manifestations, from ground-glass opacity (GGO) to pure solid nodules, which vary greatly in terms of their biological characteristics. Our current understanding of this heterogeneity is limited. To address this gap, we analyze 58 lung adenocarcinoma patients via machine learning, single-cell RNA sequencing (scRNA-seq), and whole-exome sequencing, and we identify six lung multicellular ecotypes (LMEs) correlating with distinct radiological patterns and cancer cell states. Notably, GGO-associated neoantigens in early-stage cancers are recognized by CD8[+] T cells, indicating an immune-active environment, while solid nodules feature an immune-suppressive LME with exhausted CD8[+] T cells, driven by specific stromal cells such as CTHCR1[+] fibroblasts. This study also highlights EGFR(L858R) neoantigens in GGO samples, suggesting potential CD8[+] T cell activation. Our findings offer valuable insights into lung adenocarcinoma heterogeneity, suggesting avenues for targeted therapies in early-stage disease.
Additional Links: PMID-38554705
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Citation:
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@article {pmid38554705,
year = {2024},
author = {Deng, Y and Xia, L and Zhang, J and Deng, S and Wang, M and Wei, S and Li, K and Lai, H and Yang, Y and Bai, Y and Liu, Y and Luo, L and Yang, Z and Chen, Y and Kang, R and Gan, F and Pu, Q and Mei, J and Ma, L and Lin, F and Guo, C and Liao, H and Zhu, Y and Liu, Z and Liu, C and Hu, Y and Yuan, Y and Zha, Z and Yuan, G and Zhang, G and Chen, L and Cheng, Q and Shen, S and Liu, L},
title = {Multicellular ecotypes shape progression of lung adenocarcinoma from ground-glass opacity toward advanced stages.},
journal = {Cell reports. Medicine},
volume = {5},
number = {4},
pages = {101489},
pmid = {38554705},
issn = {2666-3791},
mesh = {Humans ; *Lung Neoplasms/genetics ; *Adenocarcinoma/genetics/pathology ; CD8-Positive T-Lymphocytes/pathology ; Ecotype ; Retrospective Studies ; *Adenocarcinoma of Lung ; },
abstract = {Lung adenocarcinoma is a type of cancer that exhibits a wide range of clinical radiological manifestations, from ground-glass opacity (GGO) to pure solid nodules, which vary greatly in terms of their biological characteristics. Our current understanding of this heterogeneity is limited. To address this gap, we analyze 58 lung adenocarcinoma patients via machine learning, single-cell RNA sequencing (scRNA-seq), and whole-exome sequencing, and we identify six lung multicellular ecotypes (LMEs) correlating with distinct radiological patterns and cancer cell states. Notably, GGO-associated neoantigens in early-stage cancers are recognized by CD8[+] T cells, indicating an immune-active environment, while solid nodules feature an immune-suppressive LME with exhausted CD8[+] T cells, driven by specific stromal cells such as CTHCR1[+] fibroblasts. This study also highlights EGFR(L858R) neoantigens in GGO samples, suggesting potential CD8[+] T cell activation. Our findings offer valuable insights into lung adenocarcinoma heterogeneity, suggesting avenues for targeted therapies in early-stage disease.},
}
MeSH Terms:
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Humans
*Lung Neoplasms/genetics
*Adenocarcinoma/genetics/pathology
CD8-Positive T-Lymphocytes/pathology
Ecotype
Retrospective Studies
*Adenocarcinoma of Lung
RevDate: 2024-04-09
CmpDate: 2024-04-09
Functional characterization of serine proteinase inhibitor Kazal-Type in the red claw crayfish Cherax quadricarinatus.
Fish & shellfish immunology, 148:109525.
Serine protease inhibitors Kazal type (SPINKs) function in physiological and immunological processes across multicellular organisms. In the present study, we identified a SPINK gene, designated as CqSPINK, in the red claw crayfish Cherax quadricarinatus, which is the ortholog of human SPINK5. The deduced CqSPINK contains two Kazal domains consisting of 45 amino acid residues with a typical signature motif C-X3-C-X5-PVCG-X5-Y-X3-C-X6-C-X12-14-C. Each Kazal domain contains six conserved cysteine residues forming three pairs of disulfide bonds, segmenting the structure into three rings. Phylogenetic analysis revealed CqSPINK as a homolog of human SPINK5. CqSPINK expression was detected exclusively in hepatopancreas and epithelium, with rapid up-regulation in hepatopancreas upon Vibrio parahaemolyticus E1 challenge. Recombinant CqSPINK protein (rCqSPINK) was heterologously expressed in Escherichia coli and purified for further study. Proteinase inhibition assays demonstrated that rCqSPINK could potently inhibit proteinase K and subtilisin A, weakly inhibit α-chymotrypsin and elastase, but extremely weak inhibit trypsin. Furthermore, CqSPINK inhibited bacterial secretory proteinase activity from Bacillus subtilis, E. coli, and Staphylococcus aureus, and inhibited B. subtilis growth. These findings suggest CqSPINK's involvement in antibacterial immunity through direct inhibition of bacterial proteases, contributing to resistance against pathogen invasion.
Additional Links: PMID-38537926
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@article {pmid38537926,
year = {2024},
author = {Shao, S and Liu, K and Du, J and Yin, C and Wang, M and Wang, Y},
title = {Functional characterization of serine proteinase inhibitor Kazal-Type in the red claw crayfish Cherax quadricarinatus.},
journal = {Fish & shellfish immunology},
volume = {148},
number = {},
pages = {109525},
doi = {10.1016/j.fsi.2024.109525},
pmid = {38537926},
issn = {1095-9947},
mesh = {Humans ; Animals ; *Serine Proteinase Inhibitors/genetics/chemistry ; *Astacoidea ; Phylogeny ; Escherichia coli ; Recombinant Proteins/genetics ; Bacteria/metabolism ; },
abstract = {Serine protease inhibitors Kazal type (SPINKs) function in physiological and immunological processes across multicellular organisms. In the present study, we identified a SPINK gene, designated as CqSPINK, in the red claw crayfish Cherax quadricarinatus, which is the ortholog of human SPINK5. The deduced CqSPINK contains two Kazal domains consisting of 45 amino acid residues with a typical signature motif C-X3-C-X5-PVCG-X5-Y-X3-C-X6-C-X12-14-C. Each Kazal domain contains six conserved cysteine residues forming three pairs of disulfide bonds, segmenting the structure into three rings. Phylogenetic analysis revealed CqSPINK as a homolog of human SPINK5. CqSPINK expression was detected exclusively in hepatopancreas and epithelium, with rapid up-regulation in hepatopancreas upon Vibrio parahaemolyticus E1 challenge. Recombinant CqSPINK protein (rCqSPINK) was heterologously expressed in Escherichia coli and purified for further study. Proteinase inhibition assays demonstrated that rCqSPINK could potently inhibit proteinase K and subtilisin A, weakly inhibit α-chymotrypsin and elastase, but extremely weak inhibit trypsin. Furthermore, CqSPINK inhibited bacterial secretory proteinase activity from Bacillus subtilis, E. coli, and Staphylococcus aureus, and inhibited B. subtilis growth. These findings suggest CqSPINK's involvement in antibacterial immunity through direct inhibition of bacterial proteases, contributing to resistance against pathogen invasion.},
}
MeSH Terms:
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Humans
Animals
*Serine Proteinase Inhibitors/genetics/chemistry
*Astacoidea
Phylogeny
Escherichia coli
Recombinant Proteins/genetics
Bacteria/metabolism
RevDate: 2024-03-29
CmpDate: 2024-03-25
The Hippo kinase cascade regulates a contractile cell behavior and cell density in a close unicellular relative of animals.
eLife, 12:.
The genomes of close unicellular relatives of animals encode orthologs of many genes that regulate animal development. However, little is known about the function of such genes in unicellular organisms or the evolutionary process by which these genes came to function in multicellular development. The Hippo pathway, which regulates cell proliferation and tissue size in animals, is present in some of the closest unicellular relatives of animals, including the amoeboid organism Capsaspora owczarzaki. We previously showed that the Capsaspora ortholog of the Hippo pathway nuclear effector Yorkie/YAP/TAZ (coYki) regulates actin dynamics and the three-dimensional morphology of Capsaspora cell aggregates, but is dispensable for cell proliferation control (Phillips et al., 2022). However, the function of upstream Hippo pathway components, and whether and how they regulate coYki in Capsaspora, remained unknown. Here, we analyze the function of the upstream Hippo pathway kinases coHpo and coWts in Capsaspora by generating mutant lines for each gene. Loss of either kinase results in increased nuclear localization of coYki, indicating an ancient, premetazoan origin of this Hippo pathway regulatory mechanism. Strikingly, we find that loss of either kinase causes a contractile cell behavior and increased density of cell packing within Capsaspora aggregates. We further show that this increased cell density is not due to differences in proliferation, but rather actomyosin-dependent changes in the multicellular architecture of aggregates. Given its well-established role in cell density-regulated proliferation in animals, the increased density of cell packing in coHpo and coWts mutants suggests a shared and possibly ancient and conserved function of the Hippo pathway in cell density control. Together, these results implicate cytoskeletal regulation but not proliferation as an ancestral function of the Hippo pathway kinase cascade and uncover a novel role for Hippo signaling in regulating cell density in a proliferation-independent manner.
Additional Links: PMID-38517944
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@article {pmid38517944,
year = {2024},
author = {Phillips, JE and Pan, D},
title = {The Hippo kinase cascade regulates a contractile cell behavior and cell density in a close unicellular relative of animals.},
journal = {eLife},
volume = {12},
number = {},
pages = {},
pmid = {38517944},
issn = {2050-084X},
support = {R01 EY015708/EY/NEI NIH HHS/United States ; EY015708/EY/NEI NIH HHS/United States ; },
mesh = {Animals ; *Signal Transduction/genetics ; *Protein Serine-Threonine Kinases/genetics/metabolism ; Hippo Signaling Pathway ; Biological Evolution ; Cell Proliferation ; },
abstract = {The genomes of close unicellular relatives of animals encode orthologs of many genes that regulate animal development. However, little is known about the function of such genes in unicellular organisms or the evolutionary process by which these genes came to function in multicellular development. The Hippo pathway, which regulates cell proliferation and tissue size in animals, is present in some of the closest unicellular relatives of animals, including the amoeboid organism Capsaspora owczarzaki. We previously showed that the Capsaspora ortholog of the Hippo pathway nuclear effector Yorkie/YAP/TAZ (coYki) regulates actin dynamics and the three-dimensional morphology of Capsaspora cell aggregates, but is dispensable for cell proliferation control (Phillips et al., 2022). However, the function of upstream Hippo pathway components, and whether and how they regulate coYki in Capsaspora, remained unknown. Here, we analyze the function of the upstream Hippo pathway kinases coHpo and coWts in Capsaspora by generating mutant lines for each gene. Loss of either kinase results in increased nuclear localization of coYki, indicating an ancient, premetazoan origin of this Hippo pathway regulatory mechanism. Strikingly, we find that loss of either kinase causes a contractile cell behavior and increased density of cell packing within Capsaspora aggregates. We further show that this increased cell density is not due to differences in proliferation, but rather actomyosin-dependent changes in the multicellular architecture of aggregates. Given its well-established role in cell density-regulated proliferation in animals, the increased density of cell packing in coHpo and coWts mutants suggests a shared and possibly ancient and conserved function of the Hippo pathway in cell density control. Together, these results implicate cytoskeletal regulation but not proliferation as an ancestral function of the Hippo pathway kinase cascade and uncover a novel role for Hippo signaling in regulating cell density in a proliferation-independent manner.},
}
MeSH Terms:
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Animals
*Signal Transduction/genetics
*Protein Serine-Threonine Kinases/genetics/metabolism
Hippo Signaling Pathway
Biological Evolution
Cell Proliferation
RevDate: 2024-07-09
CmpDate: 2024-05-07
Characterization of the Pristionchus pacificus "epigenetic toolkit" reveals the evolutionary loss of the histone methyltransferase complex PRC2.
Genetics, 227(1):.
Comparative approaches have revealed both divergent and convergent paths to achieving shared developmental outcomes. Thus, only through assembling multiple case studies can we understand biological principles. Yet, despite appreciating the conservation-or lack thereof-of developmental networks, the conservation of epigenetic mechanisms regulating these networks is poorly understood. The nematode Pristionchus pacificus has emerged as a model system of plasticity and epigenetic regulation as it exhibits a bacterivorous or omnivorous morph depending on its environment. Here, we determined the "epigenetic toolkit" available to P. pacificus as a resource for future functional work on plasticity, and as a comparison with Caenorhabditis elegans to investigate the conservation of epigenetic mechanisms. Broadly, we observed a similar cast of genes with putative epigenetic function between C. elegans and P. pacificus. However, we also found striking differences. Most notably, the histone methyltransferase complex PRC2 appears to be missing in P. pacificus. We described the deletion/pseudogenization of the PRC2 genes mes-2 and mes-6 and concluded that both were lost in the last common ancestor of P. pacificus and a related species P. arcanus. Interestingly, we observed the enzymatic product of PRC2 (H3K27me3) by mass spectrometry and immunofluorescence, suggesting that a currently unknown methyltransferase has been co-opted for heterochromatin silencing. Altogether, we have provided an inventory of epigenetic genes in P. pacificus to compare with C. elegans. This inventory will enable reverse-genetic experiments related to plasticity and has revealed the first loss of PRC2 in a multicellular organism.
Additional Links: PMID-38513719
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@article {pmid38513719,
year = {2024},
author = {Brown, AL and Meiborg, AB and Franz-Wachtel, M and Macek, B and Gordon, S and Rog, O and Weadick, CJ and Werner, MS},
title = {Characterization of the Pristionchus pacificus "epigenetic toolkit" reveals the evolutionary loss of the histone methyltransferase complex PRC2.},
journal = {Genetics},
volume = {227},
number = {1},
pages = {},
pmid = {38513719},
issn = {1943-2631},
support = {R35GM150720/GM/NIGMS NIH HHS/United States ; R35 GM128804/GM/NIGMS NIH HHS/United States ; T32-GM122740/GF/NIH HHS/United States ; R35 GM150720/GM/NIGMS NIH HHS/United States ; T32 GM122740/GM/NIGMS NIH HHS/United States ; },
mesh = {Animals ; *Epigenesis, Genetic ; *Evolution, Molecular ; *Caenorhabditis elegans/genetics ; Polycomb Repressive Complex 2/genetics/metabolism ; Histone Methyltransferases/metabolism/genetics ; Nematoda/genetics ; Helminth Proteins/genetics/metabolism ; },
abstract = {Comparative approaches have revealed both divergent and convergent paths to achieving shared developmental outcomes. Thus, only through assembling multiple case studies can we understand biological principles. Yet, despite appreciating the conservation-or lack thereof-of developmental networks, the conservation of epigenetic mechanisms regulating these networks is poorly understood. The nematode Pristionchus pacificus has emerged as a model system of plasticity and epigenetic regulation as it exhibits a bacterivorous or omnivorous morph depending on its environment. Here, we determined the "epigenetic toolkit" available to P. pacificus as a resource for future functional work on plasticity, and as a comparison with Caenorhabditis elegans to investigate the conservation of epigenetic mechanisms. Broadly, we observed a similar cast of genes with putative epigenetic function between C. elegans and P. pacificus. However, we also found striking differences. Most notably, the histone methyltransferase complex PRC2 appears to be missing in P. pacificus. We described the deletion/pseudogenization of the PRC2 genes mes-2 and mes-6 and concluded that both were lost in the last common ancestor of P. pacificus and a related species P. arcanus. Interestingly, we observed the enzymatic product of PRC2 (H3K27me3) by mass spectrometry and immunofluorescence, suggesting that a currently unknown methyltransferase has been co-opted for heterochromatin silencing. Altogether, we have provided an inventory of epigenetic genes in P. pacificus to compare with C. elegans. This inventory will enable reverse-genetic experiments related to plasticity and has revealed the first loss of PRC2 in a multicellular organism.},
}
MeSH Terms:
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hide MeSH Terms
Animals
*Epigenesis, Genetic
*Evolution, Molecular
*Caenorhabditis elegans/genetics
Polycomb Repressive Complex 2/genetics/metabolism
Histone Methyltransferases/metabolism/genetics
Nematoda/genetics
Helminth Proteins/genetics/metabolism
RevDate: 2024-03-19
CmpDate: 2024-03-18
Rapid evolution of an adaptive multicellular morphology of Candida auris during systemic infection.
Nature communications, 15(1):2381.
Candida auris has become a serious threat to public health. The mechanisms of how this fungal pathogen adapts to the mammalian host are poorly understood. Here we report the rapid evolution of an adaptive C. auris multicellular aggregative morphology in the murine host during systemic infection. C. auris aggregative cells accumulate in the brain and exhibit obvious advantages over the single-celled yeast-form cells during systemic infection. Genetic mutations, specifically de novo point mutations in genes associated with cell division or budding processes, underlie the rapid evolution of this aggregative phenotype. Most mutated C. auris genes are associated with the regulation of cell wall integrity, cytokinesis, cytoskeletal properties, and cellular polarization. Moreover, the multicellular aggregates are notably more recalcitrant to the host antimicrobial peptides LL-37 and PACAP relative to the single-celled yeast-form cells. Overall, to survive in the host, C. auris can rapidly evolve a multicellular aggregative morphology via genetic mutations.
Additional Links: PMID-38493178
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@article {pmid38493178,
year = {2024},
author = {Bing, J and Guan, Z and Zheng, T and Ennis, CL and Nobile, CJ and Chen, C and Chu, H and Huang, G},
title = {Rapid evolution of an adaptive multicellular morphology of Candida auris during systemic infection.},
journal = {Nature communications},
volume = {15},
number = {1},
pages = {2381},
pmid = {38493178},
issn = {2041-1723},
support = {31930005 and 82272359//National Natural Science Foundation of China (National Science Foundation of China)/ ; 32170193 and 32000018//National Natural Science Foundation of China (National Science Foundation of China)/ ; 32170193 and 32000018//National Natural Science Foundation of China (National Science Foundation of China)/ ; R35GM124594//U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (NIGMS)/ ; },
mesh = {Animals ; Mice ; Candida/genetics ; *Candidiasis/microbiology ; Candida auris ; Saccharomyces cerevisiae ; Phenotype ; *Sepsis ; Antifungal Agents ; Microbial Sensitivity Tests ; Mammals ; },
abstract = {Candida auris has become a serious threat to public health. The mechanisms of how this fungal pathogen adapts to the mammalian host are poorly understood. Here we report the rapid evolution of an adaptive C. auris multicellular aggregative morphology in the murine host during systemic infection. C. auris aggregative cells accumulate in the brain and exhibit obvious advantages over the single-celled yeast-form cells during systemic infection. Genetic mutations, specifically de novo point mutations in genes associated with cell division or budding processes, underlie the rapid evolution of this aggregative phenotype. Most mutated C. auris genes are associated with the regulation of cell wall integrity, cytokinesis, cytoskeletal properties, and cellular polarization. Moreover, the multicellular aggregates are notably more recalcitrant to the host antimicrobial peptides LL-37 and PACAP relative to the single-celled yeast-form cells. Overall, to survive in the host, C. auris can rapidly evolve a multicellular aggregative morphology via genetic mutations.},
}
MeSH Terms:
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Animals
Mice
Candida/genetics
*Candidiasis/microbiology
Candida auris
Saccharomyces cerevisiae
Phenotype
*Sepsis
Antifungal Agents
Microbial Sensitivity Tests
Mammals
RevDate: 2024-06-03
CmpDate: 2024-05-31
Extraction and identification of exosomes from three different sources of human ovarian granulosa cells and analysis of their differential miRNA expression profiles.
Journal of assisted reproduction and genetics, 41(5):1371-1385.
OBJECTIVE: As important functional cells in the ovary, ovarian granulosa cells are involved in the regulation of oocyte growth and development and play an important role in the study of female fertility preservation. Based on the importance of granulosa cell functionalism, in this study, we analyzed the exosome secretion capacity of human ovarian granulosa cells (SVOG/KGN-cell line, PGC-primary cells) and the differences in their miRNA expression.
METHODS: Cells were identified by hematoxylin-eosin staining (HE) and FSHR immunofluorescence staining; CCK8 and colony-forming assay were performed to compare cell proliferation capacity; exosomes were extracted and identified by ultra-high speed centrifugation, transmission electron microscopy (TEM), nanoparticle tracking analysis (NTA), and western blot analysis (WB), and the expression profile of each cellular exosomal miRNA was analyzed by miRNA high-throughput sequencing.
RESULTS: The proliferative abilities of the three granulosa cells differed, but all had the ability to secrete exosomes. In the exosomes of SVOG, KGN, and PGC cells, 218, 327, and 471 miRNAs were detected, respectively. When compared to the exosomal miRNAs of PGC cells, 111 miRNAs were significantly different in SVOG, and 70 miRNAs were washed two significantly different in KGN cells. These differential miRNA functions were mainly enriched in the cell cycle, cell division/differentiation, multicellular biogenesis, and protein binding.
CONCLUSION: Human ovarian granulosa cells of different origins are capable of secreting exosomes, but there are still some differences in their exosomes and exosomal miRNAs, and experimental subjects should be selected rationally according to the actual situation.
Additional Links: PMID-38492155
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@article {pmid38492155,
year = {2024},
author = {Li, X and Gao, T and Ma, X and Zhong, J and Qin, L and Nian, Y and Wang, X and Luo, Y},
title = {Extraction and identification of exosomes from three different sources of human ovarian granulosa cells and analysis of their differential miRNA expression profiles.},
journal = {Journal of assisted reproduction and genetics},
volume = {41},
number = {5},
pages = {1371-1385},
pmid = {38492155},
issn = {1573-7330},
support = {81660806//National Natural Science Foundation of China/ ; 82260947//National Natural Science Foundation of China/ ; },
mesh = {Humans ; Female ; *Exosomes/genetics/metabolism/ultrastructure ; *Granulosa Cells/metabolism ; *MicroRNAs/genetics ; *Cell Proliferation/genetics ; Gene Expression Profiling ; Cell Line ; },
abstract = {OBJECTIVE: As important functional cells in the ovary, ovarian granulosa cells are involved in the regulation of oocyte growth and development and play an important role in the study of female fertility preservation. Based on the importance of granulosa cell functionalism, in this study, we analyzed the exosome secretion capacity of human ovarian granulosa cells (SVOG/KGN-cell line, PGC-primary cells) and the differences in their miRNA expression.
METHODS: Cells were identified by hematoxylin-eosin staining (HE) and FSHR immunofluorescence staining; CCK8 and colony-forming assay were performed to compare cell proliferation capacity; exosomes were extracted and identified by ultra-high speed centrifugation, transmission electron microscopy (TEM), nanoparticle tracking analysis (NTA), and western blot analysis (WB), and the expression profile of each cellular exosomal miRNA was analyzed by miRNA high-throughput sequencing.
RESULTS: The proliferative abilities of the three granulosa cells differed, but all had the ability to secrete exosomes. In the exosomes of SVOG, KGN, and PGC cells, 218, 327, and 471 miRNAs were detected, respectively. When compared to the exosomal miRNAs of PGC cells, 111 miRNAs were significantly different in SVOG, and 70 miRNAs were washed two significantly different in KGN cells. These differential miRNA functions were mainly enriched in the cell cycle, cell division/differentiation, multicellular biogenesis, and protein binding.
CONCLUSION: Human ovarian granulosa cells of different origins are capable of secreting exosomes, but there are still some differences in their exosomes and exosomal miRNAs, and experimental subjects should be selected rationally according to the actual situation.},
}
MeSH Terms:
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hide MeSH Terms
Humans
Female
*Exosomes/genetics/metabolism/ultrastructure
*Granulosa Cells/metabolism
*MicroRNAs/genetics
*Cell Proliferation/genetics
Gene Expression Profiling
Cell Line
RevDate: 2024-05-15
CmpDate: 2024-05-14
Emergence and maintenance of stable coexistence during a long-term multicellular evolution experiment.
Nature ecology & evolution, 8(5):1010-1020.
The evolution of multicellular life spurred evolutionary radiations, fundamentally changing many of Earth's ecosystems. Yet little is known about how early steps in the evolution of multicellularity affect eco-evolutionary dynamics. Through long-term experimental evolution, we observed niche partitioning and the adaptive divergence of two specialized lineages from a single multicellular ancestor. Over 715 daily transfers, snowflake yeast were subjected to selection for rapid growth, followed by selection favouring larger group size. Small and large cluster-forming lineages evolved from a monomorphic ancestor, coexisting for over ~4,300 generations, specializing on divergent aspects of a trade-off between growth rate and survival. Through modelling and experimentation, we demonstrate that coexistence is maintained by a trade-off between organismal size and competitiveness for dissolved oxygen. Taken together, this work shows how the evolution of a new level of biological individuality can rapidly drive adaptive diversification and the expansion of a nascent multicellular niche, one of the most historically impactful emergent properties of this evolutionary transition.
Additional Links: PMID-38486107
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@article {pmid38486107,
year = {2024},
author = {Pineau, RM and Libby, E and Demory, D and Lac, DT and Day, TC and Bravo, P and Yunker, PJ and Weitz, JS and Bozdag, GO and Ratcliff, WC},
title = {Emergence and maintenance of stable coexistence during a long-term multicellular evolution experiment.},
journal = {Nature ecology & evolution},
volume = {8},
number = {5},
pages = {1010-1020},
pmid = {38486107},
issn = {2397-334X},
support = {R35 GM138030/GM/NIGMS NIH HHS/United States ; R35 GM138354/GM/NIGMS NIH HHS/United States ; },
mesh = {*Biological Evolution ; Saccharomyces cerevisiae/genetics/physiology ; Ecosystem ; },
abstract = {The evolution of multicellular life spurred evolutionary radiations, fundamentally changing many of Earth's ecosystems. Yet little is known about how early steps in the evolution of multicellularity affect eco-evolutionary dynamics. Through long-term experimental evolution, we observed niche partitioning and the adaptive divergence of two specialized lineages from a single multicellular ancestor. Over 715 daily transfers, snowflake yeast were subjected to selection for rapid growth, followed by selection favouring larger group size. Small and large cluster-forming lineages evolved from a monomorphic ancestor, coexisting for over ~4,300 generations, specializing on divergent aspects of a trade-off between growth rate and survival. Through modelling and experimentation, we demonstrate that coexistence is maintained by a trade-off between organismal size and competitiveness for dissolved oxygen. Taken together, this work shows how the evolution of a new level of biological individuality can rapidly drive adaptive diversification and the expansion of a nascent multicellular niche, one of the most historically impactful emergent properties of this evolutionary transition.},
}
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*Biological Evolution
Saccharomyces cerevisiae/genetics/physiology
Ecosystem
RevDate: 2024-04-17
CmpDate: 2024-03-15
Mechanism and endoscopic-treatment-induced evolution of biliary non-anastomotic stricture after liver transplantation revealed by single-cell RNA sequencing.
Clinical and translational medicine, 14(3):e1622.
BACKGROUND: Biliary complications, especially non-anastomotic stricture (NAS), are the main complications after liver transplantation. Insufficient sampling and no recognized animal models obstruct the investigation. Thus, the mechanisms and alterations that occur during endoscopic treatment (ET) of NAS remain unclear.
METHODS: Samples were obtained with endoscopic forceps from the hilar bile ducts of NAS patients receiving continuous biliary stent implantation after diagnosis. Retrospective analysis of multiple studies indicated that the duration of ET for NAS was approximately 1-2 years. Thus, we divided the patients into short-term treatment (STT) and long-term treatment (LTT) groups based on durations of less or more than 1 year. Samples were subjected to single-cell RNA sequencing. Transcriptomic differences between STT and normal groups were defined as the NAS mechanism. Similarly, alterations from STT to LTT groups were regarded as endoscopic-treatment-induced evolution.
RESULTS: In NAS, inflammation and immune-related pathways were upregulated in different cell types, with nonimmune cells showing hypoxia pathway upregulation and immune cells showing ATP metabolism pathway upregulation, indicating heterogeneity. We confirmed a reduction in bile acid metabolism-related SPP1[+] epithelial cells in NAS. Increases in proinflammatory and profibrotic fibroblast subclusters indicated fibrotic progression in NAS. Furthermore, immune disorders in NAS were exacerbated by an increase in plasma cells and dysfunction of NK and NKT cells. ET downregulated multicellular immune and inflammatory responses and restored epithelial and endothelial cell proportions.
CONCLUSIONS: This study reveals the pathophysiological and genetic mechanisms and evolution of NAS induced by ET, thereby providing preventive and therapeutic insights into NAS.
HIGHLIGHTS: For the first time, single-cell transcriptome sequencing was performed on the bile ducts of patients with biliary complications. scRNA-seq analysis revealed distinct changes in the proportion and phenotype of multiple cell types during Nonanastomotic stricture (NAS) and endoscopic treatment. A reduction in bile acid metabolism-related SPP1+ epithelial cells and VEGFA+ endothelial cells, along with explosive infiltration of plasma cells and dysfunction of T and NK cells in NAS patients. SPP1+ macrophages and BST2+ T cells might serve as a surrogate marker for predicting endoscopic treatment.
Additional Links: PMID-38481381
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@article {pmid38481381,
year = {2024},
author = {Wu, Z and Liu, D and Ou, Y and Xu, Z and Heng, G and Liu, W and Fu, N and Wang, J and Jiang, D and Gan, L and Dong, J and Wang, X and Chen, Z and Zhang, L and Zhang, C},
title = {Mechanism and endoscopic-treatment-induced evolution of biliary non-anastomotic stricture after liver transplantation revealed by single-cell RNA sequencing.},
journal = {Clinical and translational medicine},
volume = {14},
number = {3},
pages = {e1622},
pmid = {38481381},
issn = {2001-1326},
support = {2022TIAD-GPX0236//Technical Innovation and Application of Chongqing/ ; 2022TIAD-GPX0238//Technical Innovation and Application of Chongqing/ ; 82270687//National Natural Science Foundation of China/ ; },
mesh = {Humans ; *Liver Transplantation/adverse effects ; Constriction, Pathologic/surgery/etiology ; Retrospective Studies ; Endothelial Cells ; Sequence Analysis, RNA ; Bile Acids and Salts ; },
abstract = {BACKGROUND: Biliary complications, especially non-anastomotic stricture (NAS), are the main complications after liver transplantation. Insufficient sampling and no recognized animal models obstruct the investigation. Thus, the mechanisms and alterations that occur during endoscopic treatment (ET) of NAS remain unclear.
METHODS: Samples were obtained with endoscopic forceps from the hilar bile ducts of NAS patients receiving continuous biliary stent implantation after diagnosis. Retrospective analysis of multiple studies indicated that the duration of ET for NAS was approximately 1-2 years. Thus, we divided the patients into short-term treatment (STT) and long-term treatment (LTT) groups based on durations of less or more than 1 year. Samples were subjected to single-cell RNA sequencing. Transcriptomic differences between STT and normal groups were defined as the NAS mechanism. Similarly, alterations from STT to LTT groups were regarded as endoscopic-treatment-induced evolution.
RESULTS: In NAS, inflammation and immune-related pathways were upregulated in different cell types, with nonimmune cells showing hypoxia pathway upregulation and immune cells showing ATP metabolism pathway upregulation, indicating heterogeneity. We confirmed a reduction in bile acid metabolism-related SPP1[+] epithelial cells in NAS. Increases in proinflammatory and profibrotic fibroblast subclusters indicated fibrotic progression in NAS. Furthermore, immune disorders in NAS were exacerbated by an increase in plasma cells and dysfunction of NK and NKT cells. ET downregulated multicellular immune and inflammatory responses and restored epithelial and endothelial cell proportions.
CONCLUSIONS: This study reveals the pathophysiological and genetic mechanisms and evolution of NAS induced by ET, thereby providing preventive and therapeutic insights into NAS.
HIGHLIGHTS: For the first time, single-cell transcriptome sequencing was performed on the bile ducts of patients with biliary complications. scRNA-seq analysis revealed distinct changes in the proportion and phenotype of multiple cell types during Nonanastomotic stricture (NAS) and endoscopic treatment. A reduction in bile acid metabolism-related SPP1+ epithelial cells and VEGFA+ endothelial cells, along with explosive infiltration of plasma cells and dysfunction of T and NK cells in NAS patients. SPP1+ macrophages and BST2+ T cells might serve as a surrogate marker for predicting endoscopic treatment.},
}
MeSH Terms:
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Humans
*Liver Transplantation/adverse effects
Constriction, Pathologic/surgery/etiology
Retrospective Studies
Endothelial Cells
Sequence Analysis, RNA
Bile Acids and Salts
RevDate: 2024-03-15
CmpDate: 2024-03-14
Evolutionary and Structural Analysis of PP16 in Viridiplantae.
International journal of molecular sciences, 25(5):.
Members of the phloem protein 16 (PP16) gene family are induced by elicitors in rice and the corresponding proteins from cucurbits, which display RNA binding and intercellular transport activities, are accumulated in phloem sap. These proteins facilitate the movement of protein complexes through the phloem translocation flow and may be involved in the response to water deficit, among other functions. However, there is scant information regarding their function in other plants, including the identification of paralog genes in non-vascular plants and chlorophytes. In the present work, an evolutionary and structural analysis of the PP16 family in green plants (Viridiplantae) was carried out. Data mining in different databases indicated that PP16 likely originated from a larger gene present in an ancestral lineage that gave rise to chlorophytes and multicellular plants. This gene encodes a protein related to synaptotagmin, which is involved in vesicular transport in animal systems, although other members of this family play a role in lipid turnover in endomembranes and organelles. These proteins contain a membrane-binding C2 domain shared with PP16 proteins in vascular plants. In silico analysis of the predicted structure of the PP16 protein family identified several β-sheets, one α-helix, and intrinsically disordered regions. PP16 may have been originally involved in vesicular trafficking and/or membrane maintenance but specialized in long-distance signaling during the emergence of the plant vascular system.
Additional Links: PMID-38474088
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@article {pmid38474088,
year = {2024},
author = {Jiménez-López, D and Xoconostle-Cázares, B and Calderón-Pérez, B and Vargas-Hernández, BY and Núñez-Muñoz, LA and Ramírez-Pool, JA and Ruiz-Medrano, R},
title = {Evolutionary and Structural Analysis of PP16 in Viridiplantae.},
journal = {International journal of molecular sciences},
volume = {25},
number = {5},
pages = {},
pmid = {38474088},
issn = {1422-0067},
support = {781282//Consejo Nacional de Humanidades, Ciencias y Tecnologías/ ; },
mesh = {*Plant Proteins/genetics ; Phloem/metabolism ; Plants/metabolism ; Biological Transport ; *Viridiplantae/metabolism ; },
abstract = {Members of the phloem protein 16 (PP16) gene family are induced by elicitors in rice and the corresponding proteins from cucurbits, which display RNA binding and intercellular transport activities, are accumulated in phloem sap. These proteins facilitate the movement of protein complexes through the phloem translocation flow and may be involved in the response to water deficit, among other functions. However, there is scant information regarding their function in other plants, including the identification of paralog genes in non-vascular plants and chlorophytes. In the present work, an evolutionary and structural analysis of the PP16 family in green plants (Viridiplantae) was carried out. Data mining in different databases indicated that PP16 likely originated from a larger gene present in an ancestral lineage that gave rise to chlorophytes and multicellular plants. This gene encodes a protein related to synaptotagmin, which is involved in vesicular transport in animal systems, although other members of this family play a role in lipid turnover in endomembranes and organelles. These proteins contain a membrane-binding C2 domain shared with PP16 proteins in vascular plants. In silico analysis of the predicted structure of the PP16 protein family identified several β-sheets, one α-helix, and intrinsically disordered regions. PP16 may have been originally involved in vesicular trafficking and/or membrane maintenance but specialized in long-distance signaling during the emergence of the plant vascular system.},
}
MeSH Terms:
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*Plant Proteins/genetics
Phloem/metabolism
Plants/metabolism
Biological Transport
*Viridiplantae/metabolism
RevDate: 2024-08-06
CmpDate: 2024-05-23
Polr3b heterozygosity in mice induces both beneficial and deleterious effects on health during ageing with no effect on lifespan.
Aging cell, 23(5):e14141.
The genetic pathways that modulate ageing in multicellular organisms are typically highly conserved across wide evolutionary distances. Recently RNA polymerase III (Pol III) was shown to promote ageing in yeast, C. elegans and D. melanogaster. In this study we investigated the role of Pol III in mammalian ageing using C57BL/6N mice heterozygous for Pol III (Polr3b[+/-]). We identified sexually dimorphic, organ-specific beneficial as well as detrimental effects of the Polr3b[+/-] mutation on health. Female Polr3b[+/-] mice displayed improved bone health during ageing, but their ability to maintain an effective gut barrier function was compromised and they were susceptible to idiopathic dermatitis (ID). In contrast, male Polr3b[+/-] mice were lighter than wild-type (WT) males and had a significantly improved gut barrier function in old age. Several metabolic parameters were affected by both age and sex, but no genotype differences were detected. Neither male nor female Polr3b[+/-] mice were long-lived compared to WT controls. Overall, we find no evidence that a reduced Pol III activity extends mouse lifespan but we do find some potential organ- and sex-specific benefits for old-age health.
Additional Links: PMID-38465473
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@article {pmid38465473,
year = {2024},
author = {Borland, G and Wilkie, SE and Thomson, J and Wang, Z and Tullet, JMA and Alic, N and Selman, C},
title = {Polr3b heterozygosity in mice induces both beneficial and deleterious effects on health during ageing with no effect on lifespan.},
journal = {Aging cell},
volume = {23},
number = {5},
pages = {e14141},
pmid = {38465473},
issn = {1474-9726},
support = {BB/S014357/1/BB_/Biotechnology and Biological Sciences Research Council/United Kingdom ; MR/N013166/1/MRC_/Medical Research Council/United Kingdom ; },
mesh = {Animals ; Female ; Male ; Mice ; *Aging/genetics ; *Heterozygote ; *Longevity/genetics ; Mice, Inbred C57BL ; *RNA Polymerase III/genetics/metabolism ; },
abstract = {The genetic pathways that modulate ageing in multicellular organisms are typically highly conserved across wide evolutionary distances. Recently RNA polymerase III (Pol III) was shown to promote ageing in yeast, C. elegans and D. melanogaster. In this study we investigated the role of Pol III in mammalian ageing using C57BL/6N mice heterozygous for Pol III (Polr3b[+/-]). We identified sexually dimorphic, organ-specific beneficial as well as detrimental effects of the Polr3b[+/-] mutation on health. Female Polr3b[+/-] mice displayed improved bone health during ageing, but their ability to maintain an effective gut barrier function was compromised and they were susceptible to idiopathic dermatitis (ID). In contrast, male Polr3b[+/-] mice were lighter than wild-type (WT) males and had a significantly improved gut barrier function in old age. Several metabolic parameters were affected by both age and sex, but no genotype differences were detected. Neither male nor female Polr3b[+/-] mice were long-lived compared to WT controls. Overall, we find no evidence that a reduced Pol III activity extends mouse lifespan but we do find some potential organ- and sex-specific benefits for old-age health.},
}
MeSH Terms:
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Animals
Female
Male
Mice
*Aging/genetics
*Heterozygote
*Longevity/genetics
Mice, Inbred C57BL
*RNA Polymerase III/genetics/metabolism
RevDate: 2024-08-21
CmpDate: 2024-03-05
Polarity establishment in the plant zygote at a glance.
Journal of cell science, 137(5):.
The complex structures of multicellular organisms originate from a unicellular zygote. In most angiosperms, including Arabidopsis thaliana, the zygote is distinctly polar and divides asymmetrically to produce an apical cell, which generates the aboveground part of the plant body, and a basal cell, which generates the root tip and extraembryonic suspensor. Thus, zygote polarity is pivotal for establishing the apical-basal axis running from the shoot apex to the root tip of the plant body. The molecular mechanisms and spatiotemporal dynamics behind zygote polarization remain elusive. However, advances in live-cell imaging of plant zygotes have recently made significant insights possible. In this Cell Science at a Glance article and the accompanying poster, we summarize our understanding of the early steps in apical-basal axis formation in Arabidopsis, with a focus on de novo transcriptional activation after fertilization and the intracellular dynamics leading to the first asymmetric division of the zygote.
Additional Links: PMID-38436556
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@article {pmid38436556,
year = {2024},
author = {Matsumoto, H and Ueda, M},
title = {Polarity establishment in the plant zygote at a glance.},
journal = {Journal of cell science},
volume = {137},
number = {5},
pages = {},
doi = {10.1242/jcs.261809},
pmid = {38436556},
issn = {1477-9137},
support = {//Japan Advanced Plant Science Network/ ; JP21K20650//Japan Society for the Promotion of Science/ ; JPMJCR2121//Japan Science and Technology Agency/ ; //Suntory Rising Stars Encouragement Program in Life Sciences/ ; 20-6102//Toray Science Foundation/ ; },
mesh = {*Zygote ; Seeds ; *Arabidopsis/genetics ; Meristem ; Transcriptional Activation ; },
abstract = {The complex structures of multicellular organisms originate from a unicellular zygote. In most angiosperms, including Arabidopsis thaliana, the zygote is distinctly polar and divides asymmetrically to produce an apical cell, which generates the aboveground part of the plant body, and a basal cell, which generates the root tip and extraembryonic suspensor. Thus, zygote polarity is pivotal for establishing the apical-basal axis running from the shoot apex to the root tip of the plant body. The molecular mechanisms and spatiotemporal dynamics behind zygote polarization remain elusive. However, advances in live-cell imaging of plant zygotes have recently made significant insights possible. In this Cell Science at a Glance article and the accompanying poster, we summarize our understanding of the early steps in apical-basal axis formation in Arabidopsis, with a focus on de novo transcriptional activation after fertilization and the intracellular dynamics leading to the first asymmetric division of the zygote.},
}
MeSH Terms:
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*Zygote
Seeds
*Arabidopsis/genetics
Meristem
Transcriptional Activation
RevDate: 2024-05-06
CmpDate: 2024-04-15
A statistical method for quantifying progenitor cells reveals incipient cell fate commitments.
Nature methods, 21(4):597-608.
Quantifying the number of progenitor cells that found an organ, tissue or cell population is of fundamental importance for understanding the development and homeostasis of a multicellular organism. Previous efforts rely on marker genes that are specifically expressed in progenitors. This strategy is, however, often hindered by the lack of ideal markers. Here we propose a general statistical method to quantify the progenitors of any tissues or cell populations in an organism, even in the absence of progenitor-specific markers, by exploring the cell phylogenetic tree that records the cell division history during development. The method, termed targeting coalescent analysis (TarCA), computes the probability that two randomly sampled cells of a tissue coalesce within the tissue-specific monophyletic clades. The inverse of this probability then serves as a measure of the progenitor number of the tissue. Both mathematic modeling and computer simulations demonstrated the high accuracy of TarCA, which was then validated using real data from nematode, fruit fly and mouse, all with related cell phylogenetic trees. We further showed that TarCA can be used to identify lineage-specific upregulated genes during embryogenesis, revealing incipient cell fate commitments in mouse embryos.
Additional Links: PMID-38379073
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@article {pmid38379073,
year = {2024},
author = {Deng, S and Gong, H and Zhang, D and Zhang, M and He, X},
title = {A statistical method for quantifying progenitor cells reveals incipient cell fate commitments.},
journal = {Nature methods},
volume = {21},
number = {4},
pages = {597-608},
pmid = {38379073},
issn = {1548-7105},
support = {32293190//National Natural Science Foundation of China (National Science Foundation of China)/ ; 32200492//National Natural Science Foundation of China (National Science Foundation of China)/ ; },
mesh = {Animals ; Mice ; Phylogeny ; Cell Differentiation/genetics ; *Stem Cells ; *Embryonic Development ; Cell Division ; },
abstract = {Quantifying the number of progenitor cells that found an organ, tissue or cell population is of fundamental importance for understanding the development and homeostasis of a multicellular organism. Previous efforts rely on marker genes that are specifically expressed in progenitors. This strategy is, however, often hindered by the lack of ideal markers. Here we propose a general statistical method to quantify the progenitors of any tissues or cell populations in an organism, even in the absence of progenitor-specific markers, by exploring the cell phylogenetic tree that records the cell division history during development. The method, termed targeting coalescent analysis (TarCA), computes the probability that two randomly sampled cells of a tissue coalesce within the tissue-specific monophyletic clades. The inverse of this probability then serves as a measure of the progenitor number of the tissue. Both mathematic modeling and computer simulations demonstrated the high accuracy of TarCA, which was then validated using real data from nematode, fruit fly and mouse, all with related cell phylogenetic trees. We further showed that TarCA can be used to identify lineage-specific upregulated genes during embryogenesis, revealing incipient cell fate commitments in mouse embryos.},
}
MeSH Terms:
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Animals
Mice
Phylogeny
Cell Differentiation/genetics
*Stem Cells
*Embryonic Development
Cell Division
RevDate: 2024-09-17
CmpDate: 2024-04-23
The three-dimensional structure of the Vint domain from Tetrahymena thermophila suggests a ligand-regulated cleavage mechanism by the HINT fold.
FEBS letters, 598(8):864-874.
Vint proteins have been identified in unicellular metazoans as a novel hedgehog-related gene family, merging the von Willebrand factor type A domain and the Hedgehog/INTein (HINT) domains. We present the first three-dimensional structure of the Vint domain from Tetrahymena thermophila corresponding to the auto-processing domain of hedgehog proteins, shedding light on the unique features, including an adduct recognition region (ARR). Our results suggest a potential binding between the ARR and sulfated glycosaminoglycans like heparin sulfate. Moreover, we uncover a possible regulatory role of the ARR in the auto-processing by Vint domains, expanding our understanding of the HINT domain evolution and their use in biotechnological applications. Vint domains might have played a crucial role in the transition from unicellular to multicellular organisms.
Additional Links: PMID-38351630
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@article {pmid38351630,
year = {2024},
author = {Iwaï, H and Beyer, HM and Johansson, JEM and Li, M and Wlodawer, A},
title = {The three-dimensional structure of the Vint domain from Tetrahymena thermophila suggests a ligand-regulated cleavage mechanism by the HINT fold.},
journal = {FEBS letters},
volume = {598},
number = {8},
pages = {864-874},
doi = {10.1002/1873-3468.14817},
pmid = {38351630},
issn = {1873-3468},
support = {75N91019D00024/CA/NCI NIH HHS/United States ; 75N91019D00024/CA/NCI NIH HHS/United States ; },
mesh = {*Tetrahymena thermophila/metabolism/genetics ; *Protozoan Proteins/chemistry/metabolism/genetics ; *Protein Domains ; Ligands ; Models, Molecular ; Hedgehog Proteins/metabolism/chemistry/genetics ; Amino Acid Sequence ; Protein Folding ; },
abstract = {Vint proteins have been identified in unicellular metazoans as a novel hedgehog-related gene family, merging the von Willebrand factor type A domain and the Hedgehog/INTein (HINT) domains. We present the first three-dimensional structure of the Vint domain from Tetrahymena thermophila corresponding to the auto-processing domain of hedgehog proteins, shedding light on the unique features, including an adduct recognition region (ARR). Our results suggest a potential binding between the ARR and sulfated glycosaminoglycans like heparin sulfate. Moreover, we uncover a possible regulatory role of the ARR in the auto-processing by Vint domains, expanding our understanding of the HINT domain evolution and their use in biotechnological applications. Vint domains might have played a crucial role in the transition from unicellular to multicellular organisms.},
}
MeSH Terms:
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*Tetrahymena thermophila/metabolism/genetics
*Protozoan Proteins/chemistry/metabolism/genetics
*Protein Domains
Ligands
Models, Molecular
Hedgehog Proteins/metabolism/chemistry/genetics
Amino Acid Sequence
Protein Folding
RevDate: 2024-03-21
CmpDate: 2024-03-20
Snowball: a novel gene family required for developmental patterning of fruiting bodies of mushroom-forming fungi (Agaricomycetes).
mSystems, 9(3):e0120823.
UNLABELLED: The morphogenesis of sexual fruiting bodies of fungi is a complex process determined by a genetically encoded program. Fruiting bodies reached the highest complexity levels in the Agaricomycetes; yet, the underlying genetics is currently poorly known. In this work, we functionally characterized a highly conserved gene termed snb1, whose expression level increases rapidly during fruiting body initiation. According to phylogenetic analyses, orthologs of snb1 are present in almost all agaricomycetes and may represent a novel conserved gene family that plays a substantial role in fruiting body development. We disrupted snb1 using CRISPR/Cas9 in the agaricomycete model organism Coprinopsis cinerea. snb1 deletion mutants formed unique, snowball-shaped, rudimentary fruiting bodies that could not differentiate caps, stipes, and lamellae. We took advantage of this phenotype to study fruiting body differentiation using RNA-Seq analyses. This revealed differentially regulated genes and gene families that, based on wild-type RNA-Seq data, were upregulated early during development and showed tissue-specific expression, suggesting a potential role in differentiation. Taken together, the novel gene family of snb1 and the differentially expressed genes in the snb1 mutants provide valuable insights into the complex mechanisms underlying developmental patterning in the Agaricomycetes.
IMPORTANCE: Fruiting bodies of mushroom-forming fungi (Agaricomycetes) are complex multicellular structures, with a spatially and temporally integrated developmental program that is, however, currently poorly known. In this study, we present a novel, conserved gene family, Snowball (snb), termed after the unique, differentiation-less fruiting body morphology of snb1 knockout strains in the model mushroom Coprinopsis cinerea. snb is a gene of unknown function that is highly conserved among agaricomycetes and encodes a protein of unknown function. A comparative transcriptomic analysis of the early developmental stages of differentiated wild-type and non-differentiated mutant fruiting bodies revealed conserved differentially expressed genes which may be related to tissue differentiation and developmental patterning fruiting body development.
Additional Links: PMID-38334416
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@article {pmid38334416,
year = {2024},
author = {Földi, C and Merényi, Z and Balázs, B and Csernetics, Á and Miklovics, N and Wu, H and Hegedüs, B and Virágh, M and Hou, Z and Liu, X-B and Galgóczy, L and Nagy, LG},
title = {Snowball: a novel gene family required for developmental patterning of fruiting bodies of mushroom-forming fungi (Agaricomycetes).},
journal = {mSystems},
volume = {9},
number = {3},
pages = {e0120823},
pmid = {38334416},
issn = {2379-5077},
support = {LP2019-13/2019//Hungarian Academy of Sciences/ ; KDP-17-4/PALY-2021//Ministry of Innovation and Technology (Hungary)/ ; OTKA 142188//National Research Development and Innovation Office (Hungary)/ ; },
mesh = {Fruiting Bodies, Fungal/genetics ; Phylogeny ; Fungal Proteins/genetics ; *Agaricales/genetics ; *Basidiomycota/metabolism ; *Ascomycota/metabolism ; },
abstract = {UNLABELLED: The morphogenesis of sexual fruiting bodies of fungi is a complex process determined by a genetically encoded program. Fruiting bodies reached the highest complexity levels in the Agaricomycetes; yet, the underlying genetics is currently poorly known. In this work, we functionally characterized a highly conserved gene termed snb1, whose expression level increases rapidly during fruiting body initiation. According to phylogenetic analyses, orthologs of snb1 are present in almost all agaricomycetes and may represent a novel conserved gene family that plays a substantial role in fruiting body development. We disrupted snb1 using CRISPR/Cas9 in the agaricomycete model organism Coprinopsis cinerea. snb1 deletion mutants formed unique, snowball-shaped, rudimentary fruiting bodies that could not differentiate caps, stipes, and lamellae. We took advantage of this phenotype to study fruiting body differentiation using RNA-Seq analyses. This revealed differentially regulated genes and gene families that, based on wild-type RNA-Seq data, were upregulated early during development and showed tissue-specific expression, suggesting a potential role in differentiation. Taken together, the novel gene family of snb1 and the differentially expressed genes in the snb1 mutants provide valuable insights into the complex mechanisms underlying developmental patterning in the Agaricomycetes.
IMPORTANCE: Fruiting bodies of mushroom-forming fungi (Agaricomycetes) are complex multicellular structures, with a spatially and temporally integrated developmental program that is, however, currently poorly known. In this study, we present a novel, conserved gene family, Snowball (snb), termed after the unique, differentiation-less fruiting body morphology of snb1 knockout strains in the model mushroom Coprinopsis cinerea. snb is a gene of unknown function that is highly conserved among agaricomycetes and encodes a protein of unknown function. A comparative transcriptomic analysis of the early developmental stages of differentiated wild-type and non-differentiated mutant fruiting bodies revealed conserved differentially expressed genes which may be related to tissue differentiation and developmental patterning fruiting body development.},
}
MeSH Terms:
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Fruiting Bodies, Fungal/genetics
Phylogeny
Fungal Proteins/genetics
*Agaricales/genetics
*Basidiomycota/metabolism
*Ascomycota/metabolism
RevDate: 2024-09-24
CmpDate: 2024-03-21
Comparative genomic analysis of symbiotic and free-living Fluviibacter phosphoraccumulans strains provides insights into the evolutionary origins of obligate Euplotes-bacterial endosymbioses.
Applied and environmental microbiology, 90(3):e0190023.
UNLABELLED: Endosymbiosis is a widespread and important phenomenon requiring diverse model systems. Ciliates are a widespread group of protists that often form symbioses with diverse microorganisms. Endosymbioses between the ciliate Euplotes and heritable bacterial symbionts are common in nature, and four essential symbionts were described: Polynucleobacter necessarius, "Candidatus Protistobacter heckmanni," "Ca. Devosia symbiotica," and "Ca. Devosia euplotis." Among them, only the genus Polynucleobacter comprises very close free-living and symbiotic representatives, which makes it an excellent model for investigating symbiont replacements and recent symbioses. In this article, we characterized a novel endosymbiont inhabiting the cytoplasm of Euplotes octocarinatus and found that it is a close relative of the free-living bacterium Fluviibacter phosphoraccumulans (Betaproteobacteria and Rhodocyclales). We present the complete genome sequence and annotation of the symbiotic Fluviibacter. Comparative analyses indicate that the genome of symbiotic Fluviibacter is small in size and rich in pseudogenes when compared with free-living strains, which seems to fit the prediction for recently established endosymbionts undergoing genome erosion. Further comparative analysis revealed reduced metabolic capacities in symbiotic Fluviibacter, which implies that the symbiont relies on the host Euplotes for carbon sources, organic nitrogen and sulfur, and some cofactors. We also estimated substitution rates between symbiotic and free-living Fluviibacter pairs for 233 genes; the results showed that symbiotic Fluviibacter displays higher dN/dS mean value than free-living relatives, which suggested that genetic drift is the main driving force behind molecular evolution in endosymbionts.
IMPORTANCE: In the long history of symbiosis research, most studies focused mainly on organelles or bacteria within multicellular hosts. The single-celled protists receive little attention despite harboring an immense diversity of symbiotic associations with bacteria and archaea. One subgroup of the ciliate Euplotes species is strictly dependent on essential symbionts for survival and has emerged as a valuable model for understanding symbiont replacements and recent symbioses. However, almost all of our knowledge about the evolution and functions of Euplotes symbioses comes from the Euplotes-Polynucleobacter system. In this article, we report a novel essential symbiont, which also has very close free-living relatives. Genome analysis indicated that it is a recently established endosymbiont undergoing genome erosion and relies on the Euplotes host for many essential molecules. Our results provide support for the notion that essential symbionts of the ciliate Euplotes evolve from free-living progenitors in the natural water environment.
Additional Links: PMID-38334408
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@article {pmid38334408,
year = {2024},
author = {Wang, R and Meng, Q and Wang, X and Xiao, Y and Sun, R and Zhang, Z and Fu, Y and Di Giuseppe, G and Liang, A},
title = {Comparative genomic analysis of symbiotic and free-living Fluviibacter phosphoraccumulans strains provides insights into the evolutionary origins of obligate Euplotes-bacterial endosymbioses.},
journal = {Applied and environmental microbiology},
volume = {90},
number = {3},
pages = {e0190023},
pmid = {38334408},
issn = {1098-5336},
support = {32270447//MOST | National Natural Science Foundation of China (NSFC)/ ; 31372199//MOST | National Natural Science Foundation of China (NSFC)/ ; 20220302121320//Fundamental Research Program of Shanxi Province/ ; },
mesh = {Phylogeny ; Symbiosis/genetics ; *Euplotes/genetics/microbiology ; *Betaproteobacteria/genetics ; Bacteria/genetics ; Genome, Bacterial ; Genomics ; },
abstract = {UNLABELLED: Endosymbiosis is a widespread and important phenomenon requiring diverse model systems. Ciliates are a widespread group of protists that often form symbioses with diverse microorganisms. Endosymbioses between the ciliate Euplotes and heritable bacterial symbionts are common in nature, and four essential symbionts were described: Polynucleobacter necessarius, "Candidatus Protistobacter heckmanni," "Ca. Devosia symbiotica," and "Ca. Devosia euplotis." Among them, only the genus Polynucleobacter comprises very close free-living and symbiotic representatives, which makes it an excellent model for investigating symbiont replacements and recent symbioses. In this article, we characterized a novel endosymbiont inhabiting the cytoplasm of Euplotes octocarinatus and found that it is a close relative of the free-living bacterium Fluviibacter phosphoraccumulans (Betaproteobacteria and Rhodocyclales). We present the complete genome sequence and annotation of the symbiotic Fluviibacter. Comparative analyses indicate that the genome of symbiotic Fluviibacter is small in size and rich in pseudogenes when compared with free-living strains, which seems to fit the prediction for recently established endosymbionts undergoing genome erosion. Further comparative analysis revealed reduced metabolic capacities in symbiotic Fluviibacter, which implies that the symbiont relies on the host Euplotes for carbon sources, organic nitrogen and sulfur, and some cofactors. We also estimated substitution rates between symbiotic and free-living Fluviibacter pairs for 233 genes; the results showed that symbiotic Fluviibacter displays higher dN/dS mean value than free-living relatives, which suggested that genetic drift is the main driving force behind molecular evolution in endosymbionts.
IMPORTANCE: In the long history of symbiosis research, most studies focused mainly on organelles or bacteria within multicellular hosts. The single-celled protists receive little attention despite harboring an immense diversity of symbiotic associations with bacteria and archaea. One subgroup of the ciliate Euplotes species is strictly dependent on essential symbionts for survival and has emerged as a valuable model for understanding symbiont replacements and recent symbioses. However, almost all of our knowledge about the evolution and functions of Euplotes symbioses comes from the Euplotes-Polynucleobacter system. In this article, we report a novel essential symbiont, which also has very close free-living relatives. Genome analysis indicated that it is a recently established endosymbiont undergoing genome erosion and relies on the Euplotes host for many essential molecules. Our results provide support for the notion that essential symbionts of the ciliate Euplotes evolve from free-living progenitors in the natural water environment.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Phylogeny
Symbiosis/genetics
*Euplotes/genetics/microbiology
*Betaproteobacteria/genetics
Bacteria/genetics
Genome, Bacterial
Genomics
RevDate: 2024-07-12
CmpDate: 2024-07-12
Chemotherapy Assessment in Advanced Multicellular 3D Models of Pancreatic Cancer: Unravelling the Importance of Spatiotemporal Mimicry of the Tumor Microenvironment.
Advanced biology, 8(7):e2300580.
Pancreatic ductal adenocarcinoma (PDAC) is a challenge for global health with very low survival rate and high therapeutic resistance. Hence, advanced preclinical models for treatment screening are of paramount importance. Herein, chemotherapeutic (gemcitabine) assessment on novel (polyurethane) scaffold-based spatially advanced 3D multicellular PDAC models is carried out. Through comprehensive image-based analysis at the protein level, and expression analysis at the mRNA level, the importance of stromal cells is confirmed, primarily activated stellate cells in the chemoresistance of PDAC cells within the models. Furthermore, it is demonstrated that, in addition to the presence of activated stellate cells, the spatial architecture of the scaffolds, i.e., segregation/compartmentalization of the cancer and stromal zones, affect the cellular evolution and is necessary for the development of chemoresistance. These results highlight that, further to multicellularity, mapping the tumor structure/architecture and zonal complexity in 3D cancer models is important for better mimicry of the in vivo therapeutic response.
Additional Links: PMID-38327154
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PubMed:
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@article {pmid38327154,
year = {2024},
author = {Gupta, P and Bermejo-Rodriguez, C and Kocher, H and Pérez-Mancera, PA and Velliou, EG},
title = {Chemotherapy Assessment in Advanced Multicellular 3D Models of Pancreatic Cancer: Unravelling the Importance of Spatiotemporal Mimicry of the Tumor Microenvironment.},
journal = {Advanced biology},
volume = {8},
number = {7},
pages = {e2300580},
doi = {10.1002/adbi.202300580},
pmid = {38327154},
issn = {2701-0198},
support = {MR/V028553/1/MRC_/Medical Research Council/United Kingdom ; MR/R025762/1//3D bioNet UKRI/ ; NC/V001167/1//National Centre for the Replacement Refinement and Reduction of Animals in Research/ ; },
mesh = {*Tumor Microenvironment/drug effects ; Humans ; *Pancreatic Neoplasms/drug therapy/pathology/genetics ; *Carcinoma, Pancreatic Ductal/drug therapy/pathology ; Deoxycytidine/analogs & derivatives/pharmacology/therapeutic use ; Cell Line, Tumor ; Gemcitabine ; Drug Resistance, Neoplasm ; Tissue Scaffolds ; },
abstract = {Pancreatic ductal adenocarcinoma (PDAC) is a challenge for global health with very low survival rate and high therapeutic resistance. Hence, advanced preclinical models for treatment screening are of paramount importance. Herein, chemotherapeutic (gemcitabine) assessment on novel (polyurethane) scaffold-based spatially advanced 3D multicellular PDAC models is carried out. Through comprehensive image-based analysis at the protein level, and expression analysis at the mRNA level, the importance of stromal cells is confirmed, primarily activated stellate cells in the chemoresistance of PDAC cells within the models. Furthermore, it is demonstrated that, in addition to the presence of activated stellate cells, the spatial architecture of the scaffolds, i.e., segregation/compartmentalization of the cancer and stromal zones, affect the cellular evolution and is necessary for the development of chemoresistance. These results highlight that, further to multicellularity, mapping the tumor structure/architecture and zonal complexity in 3D cancer models is important for better mimicry of the in vivo therapeutic response.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Tumor Microenvironment/drug effects
Humans
*Pancreatic Neoplasms/drug therapy/pathology/genetics
*Carcinoma, Pancreatic Ductal/drug therapy/pathology
Deoxycytidine/analogs & derivatives/pharmacology/therapeutic use
Cell Line, Tumor
Gemcitabine
Drug Resistance, Neoplasm
Tissue Scaffolds
RevDate: 2024-03-01
CmpDate: 2024-03-01
Conservation of Affinity Rather Than Sequence Underlies a Dynamic Evolution of the Motif-Mediated p53/MDM2 Interaction in Ray-Finned Fishes.
Molecular biology and evolution, 41(2):.
The transcription factor and cell cycle regulator p53 is marked for degradation by the ubiquitin ligase MDM2. The interaction between these 2 proteins is mediated by a conserved binding motif in the disordered p53 transactivation domain (p53TAD) and the folded SWIB domain in MDM2. The conserved motif in p53TAD from zebrafish displays a 20-fold weaker interaction with MDM2, compared to the interaction in human and chicken. To investigate this apparent difference, we tracked the molecular evolution of the p53TAD/MDM2 interaction among ray-finned fishes (Actinopterygii), the largest vertebrate clade. Intriguingly, phylogenetic analyses, ancestral sequence reconstructions, and binding experiments showed that different loss-of-affinity changes in the canonical binding motif within p53TAD have occurred repeatedly and convergently in different fish lineages, resulting in relatively low extant affinities (KD = 0.5 to 5 μM). However, for 11 different fish p53TAD/MDM2 interactions, nonconserved regions flanking the canonical motif increased the affinity 4- to 73-fold to be on par with the human interaction. Our findings suggest that compensating changes at conserved and nonconserved positions within the motif, as well as in flanking regions of low conservation, underlie a stabilizing selection of "functional affinity" in the p53TAD/MDM2 interaction. Such interplay complicates bioinformatic prediction of binding and calls for experimental validation. Motif-mediated protein-protein interactions involving short binding motifs and folded interaction domains are very common across multicellular life. It is likely that the evolution of affinity in motif-mediated interactions often involves an interplay between specific interactions made by conserved motif residues and nonspecific interactions by nonconserved disordered regions.
Additional Links: PMID-38301272
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Citation:
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@article {pmid38301272,
year = {2024},
author = {Mihalič, F and Arcila, D and Pettersson, ME and Farkhondehkish, P and Andersson, E and Andersson, L and Betancur-R, R and Jemth, P},
title = {Conservation of Affinity Rather Than Sequence Underlies a Dynamic Evolution of the Motif-Mediated p53/MDM2 Interaction in Ray-Finned Fishes.},
journal = {Molecular biology and evolution},
volume = {41},
number = {2},
pages = {},
pmid = {38301272},
issn = {1537-1719},
mesh = {Animals ; Humans ; *Tumor Suppressor Protein p53/genetics/chemistry/metabolism ; *Zebrafish ; Phylogeny ; Protein Structure, Tertiary ; Protein Binding ; Proto-Oncogene Proteins c-mdm2/genetics/chemistry/metabolism ; },
abstract = {The transcription factor and cell cycle regulator p53 is marked for degradation by the ubiquitin ligase MDM2. The interaction between these 2 proteins is mediated by a conserved binding motif in the disordered p53 transactivation domain (p53TAD) and the folded SWIB domain in MDM2. The conserved motif in p53TAD from zebrafish displays a 20-fold weaker interaction with MDM2, compared to the interaction in human and chicken. To investigate this apparent difference, we tracked the molecular evolution of the p53TAD/MDM2 interaction among ray-finned fishes (Actinopterygii), the largest vertebrate clade. Intriguingly, phylogenetic analyses, ancestral sequence reconstructions, and binding experiments showed that different loss-of-affinity changes in the canonical binding motif within p53TAD have occurred repeatedly and convergently in different fish lineages, resulting in relatively low extant affinities (KD = 0.5 to 5 μM). However, for 11 different fish p53TAD/MDM2 interactions, nonconserved regions flanking the canonical motif increased the affinity 4- to 73-fold to be on par with the human interaction. Our findings suggest that compensating changes at conserved and nonconserved positions within the motif, as well as in flanking regions of low conservation, underlie a stabilizing selection of "functional affinity" in the p53TAD/MDM2 interaction. Such interplay complicates bioinformatic prediction of binding and calls for experimental validation. Motif-mediated protein-protein interactions involving short binding motifs and folded interaction domains are very common across multicellular life. It is likely that the evolution of affinity in motif-mediated interactions often involves an interplay between specific interactions made by conserved motif residues and nonspecific interactions by nonconserved disordered regions.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
Humans
*Tumor Suppressor Protein p53/genetics/chemistry/metabolism
*Zebrafish
Phylogeny
Protein Structure, Tertiary
Protein Binding
Proto-Oncogene Proteins c-mdm2/genetics/chemistry/metabolism
RevDate: 2024-02-06
CmpDate: 2024-01-26
Colony level fitness analysis identifies a trade-off between population growth rate and dauer yield in Caenorhabditis elegans.
BMC ecology and evolution, 24(1):13.
BACKGROUND: In the evolution from unicellular to multicellular life forms, natural selection favored reduced cell proliferation and even programmed cell death if this increased organismal fitness. Could reduced individual fertility or even programmed organismal death similarly increase the fitness of colonies of closely-related metazoan organisms? This possibility is at least consistent with evolutionary theory, and has been supported by computer modelling. Caenorhabditis elegans has a boom and bust life history, where populations of nematodes that are sometimes near clonal subsist on and consume food patches, and then generate dauer larva dispersal propagules. A recent study of an in silico model of C. elegans predicted that one determinant of colony fitness (measured as dauer yield) is minimization of futile food consumption (i.e. that which does not contribute to dauer yield). One way to achieve this is to optimize colony population structure by adjustment of individual fertility.
RESULTS: Here we describe development of a C. elegans colony fitness assay, and its use to investigate the effect of altering population structure on colony fitness after population bust. Fitness metrics measured were speed of dauer production, and dauer yield, an indirect measure of efficiency of resource utilization (i.e. conversion of food into dauers). We find that with increasing founder number, speed of dauer production increases (due to earlier bust) but dauer yield rises and falls. In addition, some dauer recovery was detected soon after the post-colony bust peak of dauer yield, suggesting possible bet hedging among dauers.
CONCLUSIONS: These results suggest the presence of a fitness trade-off at colony level between speed and efficiency of resource utilization in C. elegans. They also provide indirect evidence that population structure is a determinant of colony level fitness, potentially by affecting level of futile food consumption.
Additional Links: PMID-38267842
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Citation:
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@article {pmid38267842,
year = {2024},
author = {Chapman, H and Hsiung, KC and Rawlinson, I and Galimov, ER and Gems, D},
title = {Colony level fitness analysis identifies a trade-off between population growth rate and dauer yield in Caenorhabditis elegans.},
journal = {BMC ecology and evolution},
volume = {24},
number = {1},
pages = {13},
pmid = {38267842},
issn = {2730-7182},
mesh = {Animals ; *Caenorhabditis elegans ; *Population Growth ; Apoptosis ; Benchmarking ; Biological Assay ; },
abstract = {BACKGROUND: In the evolution from unicellular to multicellular life forms, natural selection favored reduced cell proliferation and even programmed cell death if this increased organismal fitness. Could reduced individual fertility or even programmed organismal death similarly increase the fitness of colonies of closely-related metazoan organisms? This possibility is at least consistent with evolutionary theory, and has been supported by computer modelling. Caenorhabditis elegans has a boom and bust life history, where populations of nematodes that are sometimes near clonal subsist on and consume food patches, and then generate dauer larva dispersal propagules. A recent study of an in silico model of C. elegans predicted that one determinant of colony fitness (measured as dauer yield) is minimization of futile food consumption (i.e. that which does not contribute to dauer yield). One way to achieve this is to optimize colony population structure by adjustment of individual fertility.
RESULTS: Here we describe development of a C. elegans colony fitness assay, and its use to investigate the effect of altering population structure on colony fitness after population bust. Fitness metrics measured were speed of dauer production, and dauer yield, an indirect measure of efficiency of resource utilization (i.e. conversion of food into dauers). We find that with increasing founder number, speed of dauer production increases (due to earlier bust) but dauer yield rises and falls. In addition, some dauer recovery was detected soon after the post-colony bust peak of dauer yield, suggesting possible bet hedging among dauers.
CONCLUSIONS: These results suggest the presence of a fitness trade-off at colony level between speed and efficiency of resource utilization in C. elegans. They also provide indirect evidence that population structure is a determinant of colony level fitness, potentially by affecting level of futile food consumption.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Caenorhabditis elegans
*Population Growth
Apoptosis
Benchmarking
Biological Assay
RevDate: 2024-06-17
CmpDate: 2024-01-24
From Churchill to Elephants: The Role of Protective Genes against Cancer.
Genes, 15(1):.
Richard Peto's paradox, first described in 1975 from an epidemiological perspective, established an inverse correlation between the probability of developing cancer in multicellular organisms and the number of cells. Larger animals exhibit fewer tumors compared to smaller ones, though exceptions exist. Mice are more susceptible to cancer than humans, while elephants and whales demonstrate significantly lower cancer prevalence rates than humans. How nature and evolution have addressed the issue of cancer in the animal kingdom remains largely unexplored. In the field of medicine, much attention has been devoted to cancer-predisposing genes, as they offer avenues for intervention, including blocking, downregulating, early diagnosis, and targeted treatment. Predisposing genes also tend to manifest clinically earlier and more aggressively, making them easier to identify. However, despite significant strides in modern medicine, the role of protective genes lags behind. Identifying genes with a mild predisposing effect poses a significant challenge. Consequently, comprehending the protective function conferred by genes becomes even more elusive, and their very existence is subject to questioning. While the role of variable expressivity and penetrance defects of the same variant in a family is well-documented for many hereditary cancer syndromes, attempts to delineate the function of protective/modifier alleles have been restricted to a few instances. In this review, we endeavor to elucidate the role of protective genes observed in the animal kingdom, within certain genetic syndromes that appear to act as cancer-resistant/repressor alleles. Additionally, we explore the role of protective alleles in conditions predisposing to cancer. The ultimate goal is to discern why individuals, like Winston Churchill, managed to live up to 91 years of age, despite engaging in minimal physical activity, consuming large quantities of alcohol daily, and not abstaining from smoking.
Additional Links: PMID-38255007
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Citation:
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@article {pmid38255007,
year = {2024},
author = {Gazzellone, A and Sangiorgi, E},
title = {From Churchill to Elephants: The Role of Protective Genes against Cancer.},
journal = {Genes},
volume = {15},
number = {1},
pages = {},
pmid = {38255007},
issn = {2073-4425},
mesh = {Humans ; Animals ; Mice ; *Elephants/genetics ; Alleles ; *Neoplastic Syndromes, Hereditary ; *Medicine ; Cetacea ; },
abstract = {Richard Peto's paradox, first described in 1975 from an epidemiological perspective, established an inverse correlation between the probability of developing cancer in multicellular organisms and the number of cells. Larger animals exhibit fewer tumors compared to smaller ones, though exceptions exist. Mice are more susceptible to cancer than humans, while elephants and whales demonstrate significantly lower cancer prevalence rates than humans. How nature and evolution have addressed the issue of cancer in the animal kingdom remains largely unexplored. In the field of medicine, much attention has been devoted to cancer-predisposing genes, as they offer avenues for intervention, including blocking, downregulating, early diagnosis, and targeted treatment. Predisposing genes also tend to manifest clinically earlier and more aggressively, making them easier to identify. However, despite significant strides in modern medicine, the role of protective genes lags behind. Identifying genes with a mild predisposing effect poses a significant challenge. Consequently, comprehending the protective function conferred by genes becomes even more elusive, and their very existence is subject to questioning. While the role of variable expressivity and penetrance defects of the same variant in a family is well-documented for many hereditary cancer syndromes, attempts to delineate the function of protective/modifier alleles have been restricted to a few instances. In this review, we endeavor to elucidate the role of protective genes observed in the animal kingdom, within certain genetic syndromes that appear to act as cancer-resistant/repressor alleles. Additionally, we explore the role of protective alleles in conditions predisposing to cancer. The ultimate goal is to discern why individuals, like Winston Churchill, managed to live up to 91 years of age, despite engaging in minimal physical activity, consuming large quantities of alcohol daily, and not abstaining from smoking.},
}
MeSH Terms:
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hide MeSH Terms
Humans
Animals
Mice
*Elephants/genetics
Alleles
*Neoplastic Syndromes, Hereditary
*Medicine
Cetacea
RevDate: 2024-05-23
CmpDate: 2024-02-08
Phylogenomic insights into the first multicellular streptophyte.
Current biology : CB, 34(3):670-681.e7.
Streptophytes are best known as the clade containing the teeming diversity of embryophytes (land plants).[1][,][2][,][3][,][4] Next to embryophytes are however a range of freshwater and terrestrial algae that bear important information on the emergence of key traits of land plants. Among these, the Klebsormidiophyceae stand out. Thriving in diverse environments-from mundane (ubiquitous occurrence on tree barks and rocks) to extreme (from the Atacama Desert to the Antarctic)-Klebsormidiophyceae can exhibit filamentous body plans and display remarkable resilience as colonizers of terrestrial habitats.[5][,][6] Currently, the lack of a robust phylogenetic framework for the Klebsormidiophyceae hampers our understanding of the evolutionary history of these key traits. Here, we conducted a phylogenomic analysis utilizing advanced models that can counteract systematic biases. We sequenced 24 new transcriptomes of Klebsormidiophyceae and combined them with 14 previously published genomic and transcriptomic datasets. Using an analysis built on 845 loci and sophisticated mixture models, we establish a phylogenomic framework, dividing the six distinct genera of Klebsormidiophyceae in a novel three-order system, with a deep divergence more than 830 million years ago. Our reconstructions of ancestral states suggest (1) an evolutionary history of multiple transitions between terrestrial-aquatic habitats, with stem Klebsormidiales having conquered land earlier than embryophytes, and (2) that the body plan of the last common ancestor of Klebsormidiophyceae was multicellular, with a high probability that it was filamentous whereas the sarcinoids and unicells in Klebsormidiophyceae are likely derived states. We provide evidence that the first multicellular streptophytes likely lived about a billion years ago.
Additional Links: PMID-38244543
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@article {pmid38244543,
year = {2024},
author = {Bierenbroodspot, MJ and Darienko, T and de Vries, S and Fürst-Jansen, JMR and Buschmann, H and Pröschold, T and Irisarri, I and de Vries, J},
title = {Phylogenomic insights into the first multicellular streptophyte.},
journal = {Current biology : CB},
volume = {34},
number = {3},
pages = {670-681.e7},
pmid = {38244543},
issn = {1879-0445},
mesh = {Phylogeny ; Biological Evolution ; Plants/genetics ; *Embryophyta/genetics ; *Streptophyta ; },
abstract = {Streptophytes are best known as the clade containing the teeming diversity of embryophytes (land plants).[1][,][2][,][3][,][4] Next to embryophytes are however a range of freshwater and terrestrial algae that bear important information on the emergence of key traits of land plants. Among these, the Klebsormidiophyceae stand out. Thriving in diverse environments-from mundane (ubiquitous occurrence on tree barks and rocks) to extreme (from the Atacama Desert to the Antarctic)-Klebsormidiophyceae can exhibit filamentous body plans and display remarkable resilience as colonizers of terrestrial habitats.[5][,][6] Currently, the lack of a robust phylogenetic framework for the Klebsormidiophyceae hampers our understanding of the evolutionary history of these key traits. Here, we conducted a phylogenomic analysis utilizing advanced models that can counteract systematic biases. We sequenced 24 new transcriptomes of Klebsormidiophyceae and combined them with 14 previously published genomic and transcriptomic datasets. Using an analysis built on 845 loci and sophisticated mixture models, we establish a phylogenomic framework, dividing the six distinct genera of Klebsormidiophyceae in a novel three-order system, with a deep divergence more than 830 million years ago. Our reconstructions of ancestral states suggest (1) an evolutionary history of multiple transitions between terrestrial-aquatic habitats, with stem Klebsormidiales having conquered land earlier than embryophytes, and (2) that the body plan of the last common ancestor of Klebsormidiophyceae was multicellular, with a high probability that it was filamentous whereas the sarcinoids and unicells in Klebsormidiophyceae are likely derived states. We provide evidence that the first multicellular streptophytes likely lived about a billion years ago.},
}
MeSH Terms:
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Phylogeny
Biological Evolution
Plants/genetics
*Embryophyta/genetics
*Streptophyta
RevDate: 2024-06-24
CmpDate: 2024-04-27
Globin phylogeny, evolution and function, the newest update.
Proteins, 92(6):720-734.
Our globin census update allows us to refine our vision of globin origin, evolution, and structure to function relationship in the context of the currently accepted tree of life. The modern globin domain originates as a single domain, three-over-three α-helical folded structure before the diversification of the kingdoms of life (Bacteria, Archaea, Eukarya). Together with the diversification of prokaryotes, three monophyletic globin families (M, S, and T) emerged, most likely in Proteobacteria and Actinobacteria, displaying specific sequence and structural features, and spread by vertical and horizontal gene transfer, most probably already present in the last universal common ancestor (LUCA). Non-globin domains were added, and eventually lost again, creating multi-domain structures in key branches of M- (FHb and Adgb) and the vast majority of S globins, which with their coevolved multi-domain architectures, have predominantly "sensor" functions. Single domain T-family globins diverged into four major groups and most likely display functions related to reactive nitrogen and oxygen species (RNOS) chemistry, as well as oxygen storage/transport which drives the evolution of its major branches with their characteristic key distal residues (B10, E11, E7, and G8). M-family evolution also lead to distinctive major types (FHb and Fgb, Ngb, Adgb, GbX vertebrate Gbs), and shows the shift from high oxygen affinity controlled by TyrB10-Gln/AsnE11 likely related to RNOS chemistry in microorganisms, to a moderate oxygen affinity storage/transport function controlled by hydrophobic B10/E11-HisE7 in multicellular animals.
Additional Links: PMID-38192262
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PubMed:
Citation:
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@article {pmid38192262,
year = {2024},
author = {Schuster, CD and Salvatore, F and Moens, L and Martí, MA},
title = {Globin phylogeny, evolution and function, the newest update.},
journal = {Proteins},
volume = {92},
number = {6},
pages = {720-734},
doi = {10.1002/prot.26659},
pmid = {38192262},
issn = {1097-0134},
mesh = {*Globins/genetics/chemistry/metabolism ; *Phylogeny ; *Evolution, Molecular ; Humans ; Bacteria/genetics/metabolism ; Animals ; Archaea/genetics/metabolism ; Protein Domains ; Gene Transfer, Horizontal ; },
abstract = {Our globin census update allows us to refine our vision of globin origin, evolution, and structure to function relationship in the context of the currently accepted tree of life. The modern globin domain originates as a single domain, three-over-three α-helical folded structure before the diversification of the kingdoms of life (Bacteria, Archaea, Eukarya). Together with the diversification of prokaryotes, three monophyletic globin families (M, S, and T) emerged, most likely in Proteobacteria and Actinobacteria, displaying specific sequence and structural features, and spread by vertical and horizontal gene transfer, most probably already present in the last universal common ancestor (LUCA). Non-globin domains were added, and eventually lost again, creating multi-domain structures in key branches of M- (FHb and Adgb) and the vast majority of S globins, which with their coevolved multi-domain architectures, have predominantly "sensor" functions. Single domain T-family globins diverged into four major groups and most likely display functions related to reactive nitrogen and oxygen species (RNOS) chemistry, as well as oxygen storage/transport which drives the evolution of its major branches with their characteristic key distal residues (B10, E11, E7, and G8). M-family evolution also lead to distinctive major types (FHb and Fgb, Ngb, Adgb, GbX vertebrate Gbs), and shows the shift from high oxygen affinity controlled by TyrB10-Gln/AsnE11 likely related to RNOS chemistry in microorganisms, to a moderate oxygen affinity storage/transport function controlled by hydrophobic B10/E11-HisE7 in multicellular animals.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Globins/genetics/chemistry/metabolism
*Phylogeny
*Evolution, Molecular
Humans
Bacteria/genetics/metabolism
Animals
Archaea/genetics/metabolism
Protein Domains
Gene Transfer, Horizontal
RevDate: 2024-01-11
CmpDate: 2024-01-08
Adaptive advantages of restorative RNA editing in fungi for resolving survival-reproduction trade-offs.
Science advances, 10(1):eadk6130.
RNA editing in various organisms commonly restores RNA sequences to their ancestral state, but its adaptive advantages are debated. In fungi, restorative editing corrects premature stop codons in pseudogenes specifically during sexual reproduction. We characterized 71 pseudogenes and their restorative editing in Fusarium graminearum, demonstrating that restorative editing of 16 pseudogenes is crucial for germ tissue development in fruiting bodies. Our results also revealed that the emergence of premature stop codons is facilitated by restorative editing and that premature stop codons corrected by restorative editing are selectively favored over ancestral amino acid codons. Furthermore, we found that ancestral versions of pseudogenes have antagonistic effects on reproduction and survival. Restorative editing eliminates the survival costs of reproduction caused by antagonistic pleiotropy and provides a selective advantage in fungi. Our findings highlight the importance of restorative editing in the evolution of fungal complex multicellularity and provide empirical evidence that restorative editing serves as an adaptive mechanism enabling the resolution of genetic trade-offs.
Additional Links: PMID-38181075
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@article {pmid38181075,
year = {2024},
author = {Qi, Z and Lu, P and Long, X and Cao, X and Wu, M and Xin, K and Xue, T and Gao, X and Huang, Y and Wang, Q and Jiang, C and Xu, JR and Liu, H},
title = {Adaptive advantages of restorative RNA editing in fungi for resolving survival-reproduction trade-offs.},
journal = {Science advances},
volume = {10},
number = {1},
pages = {eadk6130},
pmid = {38181075},
issn = {2375-2548},
mesh = {*Codon, Nonsense ; RNA Editing/genetics ; Amino Acids ; *Magnoliopsida ; Reproduction ; },
abstract = {RNA editing in various organisms commonly restores RNA sequences to their ancestral state, but its adaptive advantages are debated. In fungi, restorative editing corrects premature stop codons in pseudogenes specifically during sexual reproduction. We characterized 71 pseudogenes and their restorative editing in Fusarium graminearum, demonstrating that restorative editing of 16 pseudogenes is crucial for germ tissue development in fruiting bodies. Our results also revealed that the emergence of premature stop codons is facilitated by restorative editing and that premature stop codons corrected by restorative editing are selectively favored over ancestral amino acid codons. Furthermore, we found that ancestral versions of pseudogenes have antagonistic effects on reproduction and survival. Restorative editing eliminates the survival costs of reproduction caused by antagonistic pleiotropy and provides a selective advantage in fungi. Our findings highlight the importance of restorative editing in the evolution of fungal complex multicellularity and provide empirical evidence that restorative editing serves as an adaptive mechanism enabling the resolution of genetic trade-offs.},
}
MeSH Terms:
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*Codon, Nonsense
RNA Editing/genetics
Amino Acids
*Magnoliopsida
Reproduction
RevDate: 2024-01-18
CmpDate: 2024-01-16
Long-run real-time PCR analysis of repetitive nuclear elements as a novel tool for DNA damage quantification in single cells: an approach validated on mouse oocytes and fibroblasts.
Journal of applied genetics, 65(1):181-190.
Since DNA damage is of great importance in various biological processes, its rate is frequently assessed both in research studies and in medical diagnostics. The most precise methods of quantifying DNA damage are based on real-time PCR. However, in the conventional version, they require a large amount of genetic material and therefore their usefulness is limited to multicellular samples. Here, we present a novel approach to long-run real-time PCR-based DNA-damage quantification (L1-LORD-Q), which consists in amplification of long interspersed nuclear elements (L1) and allows for analysis of single-cell genomes. The L1-LORD-Q was compared with alternative methods of measuring DNA breaks (Bioanalyzer system, γ-H2AX foci staining), which confirmed its accuracy. Furthermore, it was demonstrated that the L1-LORD-Q is sensitive enough to distinguish between different levels of UV-induced DNA damage. The method was validated on mouse oocytes and fibroblasts, but the general idea is universal and can be applied to various types of cells and species.
Additional Links: PMID-38110826
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@article {pmid38110826,
year = {2024},
author = {Kotarska, K and Gąsior, Ł and Rudnicka, J and Polański, Z},
title = {Long-run real-time PCR analysis of repetitive nuclear elements as a novel tool for DNA damage quantification in single cells: an approach validated on mouse oocytes and fibroblasts.},
journal = {Journal of applied genetics},
volume = {65},
number = {1},
pages = {181-190},
pmid = {38110826},
issn = {2190-3883},
support = {2019/03/X/NZ3/00572//Narodowe Centrum Nauki/ ; },
mesh = {Animals ; Mice ; Real-Time Polymerase Chain Reaction ; *DNA Damage/genetics ; *Fibroblasts ; Oocytes ; Genome ; },
abstract = {Since DNA damage is of great importance in various biological processes, its rate is frequently assessed both in research studies and in medical diagnostics. The most precise methods of quantifying DNA damage are based on real-time PCR. However, in the conventional version, they require a large amount of genetic material and therefore their usefulness is limited to multicellular samples. Here, we present a novel approach to long-run real-time PCR-based DNA-damage quantification (L1-LORD-Q), which consists in amplification of long interspersed nuclear elements (L1) and allows for analysis of single-cell genomes. The L1-LORD-Q was compared with alternative methods of measuring DNA breaks (Bioanalyzer system, γ-H2AX foci staining), which confirmed its accuracy. Furthermore, it was demonstrated that the L1-LORD-Q is sensitive enough to distinguish between different levels of UV-induced DNA damage. The method was validated on mouse oocytes and fibroblasts, but the general idea is universal and can be applied to various types of cells and species.},
}
MeSH Terms:
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Animals
Mice
Real-Time Polymerase Chain Reaction
*DNA Damage/genetics
*Fibroblasts
Oocytes
Genome
RevDate: 2024-04-08
CmpDate: 2024-04-08
Re-examining meristems through the lens of evo-devo.
Trends in plant science, 29(4):413-427.
The concept of the meristem was introduced in 1858 to characterize multicellular, formative, and proliferative tissues that give rise to the entire plant body, based on observations of vascular plants. Although its original definition did not encompass bryophytes, this concept has been used and continuously refined over the past 165 years to describe the diverse apices of all land plants. Here, we re-examine this matter in light of recent evo-devo research and show that, despite displaying high anatomical diversity, land plant meristems are unified by shared genetic control. We also propose a modular view of meristem function and highlight multiple evolutionary mechanisms that are likely to have contributed to the assembly and diversification of the varied meristems during the course of plant evolution.
Additional Links: PMID-38040554
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@article {pmid38040554,
year = {2024},
author = {Arnoux-Courseaux, M and Coudert, Y},
title = {Re-examining meristems through the lens of evo-devo.},
journal = {Trends in plant science},
volume = {29},
number = {4},
pages = {413-427},
doi = {10.1016/j.tplants.2023.11.003},
pmid = {38040554},
issn = {1878-4372},
mesh = {*Meristem/genetics ; *Plant Proteins/genetics ; Plants/genetics ; },
abstract = {The concept of the meristem was introduced in 1858 to characterize multicellular, formative, and proliferative tissues that give rise to the entire plant body, based on observations of vascular plants. Although its original definition did not encompass bryophytes, this concept has been used and continuously refined over the past 165 years to describe the diverse apices of all land plants. Here, we re-examine this matter in light of recent evo-devo research and show that, despite displaying high anatomical diversity, land plant meristems are unified by shared genetic control. We also propose a modular view of meristem function and highlight multiple evolutionary mechanisms that are likely to have contributed to the assembly and diversification of the varied meristems during the course of plant evolution.},
}
MeSH Terms:
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*Meristem/genetics
*Plant Proteins/genetics
Plants/genetics
RevDate: 2024-06-20
CmpDate: 2023-11-27
Genetic Interactions in Various Environmental Conditions in Caenorhabditis elegans.
Genes, 14(11):.
Although it is well known that epistasis plays an important role in many evolutionary processes (e.g., speciation, evolution of sex), our knowledge on the frequency and prevalent sign of epistatic interactions is mainly limited to unicellular organisms or cell cultures of multicellular organisms. This is even more pronounced in regard to how the environment can influence genetic interactions. To broaden our knowledge in that respect we studied gene-gene interactions in a whole multicellular organism, Caenorhabditis elegans. We screened over one thousand gene interactions, each one in standard laboratory conditions, and under three different stressors: heat shock, oxidative stress, and genotoxic stress. Depending on the condition, between 7% and 22% of gene pairs showed significant genetic interactions and an overall sign of epistasis changed depending on the condition. Sign epistasis was quite common, but reciprocal sign epistasis was extremally rare. One interaction was common to all conditions, whereas 78% of interactions were specific to only one environment. Although epistatic interactions are quite common, their impact on evolutionary processes will strongly depend on environmental factors.
Additional Links: PMID-38003023
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@article {pmid38003023,
year = {2023},
author = {Toch, K and Buczek, M and Labocha, MK},
title = {Genetic Interactions in Various Environmental Conditions in Caenorhabditis elegans.},
journal = {Genes},
volume = {14},
number = {11},
pages = {},
pmid = {38003023},
issn = {2073-4425},
support = {P40 OD010440/OD/NIH HHS/United States ; },
mesh = {Animals ; *Caenorhabditis elegans/genetics ; *Epistasis, Genetic ; },
abstract = {Although it is well known that epistasis plays an important role in many evolutionary processes (e.g., speciation, evolution of sex), our knowledge on the frequency and prevalent sign of epistatic interactions is mainly limited to unicellular organisms or cell cultures of multicellular organisms. This is even more pronounced in regard to how the environment can influence genetic interactions. To broaden our knowledge in that respect we studied gene-gene interactions in a whole multicellular organism, Caenorhabditis elegans. We screened over one thousand gene interactions, each one in standard laboratory conditions, and under three different stressors: heat shock, oxidative stress, and genotoxic stress. Depending on the condition, between 7% and 22% of gene pairs showed significant genetic interactions and an overall sign of epistasis changed depending on the condition. Sign epistasis was quite common, but reciprocal sign epistasis was extremally rare. One interaction was common to all conditions, whereas 78% of interactions were specific to only one environment. Although epistatic interactions are quite common, their impact on evolutionary processes will strongly depend on environmental factors.},
}
MeSH Terms:
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Animals
*Caenorhabditis elegans/genetics
*Epistasis, Genetic
RevDate: 2023-11-24
CmpDate: 2023-11-23
Genome-wide identification and characteristic analysis of ETS gene family in blood clam Tegillarca granosa.
BMC genomics, 24(1):700.
BACKGROUND: ETS transcription factors, known as the E26 transformation-specific factors, assume a critical role in the regulation of various vital biological processes in animals, including cell differentiation, the cell cycle, and cell apoptosis. However, their characterization in mollusks is currently lacking.
RESULTS: The current study focused on a comprehensive analysis of the ETS genes in blood clam Tegillarca granosa and other mollusk genomes. Our phylogenetic analysis revealed the absence of the SPI and ETV subfamilies in mollusks compared to humans. Additionally, several ETS genes in mollusks were found to lack the PNT domain, potentially resulting in a diminished ability of ETS proteins to bind target genes. Interestingly, the bivalve ETS1 genes exhibited significantly high expression levels during the multicellular proliferation stage and in gill tissues. Furthermore, qRT-PCR results showed that Tg-ETS-14 (ETS1) is upregulated in the high total hemocyte counts (THC) population of T. granosa, suggesting it plays a significant role in stimulating hemocyte proliferation.
CONCLUSION: Our study significantly contributes to the comprehension of the evolutionary aspects concerning the ETS gene family, while also providing valuable insights into its role in fostering hemocyte proliferation across mollusks.
Additional Links: PMID-37990147
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@article {pmid37990147,
year = {2023},
author = {Jin, H and Zhang, W and Liu, H and Bao, Y},
title = {Genome-wide identification and characteristic analysis of ETS gene family in blood clam Tegillarca granosa.},
journal = {BMC genomics},
volume = {24},
number = {1},
pages = {700},
pmid = {37990147},
issn = {1471-2164},
support = {LZ20C190001//Key Natural Science Foundation of Zhejiang/ ; 32273123//National Science Foundation of China/ ; 2021C02069-7//Zhejiang Major Program of Science and Technology/ ; LQ23C190007//Science Foundation of Zhejiang/ ; 2021S014//Ningbo Public Benefit Research Key Project/ ; },
mesh = {Humans ; Animals ; Phylogeny ; *Arcidae/genetics/metabolism ; Proto-Oncogene Proteins c-ets/genetics/metabolism ; Genome ; *Bivalvia/genetics ; },
abstract = {BACKGROUND: ETS transcription factors, known as the E26 transformation-specific factors, assume a critical role in the regulation of various vital biological processes in animals, including cell differentiation, the cell cycle, and cell apoptosis. However, their characterization in mollusks is currently lacking.
RESULTS: The current study focused on a comprehensive analysis of the ETS genes in blood clam Tegillarca granosa and other mollusk genomes. Our phylogenetic analysis revealed the absence of the SPI and ETV subfamilies in mollusks compared to humans. Additionally, several ETS genes in mollusks were found to lack the PNT domain, potentially resulting in a diminished ability of ETS proteins to bind target genes. Interestingly, the bivalve ETS1 genes exhibited significantly high expression levels during the multicellular proliferation stage and in gill tissues. Furthermore, qRT-PCR results showed that Tg-ETS-14 (ETS1) is upregulated in the high total hemocyte counts (THC) population of T. granosa, suggesting it plays a significant role in stimulating hemocyte proliferation.
CONCLUSION: Our study significantly contributes to the comprehension of the evolutionary aspects concerning the ETS gene family, while also providing valuable insights into its role in fostering hemocyte proliferation across mollusks.},
}
MeSH Terms:
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Humans
Animals
Phylogeny
*Arcidae/genetics/metabolism
Proto-Oncogene Proteins c-ets/genetics/metabolism
Genome
*Bivalvia/genetics
RevDate: 2024-02-28
CmpDate: 2024-02-27
Thermoprotection by a cell membrane-localized metacaspase in a green alga.
The Plant cell, 36(3):665-687.
Caspases are restricted to animals, while other organisms, including plants, possess metacaspases (MCAs), a more ancient and broader class of structurally related yet biochemically distinct proteases. Our current understanding of plant MCAs is derived from studies in streptophytes, and mostly in Arabidopsis (Arabidopsis thaliana) with 9 MCAs with partially redundant activities. In contrast to streptophytes, most chlorophytes contain only 1 or 2 uncharacterized MCAs, providing an excellent platform for MCA research. Here we investigated CrMCA-II, the single type-II MCA from the model chlorophyte Chlamydomonas (Chlamydomonas reinhardtii). Surprisingly, unlike other studied MCAs and similar to caspases, CrMCA-II dimerizes both in vitro and in vivo. Furthermore, activation of CrMCA-II in vivo correlated with its dimerization. Most of CrMCA-II in the cell was present as a proenzyme (zymogen) attached to the plasma membrane (PM). Deletion of CrMCA-II by genome editing compromised thermotolerance, leading to increased cell death under heat stress. Adding back either wild-type or catalytically dead CrMCA-II restored thermoprotection, suggesting that its proteolytic activity is dispensable for this effect. Finally, we connected the non-proteolytic role of CrMCA-II in thermotolerance to the ability to modulate PM fluidity. Our study reveals an ancient, MCA-dependent thermotolerance mechanism retained by Chlamydomonas and probably lost during the evolution of multicellularity.
Additional Links: PMID-37971931
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@article {pmid37971931,
year = {2024},
author = {Zou, Y and Sabljić, I and Horbach, N and Dauphinee, AN and Åsman, A and Sancho Temino, L and Minina, EA and Drag, M and Stael, S and Poreba, M and Ståhlberg, J and Bozhkov, PV},
title = {Thermoprotection by a cell membrane-localized metacaspase in a green alga.},
journal = {The Plant cell},
volume = {36},
number = {3},
pages = {665-687},
pmid = {37971931},
issn = {1532-298X},
support = {//Knut and Alice Wallenberg Foundation/ ; //Swedish Research Council Vetenskapsrådet/ ; //National Science Centre in Poland/ ; },
mesh = {Animals ; Plants/metabolism ; Caspases/genetics/chemistry/metabolism ; *Arabidopsis/genetics ; Cell Membrane/metabolism ; *Chlorophyta ; },
abstract = {Caspases are restricted to animals, while other organisms, including plants, possess metacaspases (MCAs), a more ancient and broader class of structurally related yet biochemically distinct proteases. Our current understanding of plant MCAs is derived from studies in streptophytes, and mostly in Arabidopsis (Arabidopsis thaliana) with 9 MCAs with partially redundant activities. In contrast to streptophytes, most chlorophytes contain only 1 or 2 uncharacterized MCAs, providing an excellent platform for MCA research. Here we investigated CrMCA-II, the single type-II MCA from the model chlorophyte Chlamydomonas (Chlamydomonas reinhardtii). Surprisingly, unlike other studied MCAs and similar to caspases, CrMCA-II dimerizes both in vitro and in vivo. Furthermore, activation of CrMCA-II in vivo correlated with its dimerization. Most of CrMCA-II in the cell was present as a proenzyme (zymogen) attached to the plasma membrane (PM). Deletion of CrMCA-II by genome editing compromised thermotolerance, leading to increased cell death under heat stress. Adding back either wild-type or catalytically dead CrMCA-II restored thermoprotection, suggesting that its proteolytic activity is dispensable for this effect. Finally, we connected the non-proteolytic role of CrMCA-II in thermotolerance to the ability to modulate PM fluidity. Our study reveals an ancient, MCA-dependent thermotolerance mechanism retained by Chlamydomonas and probably lost during the evolution of multicellularity.},
}
MeSH Terms:
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Animals
Plants/metabolism
Caspases/genetics/chemistry/metabolism
*Arabidopsis/genetics
Cell Membrane/metabolism
*Chlorophyta
RevDate: 2024-02-14
CmpDate: 2024-02-14
Genome-wide identification of the mitogen-activated kinase gene family from Limonium bicolor and functional characterization of LbMAPK2 under salt stress.
BMC plant biology, 23(1):565.
BACKGROUND: Mitogen-activated protein kinases (MAPKs) are ubiquitous signal transduction components in eukaryotes. In plants, MAPKs play an essential role in growth and development, phytohormone regulation, and abiotic stress responses. The typical recretohalophyte Limonium bicolor (Bunge) Kuntze has multicellular salt glands on its stems and leaves; these glands secrete excess salt ions from its cells to mitigate salt damage. The number, type, and biological function of L. bicolor MAPK genes are unknown.
RESULTS: We identified 20 candidate L. bicolor MAPK genes, which can be divided into four groups. Of these 20 genes, 17 were anchored to 7 chromosomes, while LbMAPK18, LbMAPK19, and LbMAPK20 mapped to distinct scaffolds. Structure analysis showed that the predicted protein LbMAPK19 contains the special structural motif TNY in its activation loop, whereas the other LbMAPK members harbor the conserved TEY or TDY motif. The promoters of most LbMAPK genes carry cis-acting elements related to growth and development, phytohormones, and abiotic stress. LbMAPK1, LbMAPK2, LbMAPK16, and LbMAPK20 are highly expressed in the early stages of salt gland development, whereas LbMAPK4, LbMAPK5, LbMAPK6, LbMAPK7, LbMAPK11, LbMAPK14, and LbMAPK15 are highly expressed during the late stages. These 20 LbMAPK genes all responded to salt, drought and ABA stress. We explored the function of LbMAPK2 via virus-induced gene silencing: knocking down LbMAPK2 transcript levels in L. bicolor resulted in fewer salt glands, lower salt secretion ability from leaves, and decreased salt tolerance. The expression of several genes [LbTTG1 (TRANSPARENT TESTA OF GL1), LbCPC (CAPRICE), and LbGL2 (GLABRA2)] related to salt gland development was significantly upregulated in LbMAPK2 knockdown lines, while the expression of LbEGL3 (ENHANCER OF GL3) was significantly downregulated.
CONCLUSION: These findings increase our understanding of the LbMAPK gene family and will be useful for in-depth studies of the molecular mechanisms behind salt gland development and salt secretion in L. bicolor. In addition, our analysis lays the foundation for exploring the biological functions of MAPKs in an extreme halophyte.
Additional Links: PMID-37964233
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@article {pmid37964233,
year = {2023},
author = {Zhang, C and Zhu, Z and Jiang, A and Liu, Q and Chen, M},
title = {Genome-wide identification of the mitogen-activated kinase gene family from Limonium bicolor and functional characterization of LbMAPK2 under salt stress.},
journal = {BMC plant biology},
volume = {23},
number = {1},
pages = {565},
pmid = {37964233},
issn = {1471-2229},
mesh = {*Plumbaginaceae/metabolism ; Mitogens/metabolism ; Salt Stress/genetics ; Mitogen-Activated Protein Kinases/genetics/metabolism ; Stress, Physiological/genetics ; Plant Growth Regulators/metabolism ; Gene Expression Regulation, Plant ; Phylogeny ; Plant Proteins/genetics/metabolism ; },
abstract = {BACKGROUND: Mitogen-activated protein kinases (MAPKs) are ubiquitous signal transduction components in eukaryotes. In plants, MAPKs play an essential role in growth and development, phytohormone regulation, and abiotic stress responses. The typical recretohalophyte Limonium bicolor (Bunge) Kuntze has multicellular salt glands on its stems and leaves; these glands secrete excess salt ions from its cells to mitigate salt damage. The number, type, and biological function of L. bicolor MAPK genes are unknown.
RESULTS: We identified 20 candidate L. bicolor MAPK genes, which can be divided into four groups. Of these 20 genes, 17 were anchored to 7 chromosomes, while LbMAPK18, LbMAPK19, and LbMAPK20 mapped to distinct scaffolds. Structure analysis showed that the predicted protein LbMAPK19 contains the special structural motif TNY in its activation loop, whereas the other LbMAPK members harbor the conserved TEY or TDY motif. The promoters of most LbMAPK genes carry cis-acting elements related to growth and development, phytohormones, and abiotic stress. LbMAPK1, LbMAPK2, LbMAPK16, and LbMAPK20 are highly expressed in the early stages of salt gland development, whereas LbMAPK4, LbMAPK5, LbMAPK6, LbMAPK7, LbMAPK11, LbMAPK14, and LbMAPK15 are highly expressed during the late stages. These 20 LbMAPK genes all responded to salt, drought and ABA stress. We explored the function of LbMAPK2 via virus-induced gene silencing: knocking down LbMAPK2 transcript levels in L. bicolor resulted in fewer salt glands, lower salt secretion ability from leaves, and decreased salt tolerance. The expression of several genes [LbTTG1 (TRANSPARENT TESTA OF GL1), LbCPC (CAPRICE), and LbGL2 (GLABRA2)] related to salt gland development was significantly upregulated in LbMAPK2 knockdown lines, while the expression of LbEGL3 (ENHANCER OF GL3) was significantly downregulated.
CONCLUSION: These findings increase our understanding of the LbMAPK gene family and will be useful for in-depth studies of the molecular mechanisms behind salt gland development and salt secretion in L. bicolor. In addition, our analysis lays the foundation for exploring the biological functions of MAPKs in an extreme halophyte.},
}
MeSH Terms:
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hide MeSH Terms
*Plumbaginaceae/metabolism
Mitogens/metabolism
Salt Stress/genetics
Mitogen-Activated Protein Kinases/genetics/metabolism
Stress, Physiological/genetics
Plant Growth Regulators/metabolism
Gene Expression Regulation, Plant
Phylogeny
Plant Proteins/genetics/metabolism
RevDate: 2024-02-07
CmpDate: 2023-12-07
A cell-based model for size control in the multiple fission alga Chlamydomonas reinhardtii.
Current biology : CB, 33(23):5215-5224.e5.
Understanding how population-size homeostasis emerges from stochastic individual cell behaviors remains a challenge in biology.[1][,][2][,][3][,][4][,][5][,][6][,][7] The unicellular green alga Chlamydomonas reinhardtii (Chlamydomonas) proliferates using a multiple fission cell cycle, where a prolonged G1 phase is followed by n rounds of alternating division cycles (S/M) to produce 2[n] daughters. A "Commitment" sizer in mid-G1 phase ensures sufficient cell growth before completing the cell cycle. A mitotic sizer couples mother-cell size to division number (n) such that daughter size distributions are uniform regardless of mother size distributions. Although daughter size distributions were highly robust to altered growth conditions, ∼40% of daughter cells fell outside of the 2-fold range expected from a "perfect" multiple fission sizer.[7][,][8] A simple intuitive power law model with stochastic noise failed to reproduce individual division behaviors of tracked single cells. Through additional iterative modeling, we identified an alternative modified threshold (MT) model, where cells need to cross a threshold greater than 2-fold their median starting size to become division-competent (i.e., Committed), after which their behaviors followed a power law model. The Commitment versus mitotic size threshold uncoupling in the MT model was likely a key pre-adaptation in the evolution of volvocine algal multicellularity. A similar experimental approach was used in size mutants mat3/rbr and dp1 that are, respectively, missing repressor or activator subunits of the retinoblastoma tumor suppressor complex (RBC). Both mutants showed altered relationships between Commitment and mitotic sizer, suggesting that RBC functions to decouple the two sizers.
Additional Links: PMID-37949064
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@article {pmid37949064,
year = {2023},
author = {Liu, D and Vargas-García, CA and Singh, A and Umen, J},
title = {A cell-based model for size control in the multiple fission alga Chlamydomonas reinhardtii.},
journal = {Current biology : CB},
volume = {33},
number = {23},
pages = {5215-5224.e5},
pmid = {37949064},
issn = {1879-0445},
support = {R01 GM126557/GM/NIGMS NIH HHS/United States ; R35 GM148351/GM/NIGMS NIH HHS/United States ; },
mesh = {*Chlamydomonas reinhardtii/genetics ; Cell Division ; Cell Cycle ; *Chlamydomonas ; Cell Proliferation ; },
abstract = {Understanding how population-size homeostasis emerges from stochastic individual cell behaviors remains a challenge in biology.[1][,][2][,][3][,][4][,][5][,][6][,][7] The unicellular green alga Chlamydomonas reinhardtii (Chlamydomonas) proliferates using a multiple fission cell cycle, where a prolonged G1 phase is followed by n rounds of alternating division cycles (S/M) to produce 2[n] daughters. A "Commitment" sizer in mid-G1 phase ensures sufficient cell growth before completing the cell cycle. A mitotic sizer couples mother-cell size to division number (n) such that daughter size distributions are uniform regardless of mother size distributions. Although daughter size distributions were highly robust to altered growth conditions, ∼40% of daughter cells fell outside of the 2-fold range expected from a "perfect" multiple fission sizer.[7][,][8] A simple intuitive power law model with stochastic noise failed to reproduce individual division behaviors of tracked single cells. Through additional iterative modeling, we identified an alternative modified threshold (MT) model, where cells need to cross a threshold greater than 2-fold their median starting size to become division-competent (i.e., Committed), after which their behaviors followed a power law model. The Commitment versus mitotic size threshold uncoupling in the MT model was likely a key pre-adaptation in the evolution of volvocine algal multicellularity. A similar experimental approach was used in size mutants mat3/rbr and dp1 that are, respectively, missing repressor or activator subunits of the retinoblastoma tumor suppressor complex (RBC). Both mutants showed altered relationships between Commitment and mitotic sizer, suggesting that RBC functions to decouple the two sizers.},
}
MeSH Terms:
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hide MeSH Terms
*Chlamydomonas reinhardtii/genetics
Cell Division
Cell Cycle
*Chlamydomonas
Cell Proliferation
RevDate: 2024-09-10
CmpDate: 2024-01-04
Selection on plastic adherence leads to hyper-multicellular strains and incidental virulence in the budding yeast.
eLife, 12:.
Many disease-causing microbes are not obligate pathogens; rather, they are environmental microbes taking advantage of an ecological opportunity. The existence of microbes whose life cycle does not require a host and are not normally pathogenic, yet are well-suited to host exploitation, is an evolutionary puzzle. One hypothesis posits that selection in the environment may favor traits that incidentally lead to pathogenicity and virulence, or serve as pre-adaptations for survival in a host. An example of such a trait is surface adherence. To experimentally test the idea of 'accidental virulence', replicate populations of Saccharomyces cerevisiae were evolved to attach to a plastic bead for hundreds of generations. Along with plastic adherence, two multicellular phenotypes- biofilm formation and flor formation- increased; another phenotype, pseudohyphal growth, responded to the nutrient limitation. Thus, experimental selection led to the evolution of highly-adherent, hyper-multicellular strains. Wax moth larvae injected with evolved hyper-multicellular strains were significantly more likely to die than those injected with evolved non-multicellular strains. Hence, selection on plastic adherence incidentally led to the evolution of enhanced multicellularity and increased virulence. Our results support the idea that selection for a trait beneficial in the open environment can inadvertently generate opportunistic, 'accidental' pathogens.
Additional Links: PMID-37916911
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@article {pmid37916911,
year = {2023},
author = {Ekdahl, LI and Salcedo, JA and Dungan, MM and Mason, DV and Myagmarsuren, D and Murphy, HA},
title = {Selection on plastic adherence leads to hyper-multicellular strains and incidental virulence in the budding yeast.},
journal = {eLife},
volume = {12},
number = {},
pages = {},
pmid = {37916911},
issn = {2050-084X},
support = {R15 GM122032/GM/NIGMS NIH HHS/United States ; R15 GM152938/GM/NIGMS NIH HHS/United States ; R15-GM122032/NH/NIH HHS/United States ; },
mesh = {Animals ; Virulence ; *Saccharomycetales ; Saccharomyces cerevisiae/genetics ; Life Cycle Stages ; Phenotype ; },
abstract = {Many disease-causing microbes are not obligate pathogens; rather, they are environmental microbes taking advantage of an ecological opportunity. The existence of microbes whose life cycle does not require a host and are not normally pathogenic, yet are well-suited to host exploitation, is an evolutionary puzzle. One hypothesis posits that selection in the environment may favor traits that incidentally lead to pathogenicity and virulence, or serve as pre-adaptations for survival in a host. An example of such a trait is surface adherence. To experimentally test the idea of 'accidental virulence', replicate populations of Saccharomyces cerevisiae were evolved to attach to a plastic bead for hundreds of generations. Along with plastic adherence, two multicellular phenotypes- biofilm formation and flor formation- increased; another phenotype, pseudohyphal growth, responded to the nutrient limitation. Thus, experimental selection led to the evolution of highly-adherent, hyper-multicellular strains. Wax moth larvae injected with evolved hyper-multicellular strains were significantly more likely to die than those injected with evolved non-multicellular strains. Hence, selection on plastic adherence incidentally led to the evolution of enhanced multicellularity and increased virulence. Our results support the idea that selection for a trait beneficial in the open environment can inadvertently generate opportunistic, 'accidental' pathogens.},
}
MeSH Terms:
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Animals
Virulence
*Saccharomycetales
Saccharomyces cerevisiae/genetics
Life Cycle Stages
Phenotype
RevDate: 2024-09-30
CmpDate: 2023-11-01
Identification of cell-type specific alternative transcripts in the multicellular alga Volvox carteri.
BMC genomics, 24(1):654.
BACKGROUND: Cell type specialization is a hallmark of complex multicellular organisms and is usually established through implementation of cell-type-specific gene expression programs. The multicellular green alga Volvox carteri has just two cell types, germ and soma, that have previously been shown to have very different transcriptome compositions which match their specialized roles. Here we interrogated another potential mechanism for differentiation in V. carteri, cell type specific alternative transcript isoforms (CTSAI).
METHODS: We used pre-existing predictions of alternative transcripts and de novo transcript assembly with HISAT2 and Ballgown software to compile a list of loci with two or more transcript isoforms, identified a small subset that were candidates for CTSAI, and manually curated this subset of genes to remove false positives. We experimentally verified three candidates using semi-quantitative RT-PCR to assess relative isoform abundance in each cell type.
RESULTS: Of the 1978 loci with two or more predicted transcript isoforms 67 of these also showed cell type isoform expression biases. After curation 15 strong candidates for CTSAI were identified, three of which were experimentally verified, and their predicted gene product functions were evaluated in light of potential cell type specific roles. A comparison of genes with predicted alternative splicing from Chlamydomonas reinhardtii, a unicellular relative of V. carteri, identified little overlap between ortholog pairs with alternative splicing in both species. Finally, we interrogated cell type expression patterns of 126 V. carteri predicted RNA binding protein (RBP) encoding genes and found 40 that showed either somatic or germ cell expression bias. These RBPs are potential mediators of CTSAI in V. carteri and suggest possible pre-adaptation for cell type specific RNA processing and a potential path for generating CTSAI in the early ancestors of metazoans and plants.
CONCLUSIONS: We predicted numerous instances of alternative transcript isoforms in Volvox, only a small subset of which showed cell type specific isoform expression bias. However, the validated examples of CTSAI supported existing hypotheses about cell type specialization in V. carteri, and also suggested new hypotheses about mechanisms of functional specialization for their gene products. Our data imply that CTSAI operates as a minor but important component of V. carteri cellular differentiation and could be used as a model for how alternative isoforms emerge and co-evolve with cell type specialization.
Additional Links: PMID-37904088
PubMed:
Citation:
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@article {pmid37904088,
year = {2023},
author = {Balasubramanian, RN and Gao, M and Umen, J},
title = {Identification of cell-type specific alternative transcripts in the multicellular alga Volvox carteri.},
journal = {BMC genomics},
volume = {24},
number = {1},
pages = {654},
pmid = {37904088},
issn = {1471-2164},
support = {1755430//Division of Integrative Organismal Systems/ ; },
mesh = {*Volvox/genetics ; Transcriptome ; Protein Isoforms/genetics ; },
abstract = {BACKGROUND: Cell type specialization is a hallmark of complex multicellular organisms and is usually established through implementation of cell-type-specific gene expression programs. The multicellular green alga Volvox carteri has just two cell types, germ and soma, that have previously been shown to have very different transcriptome compositions which match their specialized roles. Here we interrogated another potential mechanism for differentiation in V. carteri, cell type specific alternative transcript isoforms (CTSAI).
METHODS: We used pre-existing predictions of alternative transcripts and de novo transcript assembly with HISAT2 and Ballgown software to compile a list of loci with two or more transcript isoforms, identified a small subset that were candidates for CTSAI, and manually curated this subset of genes to remove false positives. We experimentally verified three candidates using semi-quantitative RT-PCR to assess relative isoform abundance in each cell type.
RESULTS: Of the 1978 loci with two or more predicted transcript isoforms 67 of these also showed cell type isoform expression biases. After curation 15 strong candidates for CTSAI were identified, three of which were experimentally verified, and their predicted gene product functions were evaluated in light of potential cell type specific roles. A comparison of genes with predicted alternative splicing from Chlamydomonas reinhardtii, a unicellular relative of V. carteri, identified little overlap between ortholog pairs with alternative splicing in both species. Finally, we interrogated cell type expression patterns of 126 V. carteri predicted RNA binding protein (RBP) encoding genes and found 40 that showed either somatic or germ cell expression bias. These RBPs are potential mediators of CTSAI in V. carteri and suggest possible pre-adaptation for cell type specific RNA processing and a potential path for generating CTSAI in the early ancestors of metazoans and plants.
CONCLUSIONS: We predicted numerous instances of alternative transcript isoforms in Volvox, only a small subset of which showed cell type specific isoform expression bias. However, the validated examples of CTSAI supported existing hypotheses about cell type specialization in V. carteri, and also suggested new hypotheses about mechanisms of functional specialization for their gene products. Our data imply that CTSAI operates as a minor but important component of V. carteri cellular differentiation and could be used as a model for how alternative isoforms emerge and co-evolve with cell type specialization.},
}
MeSH Terms:
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*Volvox/genetics
Transcriptome
Protein Isoforms/genetics
RevDate: 2023-11-13
CmpDate: 2023-10-30
Decoding Cancer Evolution: Integrating Genetic and Non-Genetic Insights.
Genes, 14(10):.
The development of cancer begins with cells transitioning from their multicellular nature to a state akin to unicellular organisms. This shift leads to a breakdown in the crucial regulators inherent to multicellularity, resulting in the emergence of diverse cancer cell subpopulations that have enhanced adaptability. The presence of different cell subpopulations within a tumour, known as intratumoural heterogeneity (ITH), poses challenges for cancer treatment. In this review, we delve into the dynamics of the shift from multicellularity to unicellularity during cancer onset and progression. We highlight the role of genetic and non-genetic factors, as well as tumour microenvironment, in promoting ITH and cancer evolution. Additionally, we shed light on the latest advancements in omics technologies that allow for in-depth analysis of tumours at the single-cell level and their spatial organization within the tissue. Obtaining such detailed information is crucial for deepening our understanding of the diverse evolutionary paths of cancer, allowing for the development of effective therapies targeting the key drivers of cancer evolution.
Additional Links: PMID-37895205
PubMed:
Citation:
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@article {pmid37895205,
year = {2023},
author = {Ashouri, A and Zhang, C and Gaiti, F},
title = {Decoding Cancer Evolution: Integrating Genetic and Non-Genetic Insights.},
journal = {Genes},
volume = {14},
number = {10},
pages = {},
pmid = {37895205},
issn = {2073-4425},
support = {//CIHR/Canada ; 184658//CIHR/Canada ; },
mesh = {Humans ; *Neoplasms/genetics/pathology ; Tumor Microenvironment/genetics ; },
abstract = {The development of cancer begins with cells transitioning from their multicellular nature to a state akin to unicellular organisms. This shift leads to a breakdown in the crucial regulators inherent to multicellularity, resulting in the emergence of diverse cancer cell subpopulations that have enhanced adaptability. The presence of different cell subpopulations within a tumour, known as intratumoural heterogeneity (ITH), poses challenges for cancer treatment. In this review, we delve into the dynamics of the shift from multicellularity to unicellularity during cancer onset and progression. We highlight the role of genetic and non-genetic factors, as well as tumour microenvironment, in promoting ITH and cancer evolution. Additionally, we shed light on the latest advancements in omics technologies that allow for in-depth analysis of tumours at the single-cell level and their spatial organization within the tissue. Obtaining such detailed information is crucial for deepening our understanding of the diverse evolutionary paths of cancer, allowing for the development of effective therapies targeting the key drivers of cancer evolution.},
}
MeSH Terms:
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Humans
*Neoplasms/genetics/pathology
Tumor Microenvironment/genetics
RevDate: 2024-02-10
CmpDate: 2023-10-30
Evolutionary consequences of nascent multicellular life cycles.
eLife, 12:.
A key step in the evolutionary transition to multicellularity is the origin of multicellular groups as biological individuals capable of adaptation. Comparative work, supported by theory, suggests clonal development should facilitate this transition, although this hypothesis has never been tested in a single model system. We evolved 20 replicate populations of otherwise isogenic clonally reproducing 'snowflake' yeast (Δace2/∆ace2) and aggregative 'floc' yeast (GAL1p::FLO1 /GAL1p::FLO1) with daily selection for rapid growth in liquid media, which favors faster cell division, followed by selection for rapid sedimentation, which favors larger multicellular groups. While both genotypes adapted to this regime, growing faster and having higher survival during the group-selection phase, there was a stark difference in evolutionary dynamics. Aggregative floc yeast obtained nearly all their increased fitness from faster growth, not improved group survival; indicating that selection acted primarily at the level of cells. In contrast, clonal snowflake yeast mainly benefited from higher group-dependent fitness, indicating a shift in the level of Darwinian individuality from cells to groups. Through genome sequencing and mathematical modeling, we show that the genetic bottlenecks in a clonal life cycle also drive much higher rates of genetic drift-a result with complex implications for this evolutionary transition. Our results highlight the central role that early multicellular life cycles play in the process of multicellular adaptation.
Additional Links: PMID-37889142
PubMed:
Citation:
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@article {pmid37889142,
year = {2023},
author = {Pentz, JT and MacGillivray, K and DuBose, JG and Conlin, PL and Reinhardt, E and Libby, E and Ratcliff, WC},
title = {Evolutionary consequences of nascent multicellular life cycles.},
journal = {eLife},
volume = {12},
number = {},
pages = {},
pmid = {37889142},
issn = {2050-084X},
support = {T32 GM142616/GM/NIGMS NIH HHS/United States ; T32GM142616/NH/NIH HHS/United States ; },
mesh = {Humans ; Animals ; *Saccharomyces cerevisiae/genetics ; *Biological Evolution ; Life Cycle Stages ; Models, Biological ; Models, Theoretical ; },
abstract = {A key step in the evolutionary transition to multicellularity is the origin of multicellular groups as biological individuals capable of adaptation. Comparative work, supported by theory, suggests clonal development should facilitate this transition, although this hypothesis has never been tested in a single model system. We evolved 20 replicate populations of otherwise isogenic clonally reproducing 'snowflake' yeast (Δace2/∆ace2) and aggregative 'floc' yeast (GAL1p::FLO1 /GAL1p::FLO1) with daily selection for rapid growth in liquid media, which favors faster cell division, followed by selection for rapid sedimentation, which favors larger multicellular groups. While both genotypes adapted to this regime, growing faster and having higher survival during the group-selection phase, there was a stark difference in evolutionary dynamics. Aggregative floc yeast obtained nearly all their increased fitness from faster growth, not improved group survival; indicating that selection acted primarily at the level of cells. In contrast, clonal snowflake yeast mainly benefited from higher group-dependent fitness, indicating a shift in the level of Darwinian individuality from cells to groups. Through genome sequencing and mathematical modeling, we show that the genetic bottlenecks in a clonal life cycle also drive much higher rates of genetic drift-a result with complex implications for this evolutionary transition. Our results highlight the central role that early multicellular life cycles play in the process of multicellular adaptation.},
}
MeSH Terms:
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Humans
Animals
*Saccharomyces cerevisiae/genetics
*Biological Evolution
Life Cycle Stages
Models, Biological
Models, Theoretical
RevDate: 2023-12-16
CmpDate: 2023-12-16
Phylogenomic analysis of the understudied Neisseriaceae species reveals a poly- and paraphyletic Kingella genus.
Microbiology spectrum, 11(6):e0312323.
Understanding the evolutionary relationships between the species in the Neisseriaceae family has been a persistent challenge in bacterial systematics due to high recombination rates in these species. Previous studies of this family have focused on Neisseria meningitidis and N. gonorrhoeae. However, previously understudied Neisseriaceae species are gaining new attention, with Kingella kingae now recognized as a common human pathogen and with Alysiella and Simonsiella being unique in the bacterial world as multicellular organisms. A better understanding of the genomic evolution of the Neisseriaceae can lead to the identification of specific genes and traits that underlie the remarkable diversity of this family.
Additional Links: PMID-37882538
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Citation:
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@article {pmid37882538,
year = {2023},
author = {Morreale, DP and St Geme Iii, JW and Planet, PJ},
title = {Phylogenomic analysis of the understudied Neisseriaceae species reveals a poly- and paraphyletic Kingella genus.},
journal = {Microbiology spectrum},
volume = {11},
number = {6},
pages = {e0312323},
pmid = {37882538},
issn = {2165-0497},
support = {R01 AI172841/AI/NIAID NIH HHS/United States ; T32 AI141393/AI/NIAID NIH HHS/United States ; },
mesh = {Humans ; *Neisseriaceae/genetics ; Kingella ; Phylogeny ; Genomics ; Phenotype ; Neisseria gonorrhoeae ; },
abstract = {Understanding the evolutionary relationships between the species in the Neisseriaceae family has been a persistent challenge in bacterial systematics due to high recombination rates in these species. Previous studies of this family have focused on Neisseria meningitidis and N. gonorrhoeae. However, previously understudied Neisseriaceae species are gaining new attention, with Kingella kingae now recognized as a common human pathogen and with Alysiella and Simonsiella being unique in the bacterial world as multicellular organisms. A better understanding of the genomic evolution of the Neisseriaceae can lead to the identification of specific genes and traits that underlie the remarkable diversity of this family.},
}
MeSH Terms:
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Humans
*Neisseriaceae/genetics
Kingella
Phylogeny
Genomics
Phenotype
Neisseria gonorrhoeae
RevDate: 2023-11-05
CmpDate: 2023-10-23
Unicellular and multicellular developmental variations in algal zygotes produce sporophytes.
Biology letters, 19(10):20230313.
The emergence of sporophytes, that is, diploid multicellular bodies in plants, facilitated plant diversification and the evolution of complexity. Although sporophytes may have evolved in an ancestral alga exhibiting a haplontic life cycle with a unicellular diploid and multicellular haploid (gametophyte) phase, the mechanism by which this novelty originated remains largely unknown. Ulotrichalean marine green algae (Ulvophyceae) are one of the few extant groups with haplontic-like life cycles. In this study, we show that zygotes of the ulotrichalean alga Monostroma angicava, which usually develop into unicellular cysts, exhibit a developmental variation producing multicellular reproductive sporophytes. Multicellular development likely occurred stochastically in individual zygotes, but its ratio responded plastically to growth conditions. Sporophytes showed identical morphological development to gametophytes, which should reflect the expression of the same genetic programme directing multicellular development. Considering that sporophytes were evolutionarily derived in Ulotrichales, this implies that sporophytes emerged by co-opting the gametophyte developmental programme to the diploid phase. This study suggests a possible mechanism of sporophyte formation in haplontic life cycles, contributing to the understanding of the evolutionary transition from unicellular to multicellular diploid body plans in green plants.
Additional Links: PMID-37848052
PubMed:
Citation:
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@article {pmid37848052,
year = {2023},
author = {Horinouchi, Y and Togashi, T},
title = {Unicellular and multicellular developmental variations in algal zygotes produce sporophytes.},
journal = {Biology letters},
volume = {19},
number = {10},
pages = {20230313},
pmid = {37848052},
issn = {1744-957X},
mesh = {Animals ; *Zygote ; Plants/genetics ; *Chlorophyta/genetics ; Reproduction ; Life Cycle Stages ; },
abstract = {The emergence of sporophytes, that is, diploid multicellular bodies in plants, facilitated plant diversification and the evolution of complexity. Although sporophytes may have evolved in an ancestral alga exhibiting a haplontic life cycle with a unicellular diploid and multicellular haploid (gametophyte) phase, the mechanism by which this novelty originated remains largely unknown. Ulotrichalean marine green algae (Ulvophyceae) are one of the few extant groups with haplontic-like life cycles. In this study, we show that zygotes of the ulotrichalean alga Monostroma angicava, which usually develop into unicellular cysts, exhibit a developmental variation producing multicellular reproductive sporophytes. Multicellular development likely occurred stochastically in individual zygotes, but its ratio responded plastically to growth conditions. Sporophytes showed identical morphological development to gametophytes, which should reflect the expression of the same genetic programme directing multicellular development. Considering that sporophytes were evolutionarily derived in Ulotrichales, this implies that sporophytes emerged by co-opting the gametophyte developmental programme to the diploid phase. This study suggests a possible mechanism of sporophyte formation in haplontic life cycles, contributing to the understanding of the evolutionary transition from unicellular to multicellular diploid body plans in green plants.},
}
MeSH Terms:
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Animals
*Zygote
Plants/genetics
*Chlorophyta/genetics
Reproduction
Life Cycle Stages
RevDate: 2024-05-21
CmpDate: 2024-01-01
Parallel evolution of the G protein-coupled receptor GrlG and the loss of fruiting body formation in the social amoeba Dictyostelium discoideum evolved under low relatedness.
G3 (Bethesda, Md.), 14(1):.
Aggregative multicellularity relies on cooperation among formerly independent cells to form a multicellular body. Previous work with Dictyostelium discoideum showed that experimental evolution under low relatedness profoundly decreased cooperation, as indicated by the loss of fruiting body formation in many clones and an increase of cheaters that contribute proportionally more to spores than to the dead stalk. Using whole-genome sequencing and variant analysis of these lines, we identified 38 single nucleotide polymorphisms in 29 genes. Each gene had 1 variant except for grlG (encoding a G protein-coupled receptor), which had 10 unique SNPs and 5 structural variants. Variants in the 5' half of grlG-the region encoding the signal peptide and the extracellular binding domain-were significantly associated with the loss of fruiting body formation; the association was not significant in the 3' half of the gene. These results suggest that the loss of grlG was adaptive under low relatedness and that at least the 5' half of the gene is important for cooperation and multicellular development. This is surprising given some previous evidence that grlG encodes a folate receptor involved in predation, which occurs only during the single-celled stage. However, non-fruiting mutants showed little increase in a parallel evolution experiment where the multicellular stage was prevented from happening. This shows that non-fruiting mutants are not generally selected by any predation advantage but rather by something-likely cheating-during the multicellular stage.
Additional Links: PMID-37832511
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Citation:
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@article {pmid37832511,
year = {2023},
author = {Walker, LM and Sherpa, RN and Ivaturi, S and Brock, DA and Larsen, TJ and Walker, JR and Strassmann, JE and Queller, DC},
title = {Parallel evolution of the G protein-coupled receptor GrlG and the loss of fruiting body formation in the social amoeba Dictyostelium discoideum evolved under low relatedness.},
journal = {G3 (Bethesda, Md.)},
volume = {14},
number = {1},
pages = {},
pmid = {37832511},
issn = {2160-1836},
support = {IOS 16-56756//National Science Foundation/ ; //McDonnell Genome Institute/ ; },
mesh = {*Amoeba ; Biological Evolution ; *Dictyostelium/genetics ; Reproduction ; },
abstract = {Aggregative multicellularity relies on cooperation among formerly independent cells to form a multicellular body. Previous work with Dictyostelium discoideum showed that experimental evolution under low relatedness profoundly decreased cooperation, as indicated by the loss of fruiting body formation in many clones and an increase of cheaters that contribute proportionally more to spores than to the dead stalk. Using whole-genome sequencing and variant analysis of these lines, we identified 38 single nucleotide polymorphisms in 29 genes. Each gene had 1 variant except for grlG (encoding a G protein-coupled receptor), which had 10 unique SNPs and 5 structural variants. Variants in the 5' half of grlG-the region encoding the signal peptide and the extracellular binding domain-were significantly associated with the loss of fruiting body formation; the association was not significant in the 3' half of the gene. These results suggest that the loss of grlG was adaptive under low relatedness and that at least the 5' half of the gene is important for cooperation and multicellular development. This is surprising given some previous evidence that grlG encodes a folate receptor involved in predation, which occurs only during the single-celled stage. However, non-fruiting mutants showed little increase in a parallel evolution experiment where the multicellular stage was prevented from happening. This shows that non-fruiting mutants are not generally selected by any predation advantage but rather by something-likely cheating-during the multicellular stage.},
}
MeSH Terms:
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*Amoeba
Biological Evolution
*Dictyostelium/genetics
Reproduction
RevDate: 2023-11-13
CmpDate: 2023-11-13
Origin, evolution, and diversification of the wall-associated kinase gene family in plants.
Plant cell reports, 42(12):1891-1906.
The study of the origin, evolution, and diversification of the wall-associated kinase gene family in plants facilitates their functional investigations in the future. Wall-associated kinases (WAKs) make up one subfamily of receptor-like kinases (RLKs), and function directly in plant cell elongation and responses to biotic and abiotic stresses. The biological functions of WAKs have been extensively characterized in angiosperms; however, the origin and evolutionary history of the WAK family in green plants remain unclear. Here, we performed a comprehensive analysis of the WAK family to reveal its origin, evolution, and diversification in green plants. In total, 1061 WAK genes were identified in 37 species from unicellular algae to multicellular plants, and the results showed that WAK genes probably originated before bryophyte differentiation and were widely distributed in land plants, especially angiosperms. The phylogeny indicated that the land plant WAKs gave rise to five clades and underwent lineage-specific expansion after species differentiation. Cis-acting elements and expression patterns analyses of WAK genes in Arabidopsis and rice demonstrated the functional diversity of WAK genes in these two species. Many gene gains and losses have occurred in angiosperms, leading to an increase in the number of gene copies. The evolutionary trajectory of the WAK family during polyploidization was uncovered using Gossypium species. Our results provide insights into the evolution of WAK genes in green plants, facilitating their functional investigations in the future.
Additional Links: PMID-37743376
PubMed:
Citation:
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@article {pmid37743376,
year = {2023},
author = {Zhang, Z and Huo, W and Wang, X and Ren, Z and Zhao, J and Liu, Y and He, K and Zhang, F and Li, W and Jin, S and Yang, D},
title = {Origin, evolution, and diversification of the wall-associated kinase gene family in plants.},
journal = {Plant cell reports},
volume = {42},
number = {12},
pages = {1891-1906},
pmid = {37743376},
issn = {1432-203X},
support = {232300421116//Natural Science Foundation of Henan Province/ ; },
mesh = {*Plants/genetics ; Genes, Plant/genetics ; *Arabidopsis/genetics ; Multigene Family ; },
abstract = {The study of the origin, evolution, and diversification of the wall-associated kinase gene family in plants facilitates their functional investigations in the future. Wall-associated kinases (WAKs) make up one subfamily of receptor-like kinases (RLKs), and function directly in plant cell elongation and responses to biotic and abiotic stresses. The biological functions of WAKs have been extensively characterized in angiosperms; however, the origin and evolutionary history of the WAK family in green plants remain unclear. Here, we performed a comprehensive analysis of the WAK family to reveal its origin, evolution, and diversification in green plants. In total, 1061 WAK genes were identified in 37 species from unicellular algae to multicellular plants, and the results showed that WAK genes probably originated before bryophyte differentiation and were widely distributed in land plants, especially angiosperms. The phylogeny indicated that the land plant WAKs gave rise to five clades and underwent lineage-specific expansion after species differentiation. Cis-acting elements and expression patterns analyses of WAK genes in Arabidopsis and rice demonstrated the functional diversity of WAK genes in these two species. Many gene gains and losses have occurred in angiosperms, leading to an increase in the number of gene copies. The evolutionary trajectory of the WAK family during polyploidization was uncovered using Gossypium species. Our results provide insights into the evolution of WAK genes in green plants, facilitating their functional investigations in the future.},
}
MeSH Terms:
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*Plants/genetics
Genes, Plant/genetics
*Arabidopsis/genetics
Multigene Family
RevDate: 2024-10-01
CmpDate: 2023-11-29
Programmed Cell Death in Unicellular Versus Multicellular Organisms.
Annual review of genetics, 57:435-459.
Programmed cell death (self-induced) is intrinsic to all cellular life forms, including unicellular organisms. However, cell death research has focused on animal models to understand cancer, degenerative disorders, and developmental processes. Recently delineated suicidal death mechanisms in bacteria and fungi have revealed ancient origins of animal cell death that are intertwined with immune mechanisms, allaying earlier doubts that self-inflicted cell death pathways exist in microorganisms. Approximately 20 mammalian death pathways have been partially characterized over the last 35 years. By contrast, more than 100 death mechanisms have been identified in bacteria and a few fungi in recent years. However, cell death is nearly unstudied in most human pathogenic microbes that cause major public health burdens. Here, we consider how the current understanding of programmed cell death arose through animal studies and how recently uncovered microbial cell death mechanisms in fungi and bacteria resemble and differ from mechanisms of mammalian cell death.
Additional Links: PMID-37722687
Publisher:
PubMed:
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@article {pmid37722687,
year = {2023},
author = {Kulkarni, M and Hardwick, JM},
title = {Programmed Cell Death in Unicellular Versus Multicellular Organisms.},
journal = {Annual review of genetics},
volume = {57},
number = {},
pages = {435-459},
doi = {10.1146/annurev-genet-033123-095833},
pmid = {37722687},
issn = {1545-2948},
support = {R21 AI144373/AI/NIAID NIH HHS/United States ; R21 AI183596/AI/NIAID NIH HHS/United States ; R21 NS127076/NS/NINDS NIH HHS/United States ; },
mesh = {Animals ; Humans ; *Apoptosis/genetics ; *Fungi/genetics/metabolism ; Bacteria ; Mammals ; },
abstract = {Programmed cell death (self-induced) is intrinsic to all cellular life forms, including unicellular organisms. However, cell death research has focused on animal models to understand cancer, degenerative disorders, and developmental processes. Recently delineated suicidal death mechanisms in bacteria and fungi have revealed ancient origins of animal cell death that are intertwined with immune mechanisms, allaying earlier doubts that self-inflicted cell death pathways exist in microorganisms. Approximately 20 mammalian death pathways have been partially characterized over the last 35 years. By contrast, more than 100 death mechanisms have been identified in bacteria and a few fungi in recent years. However, cell death is nearly unstudied in most human pathogenic microbes that cause major public health burdens. Here, we consider how the current understanding of programmed cell death arose through animal studies and how recently uncovered microbial cell death mechanisms in fungi and bacteria resemble and differ from mechanisms of mammalian cell death.},
}
MeSH Terms:
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Animals
Humans
*Apoptosis/genetics
*Fungi/genetics/metabolism
Bacteria
Mammals
RevDate: 2023-11-29
CmpDate: 2023-10-23
Evolution of phenotypic disparity in the plant kingdom.
Nature plants, 9(10):1618-1626.
The plant kingdom exhibits diverse bodyplans, from single-celled algae to complex multicellular land plants, but it is unclear how this phenotypic disparity was achieved. Here we show that the living divisions comprise discrete clusters within morphospace, separated largely by reproductive innovations, the extinction of evolutionary intermediates and lineage-specific evolution. Phenotypic complexity correlates not with disparity but with ploidy history, reflecting the role of genome duplication in plant macroevolution. Overall, the plant kingdom exhibits a pattern of episodically increasing disparity throughout its evolutionary history that mirrors the evolutionary floras and reflects ecological expansion facilitated by reproductive innovations. This pattern also parallels that seen in the animal and fungal kingdoms, suggesting a general pattern for the evolution of multicellular bodyplans.
Additional Links: PMID-37666963
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@article {pmid37666963,
year = {2023},
author = {Clark, JW and Hetherington, AJ and Morris, JL and Pressel, S and Duckett, JG and Puttick, MN and Schneider, H and Kenrick, P and Wellman, CH and Donoghue, PCJ},
title = {Evolution of phenotypic disparity in the plant kingdom.},
journal = {Nature plants},
volume = {9},
number = {10},
pages = {1618-1626},
pmid = {37666963},
issn = {2055-0278},
support = {NE/N002067/1//RCUK | Natural Environment Research Council (NERC)/ ; NE/P013678/1//RCUK | Natural Environment Research Council (NERC)/ ; BB/N000919/1//RCUK | Biotechnology and Biological Sciences Research Council (BBSRC)/ ; BB/T012773/1//RCUK | Biotechnology and Biological Sciences Research Council (BBSRC)/ ; RF-2022-167//Leverhulme Trust/ ; RPG-2019-004//Leverhulme Trust/ ; JTF 62574//John Templeton Foundation (JTF)/ ; },
mesh = {Animals ; *Biological Evolution ; *Plants/genetics ; },
abstract = {The plant kingdom exhibits diverse bodyplans, from single-celled algae to complex multicellular land plants, but it is unclear how this phenotypic disparity was achieved. Here we show that the living divisions comprise discrete clusters within morphospace, separated largely by reproductive innovations, the extinction of evolutionary intermediates and lineage-specific evolution. Phenotypic complexity correlates not with disparity but with ploidy history, reflecting the role of genome duplication in plant macroevolution. Overall, the plant kingdom exhibits a pattern of episodically increasing disparity throughout its evolutionary history that mirrors the evolutionary floras and reflects ecological expansion facilitated by reproductive innovations. This pattern also parallels that seen in the animal and fungal kingdoms, suggesting a general pattern for the evolution of multicellular bodyplans.},
}
MeSH Terms:
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Animals
*Biological Evolution
*Plants/genetics
RevDate: 2023-09-08
CmpDate: 2023-08-28
Strong Purifying Selection in Haploid Tissue-Specific Genes of Scots Pine Supports the Masking Theory.
Molecular biology and evolution, 40(8):.
The masking theory states that genes expressed in a haploid stage will be under more efficient selection. In contrast, selection will be less efficient in genes expressed in a diploid stage, where the fitness effects of recessive deleterious or beneficial mutations can be hidden from selection in heterozygous form. This difference can influence several evolutionary processes such as the maintenance of genetic variation, adaptation rate, and genetic load. Masking theory expectations have been confirmed in single-cell haploid and diploid organisms. However, in multicellular organisms, such as plants, the effects of haploid selection are not clear-cut. In plants, the great majority of studies indicating haploid selection have been carried out using male haploid tissues in angiosperms. Hence, evidence in these systems is confounded with the effects of sexual selection and intraspecific competition. Evidence from other plant groups is scarce, and results show no support for the masking theory. Here, we have used a gymnosperm Scots pine megagametophyte, a maternally derived seed haploid tissue, and four diploid tissues to test the strength of purifying selection on a set of genes with tissue-specific expression. By using targeted resequencing data of those genes, we obtained estimates of genetic diversity, the site frequency spectrum of 0-fold and 4-fold sites, and inferred the distribution of fitness effects of new mutations in haploid and diploid tissue-specific genes. Our results show that purifying selection is stronger for tissue-specific genes expressed in the haploid megagametophyte tissue and that this signal of strong selection is not an artifact driven by high expression levels.
Additional Links: PMID-37565532
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Citation:
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@article {pmid37565532,
year = {2023},
author = {Cervantes, S and Kesälahti, R and Kumpula, TA and Mattila, TM and Helanterä, H and Pyhäjärvi, T},
title = {Strong Purifying Selection in Haploid Tissue-Specific Genes of Scots Pine Supports the Masking Theory.},
journal = {Molecular biology and evolution},
volume = {40},
number = {8},
pages = {},
pmid = {37565532},
issn = {1537-1719},
mesh = {Haploidy ; *Selection, Genetic ; Mutation ; *Biological Evolution ; Diploidy ; Plants ; },
abstract = {The masking theory states that genes expressed in a haploid stage will be under more efficient selection. In contrast, selection will be less efficient in genes expressed in a diploid stage, where the fitness effects of recessive deleterious or beneficial mutations can be hidden from selection in heterozygous form. This difference can influence several evolutionary processes such as the maintenance of genetic variation, adaptation rate, and genetic load. Masking theory expectations have been confirmed in single-cell haploid and diploid organisms. However, in multicellular organisms, such as plants, the effects of haploid selection are not clear-cut. In plants, the great majority of studies indicating haploid selection have been carried out using male haploid tissues in angiosperms. Hence, evidence in these systems is confounded with the effects of sexual selection and intraspecific competition. Evidence from other plant groups is scarce, and results show no support for the masking theory. Here, we have used a gymnosperm Scots pine megagametophyte, a maternally derived seed haploid tissue, and four diploid tissues to test the strength of purifying selection on a set of genes with tissue-specific expression. By using targeted resequencing data of those genes, we obtained estimates of genetic diversity, the site frequency spectrum of 0-fold and 4-fold sites, and inferred the distribution of fitness effects of new mutations in haploid and diploid tissue-specific genes. Our results show that purifying selection is stronger for tissue-specific genes expressed in the haploid megagametophyte tissue and that this signal of strong selection is not an artifact driven by high expression levels.},
}
MeSH Terms:
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hide MeSH Terms
Haploidy
*Selection, Genetic
Mutation
*Biological Evolution
Diploidy
Plants
RevDate: 2023-12-18
CmpDate: 2023-12-18
Programmed Necrosis in Host Defense.
Current topics in microbiology and immunology, 442:1-40.
Host control over infectious disease relies on the ability of cells in multicellular organisms to detect and defend against pathogens to prevent disease. Evolution affords mammals with a wide variety of independent immune mechanisms to control or eliminate invading infectious agents. Many pathogens acquire functions to deflect these immune mechanisms and promote infection. Following successful invasion of a host, cell autonomous signaling pathways drive the production of inflammatory cytokines, deployment of restriction factors and induction of cell death. Combined, these innate immune mechanisms attract dendritic cells, neutrophils and macrophages as well as innate lymphoid cells such as natural killer cells that all help control infection. Eventually, the development of adaptive pathogen-specific immunity clears infection and provides immune memory of the encounter. For obligate intracellular pathogens such as viruses, diverse cell death pathways make a pivotal contribution to early control by eliminating host cells before progeny are produced. Pro-apoptotic caspase-8 activity (along with caspase-10 in humans) executes extrinsic apoptosis, a nonlytic form of cell death triggered by TNF family death receptors (DRs). Over the past two decades, alternate extrinsic apoptosis and necroptosis outcomes have been described. Programmed necrosis, or necroptosis, occurs when receptor interacting protein kinase 3 (RIPK3) activates mixed lineage kinase-like (MLKL), causing cell leakage. Thus, activation of DRs, toll-like receptors (TLRs) or pathogen sensor Z-nucleic acid binding protein 1 (ZBP1) initiates apoptosis as well as necroptosis if not blocked by virus-encoded inhibitors. Mammalian cell death pathways are blocked by herpesvirus- and poxvirus-encoded cell death suppressors. Growing evidence has revealed the importance of Z-nucleic acid sensor, ZBP1, in the cell autonomous recognition of both DNA and RNA virus infection. This volume will explore the detente between viruses and cells to manage death machinery and avoid elimination to support dissemination within the host animal.
Additional Links: PMID-37563336
PubMed:
Citation:
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@article {pmid37563336,
year = {2023},
author = {Mocarski, ES},
title = {Programmed Necrosis in Host Defense.},
journal = {Current topics in microbiology and immunology},
volume = {442},
number = {},
pages = {1-40},
pmid = {37563336},
issn = {0070-217X},
mesh = {Animals ; Humans ; Immunity, Innate ; Lymphocytes ; Apoptosis/genetics ; Necrosis/metabolism ; *Herpesviridae ; *Nucleic Acids ; Receptor-Interacting Protein Serine-Threonine Kinases/genetics/metabolism ; Mammals/metabolism ; },
abstract = {Host control over infectious disease relies on the ability of cells in multicellular organisms to detect and defend against pathogens to prevent disease. Evolution affords mammals with a wide variety of independent immune mechanisms to control or eliminate invading infectious agents. Many pathogens acquire functions to deflect these immune mechanisms and promote infection. Following successful invasion of a host, cell autonomous signaling pathways drive the production of inflammatory cytokines, deployment of restriction factors and induction of cell death. Combined, these innate immune mechanisms attract dendritic cells, neutrophils and macrophages as well as innate lymphoid cells such as natural killer cells that all help control infection. Eventually, the development of adaptive pathogen-specific immunity clears infection and provides immune memory of the encounter. For obligate intracellular pathogens such as viruses, diverse cell death pathways make a pivotal contribution to early control by eliminating host cells before progeny are produced. Pro-apoptotic caspase-8 activity (along with caspase-10 in humans) executes extrinsic apoptosis, a nonlytic form of cell death triggered by TNF family death receptors (DRs). Over the past two decades, alternate extrinsic apoptosis and necroptosis outcomes have been described. Programmed necrosis, or necroptosis, occurs when receptor interacting protein kinase 3 (RIPK3) activates mixed lineage kinase-like (MLKL), causing cell leakage. Thus, activation of DRs, toll-like receptors (TLRs) or pathogen sensor Z-nucleic acid binding protein 1 (ZBP1) initiates apoptosis as well as necroptosis if not blocked by virus-encoded inhibitors. Mammalian cell death pathways are blocked by herpesvirus- and poxvirus-encoded cell death suppressors. Growing evidence has revealed the importance of Z-nucleic acid sensor, ZBP1, in the cell autonomous recognition of both DNA and RNA virus infection. This volume will explore the detente between viruses and cells to manage death machinery and avoid elimination to support dissemination within the host animal.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
Humans
Immunity, Innate
Lymphocytes
Apoptosis/genetics
Necrosis/metabolism
*Herpesviridae
*Nucleic Acids
Receptor-Interacting Protein Serine-Threonine Kinases/genetics/metabolism
Mammals/metabolism
RevDate: 2023-08-01
CmpDate: 2023-07-31
The Price of Human Evolution: Cancer-Testis Antigens, the Decline in Male Fertility and the Increase in Cancer.
International journal of molecular sciences, 24(14):.
The increasing frequency of general and particularly male cancer coupled with the reduction in male fertility seen worldwide motivated us to seek a potential evolutionary link between these two phenomena, concerning the reproductive transcriptional modules observed in cancer and the expression of cancer-testis antigens (CTA). The phylostratigraphy analysis of the human genome allowed us to link the early evolutionary origin of cancer via the reproductive life cycles of the unicellulars and early multicellulars, potentially driving soma-germ transition, female meiosis, and the parthenogenesis of polyploid giant cancer cells (PGCCs), with the expansion of the CTA multi-families, very late during their evolution. CTA adaptation was aided by retrovirus domestication in the unstable genomes of mammals, for protecting male fertility in stress conditions, particularly that of humans, as compensation for the energy consumption of a large complex brain which also exploited retrotransposition. We found that the early and late evolutionary branches of human cancer are united by the immunity-proto-placental network, which evolved in the Cambrian and shares stress regulators with the finely-tuned sex determination system. We further propose that social stress and endocrine disruption caused by environmental pollution with organic materials, which alter sex determination in male foetuses and further spermatogenesis in adults, bias the development of PGCC-parthenogenetic cancer by default.
Additional Links: PMID-37511419
PubMed:
Citation:
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@article {pmid37511419,
year = {2023},
author = {Erenpreisa, J and Vainshelbaum, NM and Lazovska, M and Karklins, R and Salmina, K and Zayakin, P and Rumnieks, F and Inashkina, I and Pjanova, D and Erenpreiss, J},
title = {The Price of Human Evolution: Cancer-Testis Antigens, the Decline in Male Fertility and the Increase in Cancer.},
journal = {International journal of molecular sciences},
volume = {24},
number = {14},
pages = {},
pmid = {37511419},
issn = {1422-0067},
mesh = {Pregnancy ; Animals ; Humans ; Male ; Female ; *Testis/metabolism ; Placenta ; Spermatogenesis/genetics ; Reproduction ; *Neoplasms/genetics/metabolism ; Mammals ; Polyploidy ; Fertility/genetics ; },
abstract = {The increasing frequency of general and particularly male cancer coupled with the reduction in male fertility seen worldwide motivated us to seek a potential evolutionary link between these two phenomena, concerning the reproductive transcriptional modules observed in cancer and the expression of cancer-testis antigens (CTA). The phylostratigraphy analysis of the human genome allowed us to link the early evolutionary origin of cancer via the reproductive life cycles of the unicellulars and early multicellulars, potentially driving soma-germ transition, female meiosis, and the parthenogenesis of polyploid giant cancer cells (PGCCs), with the expansion of the CTA multi-families, very late during their evolution. CTA adaptation was aided by retrovirus domestication in the unstable genomes of mammals, for protecting male fertility in stress conditions, particularly that of humans, as compensation for the energy consumption of a large complex brain which also exploited retrotransposition. We found that the early and late evolutionary branches of human cancer are united by the immunity-proto-placental network, which evolved in the Cambrian and shares stress regulators with the finely-tuned sex determination system. We further propose that social stress and endocrine disruption caused by environmental pollution with organic materials, which alter sex determination in male foetuses and further spermatogenesis in adults, bias the development of PGCC-parthenogenetic cancer by default.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Pregnancy
Animals
Humans
Male
Female
*Testis/metabolism
Placenta
Spermatogenesis/genetics
Reproduction
*Neoplasms/genetics/metabolism
Mammals
Polyploidy
Fertility/genetics
RevDate: 2023-08-14
CmpDate: 2023-08-14
A Reinvestigation of Multiple Independent Evolution and Triassic-Jurassic Origins of Multicellular Volvocine Algae.
Genome biology and evolution, 15(8):.
The evolution of multicellular organisms is considered to be a major evolutionary transition, profoundly affecting the ecology and evolution of nearly all life on earth. The volvocine algae, a unique clade of chlorophytes with diverse cell morphology, provide an appealing model for investigating the evolution of multicellularity and development. However, the phylogenetic relationship and timescale of the volvocine algae are not fully resolved. Here, we use extensive taxon and gene sampling to reconstruct the phylogeny of the volvocine algae. Our results support that the colonial volvocine algae are not monophyletic group and multicellularity independently evolve at least twice in the volvocine algae, once in Tetrabaenaceae and another in the Goniaceae + Volvocaceae. The simulation analyses suggest that incomplete lineage sorting is a major factor for the tree topology discrepancy, which imply that the multispecies coalescent model better fits the data used in this study. The coalescent-based species tree supports that the Goniaceae is monophyletic and Crucicarteria is the earliest diverging lineage, followed by Hafniomonas and Radicarteria within the Volvocales. By considering the multiple uncertainties in divergence time estimation, the dating analyses indicate that the volvocine algae occurred during the Cryogenian to Ediacaran (696.6-551.1 Ma) and multicellularity in the volvocine algae originated from the Triassic to Jurassic. Our phylogeny and timeline provide an evolutionary framework for studying the evolution of key traits and the origin of multicellularity in the volvocine algae.
Additional Links: PMID-37498572
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Citation:
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@article {pmid37498572,
year = {2023},
author = {Ma, X and Shi, X and Wang, Q and Zhao, M and Zhang, Z and Zhong, B},
title = {A Reinvestigation of Multiple Independent Evolution and Triassic-Jurassic Origins of Multicellular Volvocine Algae.},
journal = {Genome biology and evolution},
volume = {15},
number = {8},
pages = {},
pmid = {37498572},
issn = {1759-6653},
mesh = {*Chlorophyta/genetics ; *Phylogeny ; Time Factors ; Calibration ; },
abstract = {The evolution of multicellular organisms is considered to be a major evolutionary transition, profoundly affecting the ecology and evolution of nearly all life on earth. The volvocine algae, a unique clade of chlorophytes with diverse cell morphology, provide an appealing model for investigating the evolution of multicellularity and development. However, the phylogenetic relationship and timescale of the volvocine algae are not fully resolved. Here, we use extensive taxon and gene sampling to reconstruct the phylogeny of the volvocine algae. Our results support that the colonial volvocine algae are not monophyletic group and multicellularity independently evolve at least twice in the volvocine algae, once in Tetrabaenaceae and another in the Goniaceae + Volvocaceae. The simulation analyses suggest that incomplete lineage sorting is a major factor for the tree topology discrepancy, which imply that the multispecies coalescent model better fits the data used in this study. The coalescent-based species tree supports that the Goniaceae is monophyletic and Crucicarteria is the earliest diverging lineage, followed by Hafniomonas and Radicarteria within the Volvocales. By considering the multiple uncertainties in divergence time estimation, the dating analyses indicate that the volvocine algae occurred during the Cryogenian to Ediacaran (696.6-551.1 Ma) and multicellularity in the volvocine algae originated from the Triassic to Jurassic. Our phylogeny and timeline provide an evolutionary framework for studying the evolution of key traits and the origin of multicellularity in the volvocine algae.},
}
MeSH Terms:
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*Chlorophyta/genetics
*Phylogeny
Time Factors
Calibration
RevDate: 2023-09-18
CmpDate: 2023-09-07
The molecular basis of tumor metastasis and current approaches to decode targeted migration-promoting events in pediatric neuroblastoma.
Biochemical pharmacology, 215:115696.
Cell motility is a crucial biological process that plays a critical role in the development of multicellular organisms and is essential for tissue formation and regeneration. However, uncontrolled cell motility can lead to the development of various diseases, including neoplasms. In this review, we discuss recent advances in the discovery of regulatory mechanisms underlying the metastatic spread of neuroblastoma, a solid pediatric tumor that originates in the embryonic migratory cells of the neural crest. The highly motile phenotype of metastatic neuroblastoma cells requires targeting of intracellular and extracellular processes, that, if affected, would be helpful for the treatment of high-risk patients with neuroblastoma, for whom current therapies remain inadequate. Development of new potentially migration-inhibiting compounds and standardized preclinical approaches for the selection of anti-metastatic drugs in neuroblastoma will also be discussed.
Additional Links: PMID-37481138
Publisher:
PubMed:
Citation:
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@article {pmid37481138,
year = {2023},
author = {Corallo, D and Dalla Vecchia, M and Lazic, D and Taschner-Mandl, S and Biffi, A and Aveic, S},
title = {The molecular basis of tumor metastasis and current approaches to decode targeted migration-promoting events in pediatric neuroblastoma.},
journal = {Biochemical pharmacology},
volume = {215},
number = {},
pages = {115696},
doi = {10.1016/j.bcp.2023.115696},
pmid = {37481138},
issn = {1873-2968},
mesh = {Humans ; *Neuroblastoma/drug therapy/genetics/pathology ; *Neoplasm Metastasis ; },
abstract = {Cell motility is a crucial biological process that plays a critical role in the development of multicellular organisms and is essential for tissue formation and regeneration. However, uncontrolled cell motility can lead to the development of various diseases, including neoplasms. In this review, we discuss recent advances in the discovery of regulatory mechanisms underlying the metastatic spread of neuroblastoma, a solid pediatric tumor that originates in the embryonic migratory cells of the neural crest. The highly motile phenotype of metastatic neuroblastoma cells requires targeting of intracellular and extracellular processes, that, if affected, would be helpful for the treatment of high-risk patients with neuroblastoma, for whom current therapies remain inadequate. Development of new potentially migration-inhibiting compounds and standardized preclinical approaches for the selection of anti-metastatic drugs in neuroblastoma will also be discussed.},
}
MeSH Terms:
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Humans
*Neuroblastoma/drug therapy/genetics/pathology
*Neoplasm Metastasis
RevDate: 2024-07-07
CmpDate: 2023-09-27
Longevity of Fungal Mycelia and Nuclear Quality Checks: a New Hypothesis for the Role of Clamp Connections in Dikaryons.
Microbiology and molecular biology reviews : MMBR, 87(3):e0002221.
This paper addresses the stability of mycelial growth in fungi and differences between ascomycetes and basidiomycetes. Starting with general evolutionary theories of multicellularity and the role of sex, we then discuss individuality in fungi. Recent research has demonstrated the deleterious consequences of nucleus-level selection in fungal mycelia, favoring cheaters with a nucleus-level benefit during spore formation but a negative effect on mycelium-level fitness. Cheaters appear to generally be loss-of-fusion (LOF) mutants, with a higher propensity to form aerial hyphae developing into asexual spores. Since LOF mutants rely on heterokaryosis with wild-type nuclei, we argue that regular single-spore bottlenecks can efficiently select against such cheater mutants. We then zoom in on ecological differences between ascomycetes being typically fast-growing but short-lived with frequent asexual-spore bottlenecks and basidiomycetes being generally slow-growing but long-lived and usually without asexual-spore bottlenecks. We argue that these life history differences have coevolved with stricter nuclear quality checks in basidiomycetes. Specifically, we propose a new function for clamp connections, structures formed during the sexual stage in ascomycetes and basidiomycetes but during somatic growth only in basidiomycete dikaryons. During dikaryon cell division, the two haploid nuclei temporarily enter a monokaryotic phase, by alternatingly entering a retrograde-growing clamp cell, which subsequently fuses with the subapical cell to recover the dikaryotic cell. We hypothesize that clamp connections act as screening devices for nuclear quality, with both nuclei continuously testing each other for fusion ability, a test that LOF mutants will fail. By linking differences in longevity of the mycelial phase to ecology and stringency of nuclear quality checks, we propose that mycelia have a constant and low lifetime cheating risk, irrespective of their size and longevity.
Additional Links: PMID-37409939
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Citation:
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@article {pmid37409939,
year = {2023},
author = {Aanen, DK and van 't Padje, A and Auxier, B},
title = {Longevity of Fungal Mycelia and Nuclear Quality Checks: a New Hypothesis for the Role of Clamp Connections in Dikaryons.},
journal = {Microbiology and molecular biology reviews : MMBR},
volume = {87},
number = {3},
pages = {e0002221},
pmid = {37409939},
issn = {1098-5557},
mesh = {*Mycelium ; *Hyphae/genetics ; Fungi ; },
abstract = {This paper addresses the stability of mycelial growth in fungi and differences between ascomycetes and basidiomycetes. Starting with general evolutionary theories of multicellularity and the role of sex, we then discuss individuality in fungi. Recent research has demonstrated the deleterious consequences of nucleus-level selection in fungal mycelia, favoring cheaters with a nucleus-level benefit during spore formation but a negative effect on mycelium-level fitness. Cheaters appear to generally be loss-of-fusion (LOF) mutants, with a higher propensity to form aerial hyphae developing into asexual spores. Since LOF mutants rely on heterokaryosis with wild-type nuclei, we argue that regular single-spore bottlenecks can efficiently select against such cheater mutants. We then zoom in on ecological differences between ascomycetes being typically fast-growing but short-lived with frequent asexual-spore bottlenecks and basidiomycetes being generally slow-growing but long-lived and usually without asexual-spore bottlenecks. We argue that these life history differences have coevolved with stricter nuclear quality checks in basidiomycetes. Specifically, we propose a new function for clamp connections, structures formed during the sexual stage in ascomycetes and basidiomycetes but during somatic growth only in basidiomycete dikaryons. During dikaryon cell division, the two haploid nuclei temporarily enter a monokaryotic phase, by alternatingly entering a retrograde-growing clamp cell, which subsequently fuses with the subapical cell to recover the dikaryotic cell. We hypothesize that clamp connections act as screening devices for nuclear quality, with both nuclei continuously testing each other for fusion ability, a test that LOF mutants will fail. By linking differences in longevity of the mycelial phase to ecology and stringency of nuclear quality checks, we propose that mycelia have a constant and low lifetime cheating risk, irrespective of their size and longevity.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Mycelium
*Hyphae/genetics
Fungi
RevDate: 2023-10-21
CmpDate: 2023-10-06
High-throughput library transgenesis in Caenorhabditis elegans via Transgenic Arrays Resulting in Diversity of Integrated Sequences (TARDIS).
eLife, 12:.
High-throughput transgenesis using synthetic DNA libraries is a powerful method for systematically exploring genetic function. Diverse synthesized libraries have been used for protein engineering, identification of protein-protein interactions, characterization of promoter libraries, developmental and evolutionary lineage tracking, and various other exploratory assays. However, the need for library transgenesis has effectively restricted these approaches to single-cell models. Here, we present Transgenic Arrays Resulting in Diversity of Integrated Sequences (TARDIS), a simple yet powerful approach to large-scale transgenesis that overcomes typical limitations encountered in multicellular systems. TARDIS splits the transgenesis process into a two-step process: creation of individuals carrying experimentally introduced sequence libraries, followed by inducible extraction and integration of individual sequences/library components from the larger library cassette into engineered genomic sites. Thus, transformation of a single individual, followed by lineage expansion and functional transgenesis, gives rise to thousands of genetically unique transgenic individuals. We demonstrate the power of this system using engineered, split selectable TARDIS sites in Caenorhabditis elegans to generate (1) a large set of individually barcoded lineages and (2) transcriptional reporter lines from predefined promoter libraries. We find that this approach increases transformation yields up to approximately 1000-fold over current single-step methods. While we demonstrate the utility of TARDIS using C. elegans, in principle the process is adaptable to any system where experimentally generated genomic loci landing pads and diverse, heritable DNA elements can be generated.
Additional Links: PMID-37401921
PubMed:
Citation:
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@article {pmid37401921,
year = {2023},
author = {Stevenson, ZC and Moerdyk-Schauwecker, MJ and Banse, SA and Patel, DS and Lu, H and Phillips, PC},
title = {High-throughput library transgenesis in Caenorhabditis elegans via Transgenic Arrays Resulting in Diversity of Integrated Sequences (TARDIS).},
journal = {eLife},
volume = {12},
number = {},
pages = {},
pmid = {37401921},
issn = {2050-084X},
support = {R01AG056436/NH/NIH HHS/United States ; R35GM131838/NH/NIH HHS/United States ; R35 GM131838/GM/NIGMS NIH HHS/United States ; R01 AG056436/AG/NIA NIH HHS/United States ; T32 GM007413/GM/NIGMS NIH HHS/United States ; },
mesh = {Animals ; Animals, Genetically Modified ; *Caenorhabditis elegans/genetics ; *Gene Library ; *Gene Transfer Techniques ; *Transgenes/genetics ; DNA Barcoding, Taxonomic ; Genetic Variation ; Promoter Regions, Genetic/genetics ; },
abstract = {High-throughput transgenesis using synthetic DNA libraries is a powerful method for systematically exploring genetic function. Diverse synthesized libraries have been used for protein engineering, identification of protein-protein interactions, characterization of promoter libraries, developmental and evolutionary lineage tracking, and various other exploratory assays. However, the need for library transgenesis has effectively restricted these approaches to single-cell models. Here, we present Transgenic Arrays Resulting in Diversity of Integrated Sequences (TARDIS), a simple yet powerful approach to large-scale transgenesis that overcomes typical limitations encountered in multicellular systems. TARDIS splits the transgenesis process into a two-step process: creation of individuals carrying experimentally introduced sequence libraries, followed by inducible extraction and integration of individual sequences/library components from the larger library cassette into engineered genomic sites. Thus, transformation of a single individual, followed by lineage expansion and functional transgenesis, gives rise to thousands of genetically unique transgenic individuals. We demonstrate the power of this system using engineered, split selectable TARDIS sites in Caenorhabditis elegans to generate (1) a large set of individually barcoded lineages and (2) transcriptional reporter lines from predefined promoter libraries. We find that this approach increases transformation yields up to approximately 1000-fold over current single-step methods. While we demonstrate the utility of TARDIS using C. elegans, in principle the process is adaptable to any system where experimentally generated genomic loci landing pads and diverse, heritable DNA elements can be generated.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
Animals, Genetically Modified
*Caenorhabditis elegans/genetics
*Gene Library
*Gene Transfer Techniques
*Transgenes/genetics
DNA Barcoding, Taxonomic
Genetic Variation
Promoter Regions, Genetic/genetics
RevDate: 2024-09-30
CmpDate: 2023-07-03
Is chimerism associated with cancer across the tree of life?.
PloS one, 18(6):e0287901.
Chimerism is a widespread phenomenon across the tree of life. It is defined as a multicellular organism composed of cells from other genetically distinct entities. This ability to 'tolerate' non-self cells may be linked to susceptibility to diseases like cancer. Here we test whether chimerism is associated with cancers across obligately multicellular organisms in the tree of life. We classified 12 obligately multicellular taxa from lowest to highest chimerism levels based on the existing literature on the presence of chimerism in these species. We then tested for associations of chimerism with tumour invasiveness, neoplasia (benign or malignant) prevalence and malignancy prevalence in 11 terrestrial mammalian species. We found that taxa with higher levels of chimerism have higher tumour invasiveness, though there was no association between malignancy or neoplasia and chimerism among mammals. This suggests that there may be an important biological relationship between chimerism and susceptibility to tissue invasion by cancerous cells. Studying chimerism might help us identify mechanisms underlying invasive cancers and also could provide insights into the detection and management of emerging transmissible cancers.
Additional Links: PMID-37384647
PubMed:
Citation:
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@article {pmid37384647,
year = {2023},
author = {Kapsetaki, SE and Fortunato, A and Compton, Z and Rupp, SM and Nour, Z and Riggs-Davis, S and Stephenson, D and Duke, EG and Boddy, AM and Harrison, TM and Maley, CC and Aktipis, A},
title = {Is chimerism associated with cancer across the tree of life?.},
journal = {PloS one},
volume = {18},
number = {6},
pages = {e0287901},
pmid = {37384647},
issn = {1932-6203},
support = {U54 CA217376/CA/NCI NIH HHS/United States ; T32 CA272303/CA/NCI NIH HHS/United States ; U2C CA233254/CA/NCI NIH HHS/United States ; P01 CA091955/CA/NCI NIH HHS/United States ; R01 CA140657/CA/NCI NIH HHS/United States ; R21 CA257980/CA/NCI NIH HHS/United States ; },
mesh = {Animals ; *Chimerism ; *Neoplasms/genetics ; Mammals ; },
abstract = {Chimerism is a widespread phenomenon across the tree of life. It is defined as a multicellular organism composed of cells from other genetically distinct entities. This ability to 'tolerate' non-self cells may be linked to susceptibility to diseases like cancer. Here we test whether chimerism is associated with cancers across obligately multicellular organisms in the tree of life. We classified 12 obligately multicellular taxa from lowest to highest chimerism levels based on the existing literature on the presence of chimerism in these species. We then tested for associations of chimerism with tumour invasiveness, neoplasia (benign or malignant) prevalence and malignancy prevalence in 11 terrestrial mammalian species. We found that taxa with higher levels of chimerism have higher tumour invasiveness, though there was no association between malignancy or neoplasia and chimerism among mammals. This suggests that there may be an important biological relationship between chimerism and susceptibility to tissue invasion by cancerous cells. Studying chimerism might help us identify mechanisms underlying invasive cancers and also could provide insights into the detection and management of emerging transmissible cancers.},
}
MeSH Terms:
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Animals
*Chimerism
*Neoplasms/genetics
Mammals
RevDate: 2023-11-24
CmpDate: 2023-06-26
m[6]A methylation reader IGF2BP2 activates endothelial cells to promote angiogenesis and metastasis of lung adenocarcinoma.
Molecular cancer, 22(1):99.
BACKGROUND: Lung adenocarcinoma (LUAD) is a common type of lung cancer with a high risk of metastasis, but the exact molecular mechanisms of metastasis are not yet understood.
METHODS: This study acquired single-cell transcriptomics profiling of 11 distal normal lung tissues, 11 primary LUAD tissues, and 4 metastatic LUAD tissues from the GSE131907 dataset. The lung multicellular ecosystems were characterized at a single-cell resolution, and the potential mechanisms underlying angiogenesis and metastasis of LUAD were explored.
RESULTS: We constructed a global single-cell landscape of 93,610 cells from primary and metastatic LUAD and found that IGF2BP2 was specifically expressed both in a LUAD cell subpopulation (termed as LUAD_IGF2BP2), and an endothelial cell subpopulation (termed as En_IGF2BP2). The LUAD_IGF2BP2 subpopulation progressively formed and dominated the ecology of metastatic LUAD during metastatic evolution. IGF2BP2 was preferentially secreted by exosomes in the LUAD_IGF2BP2 subpopulation, which was absorbed by the En_IGF2BP2 subpopulation in the tumor microenvironment. Subsequently, IGF2BP2 improved the RNA stability of FLT4 through m[6]A modification, thereby activating the PI3K-Akt signaling pathway, and eventually promoting angiogenesis and metastasis. Analysis of clinical data showed that IGF2BP2 was linked with poor overall survival and relapse-free survival for LUAD patients.
CONCLUSIONS: Overall, these findings provide a novel insight into the multicellular ecosystems of primary and metastatic LUAD, and demonstrate that a specific LUAD_IGF2BP2 subpopulation is a key orchestrator promoting angiogenesis and metastasis, with implications for the gene regulatory mechanisms of LUAD metastatic evolution, representing themselves as potential antiangiogenic targets.
Additional Links: PMID-37353784
PubMed:
Citation:
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@article {pmid37353784,
year = {2023},
author = {Fang, H and Sun, Q and Zhou, J and Zhang, H and Song, Q and Zhang, H and Yu, G and Guo, Y and Huang, C and Mou, Y and Jia, C and Song, Y and Liu, A and Song, K and Lu, C and Tian, R and Wei, S and Yang, D and Chen, Y and Li, T and Wang, K and Yu, Y and Lv, Y and Mo, K and Sun, P and Yu, X and Song, X},
title = {m[6]A methylation reader IGF2BP2 activates endothelial cells to promote angiogenesis and metastasis of lung adenocarcinoma.},
journal = {Molecular cancer},
volume = {22},
number = {1},
pages = {99},
pmid = {37353784},
issn = {1476-4598},
mesh = {Humans ; Methylation ; Ecosystem ; Endothelial Cells ; Phosphatidylinositol 3-Kinases ; Neoplasm Recurrence, Local ; *Adenocarcinoma of Lung/genetics ; *Lung Neoplasms/genetics ; Tumor Microenvironment ; RNA-Binding Proteins/genetics ; },
abstract = {BACKGROUND: Lung adenocarcinoma (LUAD) is a common type of lung cancer with a high risk of metastasis, but the exact molecular mechanisms of metastasis are not yet understood.
METHODS: This study acquired single-cell transcriptomics profiling of 11 distal normal lung tissues, 11 primary LUAD tissues, and 4 metastatic LUAD tissues from the GSE131907 dataset. The lung multicellular ecosystems were characterized at a single-cell resolution, and the potential mechanisms underlying angiogenesis and metastasis of LUAD were explored.
RESULTS: We constructed a global single-cell landscape of 93,610 cells from primary and metastatic LUAD and found that IGF2BP2 was specifically expressed both in a LUAD cell subpopulation (termed as LUAD_IGF2BP2), and an endothelial cell subpopulation (termed as En_IGF2BP2). The LUAD_IGF2BP2 subpopulation progressively formed and dominated the ecology of metastatic LUAD during metastatic evolution. IGF2BP2 was preferentially secreted by exosomes in the LUAD_IGF2BP2 subpopulation, which was absorbed by the En_IGF2BP2 subpopulation in the tumor microenvironment. Subsequently, IGF2BP2 improved the RNA stability of FLT4 through m[6]A modification, thereby activating the PI3K-Akt signaling pathway, and eventually promoting angiogenesis and metastasis. Analysis of clinical data showed that IGF2BP2 was linked with poor overall survival and relapse-free survival for LUAD patients.
CONCLUSIONS: Overall, these findings provide a novel insight into the multicellular ecosystems of primary and metastatic LUAD, and demonstrate that a specific LUAD_IGF2BP2 subpopulation is a key orchestrator promoting angiogenesis and metastasis, with implications for the gene regulatory mechanisms of LUAD metastatic evolution, representing themselves as potential antiangiogenic targets.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Methylation
Ecosystem
Endothelial Cells
Phosphatidylinositol 3-Kinases
Neoplasm Recurrence, Local
*Adenocarcinoma of Lung/genetics
*Lung Neoplasms/genetics
Tumor Microenvironment
RNA-Binding Proteins/genetics
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