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[PMID]:28457750
[Au] Autor:Li L; Dong J; Yan L; Yong J; Liu X; Hu Y; Fan X; Wu X; Guo H; Wang X; Zhu X; Li R; Yan J; Wei Y; Zhao Y; Wang W; Ren Y; Yuan P; Yan Z; Hu B; Guo F; Wen L; Tang F; Qiao J
[Ad] Endereço:Beijing Advanced Innovation Center for Genomics (ICG), College of Life Sciences, Department of Obstetrics and Gynecology, Third Hospital, Peking University, Beijing 100871, China; Biomedical Institute for Pioneering Investigation via Convergence and Center for Reproductive Medicine, Ministry of Educ
[Ti] Título:Single-Cell RNA-Seq Analysis Maps Development of Human Germline Cells and Gonadal Niche Interactions.
[So] Source:Cell Stem Cell;20(6):858-873.e4, 2017 Jun 01.
[Is] ISSN:1875-9777
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human fetal germ cells (FGCs) are precursors to sperm and eggs and are crucial for maintenance of the species. However, the developmental trajectories and heterogeneity of human FGCs remain largely unknown. Here we performed single-cell RNA-seq analysis of over 2,000 FGCs and their gonadal niche cells in female and male human embryos spanning several developmental stages. We found that female FGCs undergo four distinct sequential phases characterized by mitosis, retinoic acid signaling, meiotic prophase, and oogenesis. Male FGCs develop through stages of migration, mitosis, and cell-cycle arrest. Individual embryos of both sexes simultaneously contain several subpopulations, highlighting the asynchronous and heterogeneous nature of FGC development. Moreover, we observed reciprocal signaling interactions between FGCs and their gonadal niche cells, including activation of the bone morphogenic protein (BMP) and Notch signaling pathways. Our work provides key insights into the crucial features of human FGCs during their highly ordered mitotic, meiotic, and gametogenetic processes in vivo.
[Mh] Termos MeSH primário: Divisão Celular/fisiologia
Células Germinativas Embrionárias/metabolismo
Feto/metabolismo
Gônadas/enzimologia
Transdução de Sinais/fisiologia
Nicho de Células-Tronco/fisiologia
[Mh] Termos MeSH secundário: Proteínas Morfogenéticas Ósseas/metabolismo
Células Germinativas Embrionárias/citologia
Feminino
Feto/citologia
Gônadas/citologia
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Masculino
Receptores Notch/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bone Morphogenetic Proteins); 0 (Receptors, Notch)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


  2 / 167682 MEDLINE  
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[PMID]:28463114
[Au] Autor:Moura M; Osswald M; Leça N; Barbosa J; Pereira AJ; Maiato H; Sunkel CE; Conde C
[Ad] Endereço:i3S, Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Porto, Portugal.
[Ti] Título:Protein Phosphatase 1 inactivates Mps1 to ensure efficient Spindle Assembly Checkpoint silencing.
[So] Source:Elife;6, 2017 05 02.
[Is] ISSN:2050-084X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Faithfull genome partitioning during cell division relies on the Spindle Assembly Checkpoint (SAC), a conserved signaling pathway that delays anaphase onset until all chromosomes are attached to spindle microtubules. Mps1 kinase is an upstream SAC regulator that promotes the assembly of an anaphase inhibitor through a sequential multi-target phosphorylation cascade. Thus, the SAC is highly responsive to Mps1, whose activity peaks in early mitosis as a result of its T-loop autophosphorylation. However, the mechanism controlling Mps1 inactivation once kinetochores attach to microtubules and the SAC is satisfied remains unknown. Here we show and in that Protein Phosphatase 1 (PP1) inactivates Mps1 by dephosphorylating its T-loop. PP1-mediated dephosphorylation of Mps1 occurs at kinetochores and in the cytosol, and inactivation of both pools of Mps1 during metaphase is essential to ensure prompt and efficient SAC silencing. Overall, our findings uncover a mechanism of SAC inactivation required for timely mitotic exit.
[Mh] Termos MeSH primário: Proteínas de Ciclo Celular/metabolismo
Divisão Celular
Segregação de Cromossomos
Proteínas de Drosophila/metabolismo
Drosophila/fisiologia
Pontos de Checagem da Fase M do Ciclo Celular
Proteína Fosfatase 1/metabolismo
Proteínas Serina-Treonina Quinases/metabolismo
[Mh] Termos MeSH secundário: Animais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cell Cycle Proteins); 0 (Drosophila Proteins); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (ald protein, Drosophila); EC 3.1.3.16 (Protein Phosphatase 1)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


  3 / 167682 MEDLINE  
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[PMID]:27771340
[Au] Autor:Ambrosini A; Gracia M; Proag A; Rayer M; Monier B; Suzanne M
[Ad] Endereço:LBCMCP UMR5088, Centre de Biologie Integrative (CBI), Université de Toulouse, CNRS, UPS, France.
[Ti] Título:Apoptotic forces in tissue morphogenesis.
[So] Source:Mech Dev;144(Pt A):33-42, 2017 04.
[Is] ISSN:1872-6356
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:It is now well established that apoptosis is induced in response to mechanical strain. Indeed, increasing compressive forces induces apoptosis in confined spheroids of tumour cells, whereas releasing stress reduces apoptosis in spheroids cultivated in free suspension (Cheng et al., 2009). Apoptosis can also be induced by applying a 100 to 250MPa pressure, as shown in different cultured cells (for review, see (Frey et al., 2008)). During epithelium development, the pressure caused by a fast-growing clone can trigger apoptosis at the vicinity of the clone, mediating mechanical cell competition (Levayer et al., 2016). While the effect of strain has long been known for its role in apoptosis induction, the reciprocal mechanism has only recently been highlighted. First demonstrated at the cellular level, the effect of an apoptotic cell on its direct neighbours has been analysed in different kinds of monolayer epithelium (Gu et al., 2011; Rosenblatt et al., 2001; Kuipers et al., 2014; Lubkov & Bar-Sagi, 2014). More recently, the concept of a broader impact of apoptotic cell behaviours on tissue mechanical strain has emerged from the characterisation of tissue remodelling during Drosophila development (Toyama et al., 2008; Monier et al., 2015). In the present review, we summarize our current knowledge on the mechanical impact of apoptosis during tissue remodelling.
[Mh] Termos MeSH primário: Apoptose/genética
Drosophila melanogaster/crescimento & desenvolvimento
Células Epiteliais/citologia
Regulação da Expressão Gênica no Desenvolvimento
Morfogênese/genética
[Mh] Termos MeSH secundário: Abdome/crescimento & desenvolvimento
Animais
Divisão Celular
Proteínas de Ligação a DNA/genética
Proteínas de Ligação a DNA/metabolismo
Proteínas de Drosophila/genética
Proteínas de Drosophila/metabolismo
Drosophila melanogaster/genética
Drosophila melanogaster/metabolismo
Células Epiteliais/metabolismo
Matriz Extracelular/metabolismo
Larva/genética
Larva/crescimento & desenvolvimento
Larva/metabolismo
Modelos Biológicos
Pupa/genética
Pupa/crescimento & desenvolvimento
Pupa/metabolismo
Estresse Mecânico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA-Binding Proteins); 0 (Drosophila Proteins); 0 (dwg protein, Drosophila); 0 (reaper protein, Drosophila)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


  4 / 167682 MEDLINE  
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[PMID]:29338026
[Au] Autor:Vanzyl EJ; Rick KRC; Blackmore AB; MacFarlane EM; McKay BC
[Ad] Endereço:Department of Biology, Carleton University, Ottawa ON, Canada.
[Ti] Título:Flow cytometric analysis identifies changes in S and M phases as novel cell cycle alterations induced by the splicing inhibitor isoginkgetin.
[So] Source:PLoS One;13(1):e0191178, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The spliceosome is a large ribonucleoprotein complex that catalyzes the removal of introns from RNA polymerase II-transcribed RNAs. Spliceosome assembly occurs in a stepwise manner through specific intermediates referred to as pre-spliceosome complexes E, A, B, B* and C. It has been reported that small molecule inhibitors of the spliceosome that target the SF3B1 protein component of complex A lead to the accumulation of cells in the G1 and G2/M phases of the cell cycle. Here we performed a comprehensive flow cytometry analysis of the effects of isoginkgetin (IGG), a natural compound that interferes with spliceosome assembly at a later step, complex B formation. We found that IGG slowed cell cycle progression in multiple phases of the cell cycle (G1, S and G2) but not M phase. This pattern was somewhat similar to but distinguishable from changes associated with an SF3B1 inhibitor, pladienolide B (PB). Both drugs led to a significant decrease in nascent DNA synthesis in S phase, indicative of an S phase arrest. However, IGG led to a much more prominent S phase arrest than PB while PB exhibited a more pronounced G1 arrest that decreased the proportion of cells in S phase as well. We also found that both drugs led to a comparable decrease in the proportion of cells in M phase. This work indicates that spliceosome inhibitors affect multiple phases of the cell cycle and that some of these effects vary in an agent-specific manner despite the fact that they target splicing at similar stages of spliceosome assembly.
[Mh] Termos MeSH primário: Biflavonoides/farmacologia
Divisão Celular/efeitos dos fármacos
Processamento de RNA/efeitos dos fármacos
Fase S/efeitos dos fármacos
[Mh] Termos MeSH secundário: Ciclo Celular/efeitos dos fármacos
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Replicação do DNA/efeitos dos fármacos
Compostos de Epóxi/farmacologia
Citometria de Fluxo
Células HCT116
Seres Humanos
Macrolídeos/farmacologia
Precursores de RNA/metabolismo
Spliceossomos/efeitos dos fármacos
Spliceossomos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biflavonoids); 0 (Epoxy Compounds); 0 (Macrolides); 0 (RNA Precursors); 0 (isoginkgetin); 0 (pladienolide B)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180117
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191178


  5 / 167682 MEDLINE  
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[PMID]:28467946
[Au] Autor:Torrano V; Carracedo A
[Ad] Endereço:CIC bioGUNE, 801A Bizkaia Technology Park, 48160 Derio, Spain; CIBERONC.
[Ti] Título:Quiescence-like Metabolism to Push Cancer Out of the Race.
[So] Source:Cell Metab;25(5):997-999, 2017 May 02.
[Is] ISSN:1932-7420
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Biological features acquired or lost during the tumorigenic process are a source for the discovery of molecular cues relevant to cancer. The latest study led by the Weinberg lab (Keckesova et al., 2017) focuses on the transcriptional program underlying quiescence to uncover a novel metabolic tumor suppressor, LACTB.
[Mh] Termos MeSH primário: Proteínas de Membrana/metabolismo
Proteínas Mitocondriais/metabolismo
Neoplasias/metabolismo
beta-Lactamases/metabolismo
[Mh] Termos MeSH secundário: Animais
Carboxiliases/metabolismo
Divisão Celular
Proliferação Celular
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Proteínas de Membrana/genética
Mitocôndrias/genética
Mitocôndrias/metabolismo
Mitocôndrias/patologia
Proteínas Mitocondriais/genética
Neoplasias/genética
Neoplasias/patologia
Transdução de Sinais
Proteínas Supressoras de Tumor/genética
Proteínas Supressoras de Tumor/metabolismo
beta-Lactamases/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Membrane Proteins); 0 (Mitochondrial Proteins); 0 (Tumor Suppressor Proteins); EC 3.4.- (LACTB protein, human); EC 3.5.2.6 (beta-Lactamases); EC 4.1.1.- (Carboxy-Lyases); EC 4.1.1.65 (phosphatidylserine decarboxylase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180219
[Lr] Data última revisão:
180219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


  6 / 167682 MEDLINE  
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[PMID]:28450582
[Au] Autor:McConnell MJ; Moran JV; Abyzov A; Akbarian S; Bae T; Cortes-Ciriano I; Erwin JA; Fasching L; Flasch DA; Freed D; Ganz J; Jaffe AE; Kwan KY; Kwon M; Lodato MA; Mills RE; Paquola ACM; Rodin RE; Rosenbluh C; Sestan N; Sherman MA; Shin JH; Song S; Straub RE; Thorpe J; Weinberger DR; Urban AE; Zhou B; Gage FH; Lehner T; Senthil G; Walsh CA; Chess A; Courchesne E; Gleeson JG; Kidd JM; Park PJ; Pevsner J; Vaccarino FM; Brain Somatic Mosaicism Network
[Ti] Título:Intersection of diverse neuronal genomes and neuropsychiatric disease: The Brain Somatic Mosaicism Network.
[So] Source:Science;356(6336), 2017 Apr 28.
[Is] ISSN:1095-9203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neuropsychiatric disorders have a complex genetic architecture. Human genetic population-based studies have identified numerous heritable sequence and structural genomic variants associated with susceptibility to neuropsychiatric disease. However, these germline variants do not fully account for disease risk. During brain development, progenitor cells undergo billions of cell divisions to generate the ~80 billion neurons in the brain. The failure to accurately repair DNA damage arising during replication, transcription, and cellular metabolism amid this dramatic cellular expansion can lead to somatic mutations. Somatic mutations that alter subsets of neuronal transcriptomes and proteomes can, in turn, affect cell proliferation and survival and lead to neurodevelopmental disorders. The long life span of individual neurons and the direct relationship between neural circuits and behavior suggest that somatic mutations in small populations of neurons can significantly affect individual neurodevelopment. The Brain Somatic Mosaicism Network has been founded to study somatic mosaicism both in neurotypical human brains and in the context of complex neuropsychiatric disorders.
[Mh] Termos MeSH primário: Encéfalo/anormalidades
Transtornos Mentais/genética
Mosaicismo
Doenças do Sistema Nervoso/genética
Células-Tronco Neurais/fisiologia
Neurônios/fisiologia
[Mh] Termos MeSH secundário: Encéfalo/metabolismo
Divisão Celular/genética
Dano ao DNA
Análise Mutacional de DNA/métodos
Reparo do DNA/genética
Replicação do DNA
Genoma Humano
Células Germinativas/metabolismo
Seres Humanos
Rede Nervosa/crescimento & desenvolvimento
Rede Nervosa/metabolismo
Células-Tronco Neurais/metabolismo
Neurônios/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180219
[Lr] Data última revisão:
180219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE


  7 / 167682 MEDLINE  
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[PMID]:28466007
[Au] Autor:Peng Y; Scott P; Tao R; Wang H; Wu Y; Peng G
[Ad] Endereço:Department of Clinical Cancer Prevention, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
[Ti] Título:Dissect the Dynamic Molecular Circuits of Cell Cycle Control through Network Evolution Model.
[So] Source:Biomed Res Int;2017:2954351, 2017.
[Is] ISSN:2314-6141
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The molecular circuits of cell cycle control serve as a key hub to integrate from endogenous and environmental signals into a robust biological decision driving cell growth and division. Dysfunctional cell cycle control is highlighted in a wide spectrum of human cancers. More importantly the mainstay anticancer treatment such as radiation therapy and chemotherapy targets the hallmark of uncontrolled cell proliferation in cancer cells by causing DNA damage, cell cycle arrest, and cell death. Given the functional importance of cell cycle control, the regulatory mechanisms that drive the cell division have been extensively investigated in a huge number of studies by conventional single-gene approaches. However the complexity of cell cycle control renders a significant barrier to understand its function at a network level. In this study, we used mathematical modeling through modern graph theory and differential equation systems. We believe our network evolution model can help us understand the dynamic cell cycle control in tumor evolution and optimizing dosing schedules for radiation therapy and chemotherapy targeting cell cycle.
[Mh] Termos MeSH primário: Pontos de Checagem do Ciclo Celular/genética
Modelos Teóricos
Neoplasias/genética
[Mh] Termos MeSH secundário: Apoptose/genética
Divisão Celular/genética
Proliferação Celular/genética
Dano ao DNA/genética
Seres Humanos
Neoplasias/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1155/2017/2954351


  8 / 167682 MEDLINE  
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[PMID]:28465207
[Au] Autor:Song AT; Galli A; Leclerc S; Nattel S; Mandato C; Andelfinger G
[Ad] Endereço:Cardiovascular Genetics, Department of Pediatrics, CHU Sainte-Justine, Montreal, QC, Canada; McGill University, Department of Anatomy and Cell Biology, Montreal, QC, Canada.
[Ti] Título:Characterization of Sgo1 expression in developing and adult mouse.
[So] Source:Gene Expr Patterns;25-26:36-45, 2017 Nov.
[Is] ISSN:1872-7298
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:SGO1 has been characterized in its function in correct cell division and its role in centrosome cohesion in the nucleus. However, its organ-specific maturation-related expression pattern in vivo remains largely uncharacterized. Here, we show clear SGO1 expression in post-developmental neuronal cells and cytoplasmic localisation in nucleated cells with a transgenic mice model and immunohistochemistry of wild type mice. We demonstrate extranuclear expression of Sgo1 in the developing heart and gut, which have been shown to be dysregulated in humans with homozygous SGO1 mutation. Additionally, we show Sgo1 expression in select population of retinal cells in developing and post-developmental retina. Our expression analysis strongly suggests that the function of SGO1 goes beyond its well characterized role in cell division.
[Mh] Termos MeSH primário: Proteínas de Ciclo Celular/genética
Proteínas de Ciclo Celular/metabolismo
Citoplasma/metabolismo
Embrião de Mamíferos/metabolismo
[Mh] Termos MeSH secundário: Animais
Divisão Celular
Citoplasma/genética
Trato Gastrointestinal/crescimento & desenvolvimento
Trato Gastrointestinal/metabolismo
Regulação da Expressão Gênica no Desenvolvimento
Células HeLa
Coração/crescimento & desenvolvimento
Seres Humanos
Camundongos
Camundongos Transgênicos
Miocárdio/metabolismo
Neurônios/metabolismo
Especificidade de Órgãos
Retina/crescimento & desenvolvimento
Retina/metabolismo
Distribuição Tecidual
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cell Cycle Proteins); 0 (shugoshin protein, mouse)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


  9 / 167682 MEDLINE  
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[PMID]:28465423
[Au] Autor:Wagstaff JM; Tsim M; Oliva MA; García-Sanchez A; Kureisaite-Ciziene D; Andreu JM; Löwe J
[Ad] Endereço:MRC Laboratory of Molecular Biology, Cambridge, United Kingdom.
[Ti] Título:A Polymerization-Associated Structural Switch in FtsZ That Enables Treadmilling of Model Filaments.
[So] Source:MBio;8(3), 2017 May 02.
[Is] ISSN:2150-7511
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bacterial cell division in many organisms involves a constricting cytokinetic ring that is orchestrated by the tubulin-like protein FtsZ. FtsZ forms dynamic filaments close to the membrane at the site of division that have recently been shown to treadmill around the division ring, guiding septal wall synthesis. Here, using X-ray crystallography of FtsZ (SaFtsZ), we reveal how an FtsZ can adopt two functionally distinct conformations, open and closed. The open form is found in SaFtsZ filaments formed in crystals and also in soluble filaments of FtsZ as deduced by electron cryomicroscopy. The closed form is found within several crystal forms of two nonpolymerizing SaFtsZ mutants and corresponds to many previous FtsZ structures from other organisms. We argue that FtsZ's conformational switch is polymerization-associated, driven by the formation of the longitudinal intersubunit interfaces along the filament. We show that such a switch provides explanations for both how treadmilling may occur within a single-stranded filament and why filament assembly is cooperative. The FtsZ protein is a key molecule during bacterial cell division. FtsZ forms filaments that organize cell membrane constriction, as well as remodeling of the cell wall, to divide cells. FtsZ functions through nucleotide-driven filament dynamics that are poorly understood at the molecular level. In particular, mechanisms for cooperative assembly (nonlinear dependency on concentration) and treadmilling (preferential growth at one filament end and loss at the other) have remained elusive. Here, we show that most likely all FtsZ proteins have two distinct conformations, a "closed" form in monomeric FtsZ and an "open" form in filaments. The conformational switch that occurs upon polymerization explains cooperativity and, in concert with polymerization-dependent nucleotide hydrolysis, efficient treadmilling of FtsZ polymers.
[Mh] Termos MeSH primário: Proteínas de Bactérias/química
Proteínas de Bactérias/metabolismo
Proteínas do Citoesqueleto/química
Proteínas do Citoesqueleto/metabolismo
Citoesqueleto/metabolismo
Staphylococcus aureus/metabolismo
[Mh] Termos MeSH secundário: Divisão Celular
Microscopia Crioeletrônica
Cristalografia por Raios X
Citoesqueleto/química
Escherichia coli/metabolismo
Mutação
Polimerização
Conformação Proteica
Staphylococcus aureus/química
Staphylococcus aureus/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Cytoskeletal Proteins); 0 (FtsZ protein, Bacteria)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180126
[Lr] Data última revisão:
180126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


  10 / 167682 MEDLINE  
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[PMID]:29212000
[Au] Autor:Andrade-Restrepo M
[Ad] Endereço:Institut Jacques Monod, CNRS UMR 7592, Université Paris Diderot, Sorbonne Paris Cité, Paris, France. Electronic address: martinandraderestrepo@gmail.com.
[Ti] Título:Is Aggregate-Dependent Yeast Aging Fortuitous? A Model of Damage Segregation and Aggregate Dynamics.
[So] Source:Biophys J;113(11):2464-2476, 2017 Dec 05.
[Is] ISSN:1542-0086
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:During cytokinesis in Saccharomyces cerevisiae, damaged proteins are distributed unequally between the daughter and mother cells. The retention of these proteins is correlated with yeast aging. Even though evidence suggests that aggregates are retained due to an underlying molecular mechanism, the debate on whether an active mechanism is necessary for this asymmetry remains unsolved. In particular, passive diffusion and a bud-specific dilution remain as possible explanations. Here, a computational and mathematical model is provided to test whether passive mechanisms alone are sufficient to account for the aggregate distribution patterns and the aggregate kinetics observed in living cells. To this author's knowledge, this is the most comprehensive model available on this subject and the only one combining key potentially essential passive-only mechanisms proposed in existing bibliography-namely, the geometrical effect of the dividing yeast cell on the diffusion of protein aggregates, and the possibility of aggregate binding and aggregate formation at different rates. Results suggest that although passive processes alone can reproduce certain averaged observables from experimental bibliography, they are insufficient to vindicate aggregate activity observed in living budding yeast cells. These results are complemented by showing that under basic forms of active quality control, discrepancies between the outputs of the model and experimental bibliography are reduced.
[Mh] Termos MeSH primário: Modelos Biológicos
Saccharomyces cerevisiae/citologia
[Mh] Termos MeSH secundário: Divisão Celular
Cinética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180119
[Lr] Data última revisão:
180119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171207
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BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde