Base de dados : MEDLINE
Pesquisa : G04.144.220.109 [Categoria DeCS]
Referências encontradas : 261 [refinar]
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  1 / 261 MEDLINE  
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[PMID]:27771141
[Au] Autor:Kaminski MM; Liedmann S; Milasta S; Green DR
[Ad] Endereço:Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN, 38105, USA.
[Ti] Título:Polarization and asymmetry in T cell metabolism.
[So] Source:Semin Immunol;28(5):525-534, 2016 Oct.
[Is] ISSN:1096-3618
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:T cell activation results in a rapidly proliferating T cell endowed with a metabolic phenotype necessary for growth and division. However, before the cell can proceed towards this burst of cell division a phase of quiescence occurs, during which the basic mechanisms governing regulation of metabolic reprograming are established. This review focuses on key cellular processes controlling early metabolic regulation and how these circuits of metabolic control dictate distinct cellular fates upon the first asymmetric division.
[Mh] Termos MeSH primário: Divisão Celular Assimétrica
Metabolismo Energético
Ativação Linfocitária/imunologia
Linfócitos T/imunologia
Linfócitos T/metabolismo
[Mh] Termos MeSH secundário: Animais
Divisão Celular Assimétrica/genética
Divisão Celular Assimétrica/imunologia
Biomarcadores
Regulação da Expressão Gênica
Seres Humanos
Ativação Linfocitária/genética
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biomarkers)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180113
[Lr] Data última revisão:
180113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


  2 / 261 MEDLINE  
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[PMID]:28851710
[Au] Autor:Mellott DO; Thisdelle J; Burke RD
[Ad] Endereço:Biochemistry and Microbiology, University of Victoria, Victoria, BC, Canada V8W 2Y2.
[Ti] Título:Notch signaling patterns neurogenic ectoderm and regulates the asymmetric division of neural progenitors in sea urchin embryos.
[So] Source:Development;144(19):3602-3611, 2017 10 01.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We have examined regulation of neurogenesis by Delta/Notch signaling in sea urchin embryos. At gastrulation, neural progenitors enter S phase coincident with expression of Sp-SoxC. We used a BAC containing knocked into the locus to label neural progenitors. Live imaging and immunolocalizations indicate that Sp-SoxC-expressing cells divide to produce pairs of adjacent cells expressing GFP. Over an interval of about 6 h, one cell fragments, undergoes apoptosis and expresses high levels of activated Caspase3. A Notch reporter indicates that Notch signaling is activated in cells adjacent to cells expressing Sp-SoxC. Inhibition of γ-secretase, injection of Sp-Delta morpholinos or CRISPR/Cas9-induced mutation of results in supernumerary neural progenitors and neurons. Interfering with Notch signaling increases neural progenitor recruitment and pairs of neural progenitors. Thus, Notch signaling restricts the number of neural progenitors recruited and regulates the fate of progeny of the asymmetric division. We propose a model in which localized signaling converts ectodermal and ciliary band cells to neural progenitors that divide asymmetrically to produce a neural precursor and an apoptotic cell.
[Mh] Termos MeSH primário: Divisão Celular Assimétrica
Embrião não Mamífero/metabolismo
Células-Tronco Neurais/citologia
Neurogênese
Receptores Notch/metabolismo
Ouriços-do-Mar/embriologia
Ouriços-do-Mar/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Apoptose
Padronização Corporal
Ectoderma/citologia
Ectoderma/metabolismo
Embrião não Mamífero/citologia
Proteínas de Fluorescência Verde/metabolismo
Mitose
Modelos Biológicos
Células-Tronco Neurais/metabolismo
Neurônios/citologia
Neurônios/metabolismo
Fatores de Transcrição SOX/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Receptors, Notch); 0 (SOX Transcription Factors); 147336-22-9 (Green Fluorescent Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170831
[St] Status:MEDLINE
[do] DOI:10.1242/dev.151720


  3 / 261 MEDLINE  
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[PMID]:28827395
[Au] Autor:Winter ES; Schwarz A; Fabig G; Feldman JL; Pires-daSilva A; Müller-Reichert T; Sadler PL; Shakes DC
[Ad] Endereço:Department of Biology, College of William and Mary, Williamsburg, VA 23187, USA.
[Ti] Título:Cytoskeletal variations in an asymmetric cell division support diversity in nematode sperm size and sex ratios.
[So] Source:Development;144(18):3253-3263, 2017 09 15.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Asymmetric partitioning is an essential component of many developmental processes. As spermatogenesis concludes, sperm are streamlined by discarding unnecessary cellular components into cellular wastebags called residual bodies (RBs). During nematode spermatogenesis, this asymmetric partitioning event occurs shortly after anaphase II, and both microtubules and actin partition into a central RB. Here, we use fluorescence and transmission electron microscopy to elucidate and compare the intermediate steps of RB formation in , sp. SB347 (recently named ) and related nematodes. In all cases, intact microtubules reorganize and move from centrosomal to non-centrosomal sites at the RB-sperm boundary whereas actin reorganizes through cortical ring expansion and clearance from the poles. However, in species with tiny spermatocytes, these cytoskeletal changes are restricted to one pole. Consequently, partitioning yields one functional sperm with the X-bearing chromosome complement and an RB with the other chromosome set. Unipolar partitioning may not require an unpaired X, as it also occurs in XX spermatocytes. Instead, constraints related to spermatocyte downsizing may have contributed to the evolution of a sperm cell equivalent to female polar bodies.
[Mh] Termos MeSH primário: Divisão Celular Assimétrica
Caenorhabditis elegans/citologia
Tamanho Celular
Citoesqueleto/metabolismo
Razão de Masculinidade
Espermatozoides/citologia
[Mh] Termos MeSH secundário: Actinas/metabolismo
Animais
Centrossomo/metabolismo
Citoesqueleto/ultraestrutura
Feminino
Organismos Hermafroditas/citologia
Masculino
Meiose
Microtúbulos/metabolismo
Modelos Biológicos
Espermatócitos/citologia
Espermatócitos/ultraestrutura
Espermatogênese
Espermatozoides/ultraestrutura
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Actins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170823
[St] Status:MEDLINE
[do] DOI:10.1242/dev.153841


  4 / 261 MEDLINE  
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[PMID]:28712722
[Au] Autor:Tsankova A; Pham TT; Garcia DS; Otte F; Cabernard C
[Ad] Endereço:Biozentrum, University of Basel, Klingelbergstrasse 50-70, 4056 Basel, Switzerland.
[Ti] Título:Cell Polarity Regulates Biased Myosin Activity and Dynamics during Asymmetric Cell Division via Drosophila Rho Kinase and Protein Kinase N.
[So] Source:Dev Cell;42(2):143-155.e5, 2017 Jul 24.
[Is] ISSN:1878-1551
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cell and tissue morphogenesis depends on the correct regulation of non-muscle Myosin II, but how this motor protein is spatiotemporally controlled is incompletely understood. Here, we show that in asymmetrically dividing Drosophila neural stem cells, cell intrinsic polarity cues provide spatial and temporal information to regulate biased Myosin activity. Using live cell imaging and a genetically encoded Myosin activity sensor, we found that Drosophila Rho kinase (Rok) enriches for activated Myosin on the neuroblast cortex prior to nuclear envelope breakdown (NEB). After NEB, the conserved polarity protein Partner of Inscuteable (Pins) sequentially enriches Rok and Protein Kinase N (Pkn) on the apical neuroblast cortex. Our data suggest that apical Rok first increases phospho-Myosin, followed by Pkn-mediated Myosin downregulation, possibly through Rok inhibition. We propose that polarity-induced spatiotemporal control of Rok and Pkn is important for unequal cortical expansion, ensuring correct cleavage furrow positioning and the establishment of physical asymmetry.
[Mh] Termos MeSH primário: Divisão Celular Assimétrica
Polaridade Celular
Proteínas de Drosophila/metabolismo
Drosophila melanogaster/citologia
Drosophila melanogaster/enzimologia
Miosinas/metabolismo
Proteína Quinase C/metabolismo
Quinases Associadas a rho/metabolismo
[Mh] Termos MeSH secundário: Anáfase
Animais
Forma Celular
Mutação/genética
Neurônios/citologia
Neurônios/metabolismo
Fosforilação
Transporte Proteico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Drosophila Proteins); EC 2.7.1.- (protein kinase N); EC 2.7.11.1 (rho-Associated Kinases); EC 2.7.11.13 (Protein Kinase C); EC 3.6.4.1 (Myosins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170718
[St] Status:MEDLINE


  5 / 261 MEDLINE  
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[PMID]:28632741
[Au] Autor:Nakaoka H; Wakamoto Y
[Ad] Endereço:Department of Basic Science, Graduate School of Arts and Sciences, University of Tokyo, Komaba, Meguro-ku, Tokyo, Japan.
[Ti] Título:Aging, mortality, and the fast growth trade-off of Schizosaccharomyces pombe.
[So] Source:PLoS Biol;15(6):e2001109, 2017 Jun.
[Is] ISSN:1545-7885
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Replicative aging has been demonstrated in asymmetrically dividing unicellular organisms, seemingly caused by unequal damage partitioning. Although asymmetric segregation and inheritance of potential aging factors also occur in symmetrically dividing species, it nevertheless remains controversial whether this results in aging. Based on large-scale single-cell lineage data obtained by time-lapse microscopy with a microfluidic device, in this report, we demonstrate the absence of replicative aging in old-pole cell lineages of Schizosaccharomyces pombe cultured under constant favorable conditions. By monitoring more than 1,500 cell lineages in 7 different culture conditions, we showed that both cell division and death rates are remarkably constant for at least 50-80 generations. Our measurements revealed that the death rate per cellular generation increases with the division rate, pointing to a physiological trade-off with fast growth under balanced growth conditions. We also observed the formation and inheritance of Hsp104-associated protein aggregates, which are a potential aging factor in old-pole cell lineages, and found that these aggregates exhibited a tendency to preferentially remain at the old poles for several generations. However, the aggregates were eventually segregated from old-pole cells upon cell division and probabilistically allocated to new-pole cells. We found that cell deaths were typically preceded by sudden acceleration of protein aggregation; thus, a relatively large amount of protein aggregates existed at the very ends of the dead cell lineages. Our lineage tracking analyses, however, revealed that the quantity and inheritance of protein aggregates increased neither cellular generation time nor cell death initiation rates. Furthermore, our results demonstrated that unusually large amounts of protein aggregates induced by oxidative stress exposure did not result in aging; old-pole cells resumed normal growth upon stress removal, despite the fact that most of them inherited significant quantities of aggregates. These results collectively indicate that protein aggregates are not a major determinant of triggering cell death in S. pombe and thus cannot be an appropriate molecular marker or index for replicative aging under both favorable and stressful environmental conditions.
[Mh] Termos MeSH primário: Divisão Celular Assimétrica
Agregados Proteicos
Schizosaccharomyces/crescimento & desenvolvimento
Polos do Fuso/metabolismo
Estresse Fisiológico
[Mh] Termos MeSH secundário: Adenosina Trifosfatases/química
Adenosina Trifosfatases/genética
Adenosina Trifosfatases/metabolismo
Biomarcadores/metabolismo
Rastreamento de Células
Replicação do DNA
Deleção de Genes
Proteínas de Choque Térmico/química
Proteínas de Choque Térmico/genética
Proteínas de Choque Térmico/metabolismo
Proteínas Luminescentes/química
Proteínas Luminescentes/genética
Proteínas Luminescentes/metabolismo
Viabilidade Microbiana
Microfluídica/instrumentação
Microscopia Confocal
Microscopia de Fluorescência
Orthoreovirus/metabolismo
Estresse Oxidativo
Fragmentos de Peptídeos/química
Fragmentos de Peptídeos/genética
Fragmentos de Peptídeos/metabolismo
Proteínas Recombinantes de Fusão/química
Proteínas Recombinantes de Fusão/metabolismo
Schizosaccharomyces/citologia
Schizosaccharomyces/fisiologia
Proteínas de Schizosaccharomyces pombe/química
Proteínas de Schizosaccharomyces pombe/genética
Proteínas de Schizosaccharomyces pombe/metabolismo
Análise de Célula Única
Imagem com Lapso de Tempo
Proteínas não Estruturais Virais/química
Proteínas não Estruturais Virais/genética
Proteínas não Estruturais Virais/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Heat-Shock Proteins); 0 (Luminescent Proteins); 0 (Peptide Fragments); 0 (Protein Aggregates); 0 (Recombinant Fusion Proteins); 0 (Schizosaccharomyces pombe Proteins); 0 (Viral Nonstructural Proteins); EC 3.6.1.- (Adenosine Triphosphatases); EC 3.6.1.- (HSP104 protein, S pombe)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170621
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pbio.2001109


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[PMID]:28630123
[Au] Autor:Howell M; Aliashkevich A; Salisbury AK; Cava F; Bowman GR; Brown PJB
[Ad] Endereço:Division of Biological Sciences, University of Missouri, Columbia, Missouri, USA.
[Ti] Título:Absence of the Polar Organizing Protein PopZ Results in Reduced and Asymmetric Cell Division in Agrobacterium tumefaciens.
[So] Source:J Bacteriol;199(17), 2017 Sep 01.
[Is] ISSN:1098-5530
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:is a rod-shaped bacterium that grows by polar insertion of new peptidoglycan during cell elongation. As the cell cycle progresses, peptidoglycan synthesis at the pole ceases prior to insertion of new peptidoglycan at midcell to enable cell division. The homolog of the polar organelle development protein PopZ has been identified as a growth pole marker and a candidate polar growth-promoting factor. Here, we characterize the function of PopZ in cell growth and division of Consistent with previous observations, we observe that PopZ localizes specifically to the growth pole in wild-type cells. Despite the striking localization pattern of PopZ, we find the absence of the protein does not impair polar elongation or cause major changes in the peptidoglycan composition. Instead, we observe an atypical cell length distribution, including minicells, elongated cells, and cells with ectopic poles. Most minicells lack DNA, suggesting a defect in chromosome segregation. Furthermore, the canonical cell division proteins FtsZ and FtsA are misplaced, leading to asymmetric sites of cell constriction. Together, these data suggest that PopZ plays an important role in the regulation of chromosome segregation and cell division. is a bacterial plant pathogen and a natural genetic engineer. However, very little is known about the spatial and temporal regulation of cell wall biogenesis that leads to polar growth in this bacterium. Understanding the molecular basis of growth may allow for the development of innovations to prevent disease or to promote growth during biotechnology applications. Finally, since many closely related plant and animal pathogens exhibit polar growth, discoveries in may be broadly applicable for devising antimicrobial strategies.
[Mh] Termos MeSH primário: Agrobacterium tumefaciens/citologia
Divisão Celular Assimétrica
Proteínas de Bactérias/metabolismo
Proteínas de Ciclo Celular/metabolismo
Divisão Celular
Segregação de Cromossomos
[Mh] Termos MeSH secundário: Agrobacterium tumefaciens/fisiologia
Proteínas de Bactérias/genética
Proteínas de Ciclo Celular/genética
Parede Celular/química
Peptidoglicano/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Cell Cycle Proteins); 0 (Peptidoglycan)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170827
[Lr] Data última revisão:
170827
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170621
[St] Status:MEDLINE


  7 / 261 MEDLINE  
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[PMID]:28619817
[Au] Autor:Rives-Quinto N; Franco M; de Torres-Jurado A; Carmena A
[Ad] Endereço:Instituto de Neurociencias, Consejo Superior de Investigaciones Científicas/Universidad Miguel Hernández, 03550 Sant Joan d'Alacant, Alicante, Spain.
[Ti] Título:Synergism between and mutations causes tumor-like overgrowth via Ras activation in neural stem cells and epithelia.
[So] Source:Development;144(14):2570-2583, 2017 07 15.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Over the past decade an intriguing connection between asymmetric cell division, stem cells and tumorigenesis has emerged. Neuroblasts, which are the neural stem cells of the central nervous system, divide asymmetrically and constitute an excellent paradigm for investigating this connection further. Here we show that the simultaneous loss of the asymmetric cell division regulators Canoe (afadin in mammals) and Scribble in neuroblast clones leads to tumor-like overgrowth through both a severe disruption of the asymmetric cell division process and loss-mediated Ras-PI3K-Akt activation. Moreover, loss also interacts synergistically with loss to promote overgrowth in epithelial tissues, here just by activating the Ras-Raf-MAPK pathway. and , which are functionally related to , contribute to repress the Ras-MAPK signaling cascade in epithelia. Hence, our work uncovers novel cooperative interactions between all these well-conserved tumor suppressors that ensure tight regulation of the Ras signaling pathway.
[Mh] Termos MeSH primário: Proteínas de Drosophila/genética
Proteínas de Drosophila/metabolismo
IMP Desidrogenase/metabolismo
Proteínas de Membrana/genética
Mutação
Células-Tronco Neurais/citologia
Células-Tronco Neurais/metabolismo
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Apoptose
Divisão Celular Assimétrica/genética
Transformação Celular Neoplásica/genética
Transformação Celular Neoplásica/metabolismo
Transformação Celular Neoplásica/patologia
Proteínas de Drosophila/deficiência
Drosophila melanogaster/citologia
Drosophila melanogaster/genética
Drosophila melanogaster/metabolismo
Células Epiteliais/citologia
Células Epiteliais/metabolismo
Feminino
Técnicas de Inativação de Genes
Genes de Insetos
IMP Desidrogenase/genética
Sistema de Sinalização das MAP Quinases
Masculino
Proteínas de Membrana/deficiência
Proteínas de Membrana/metabolismo
Modelos Biológicos
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Drosophila Proteins); 0 (Membrane Proteins); 0 (Scribble protein, Drosophila); 0 (canoe protein, Drosophila); EC 1.1.1.205 (IMP Dehydrogenase); EC 1.1.1.205 (raspberry protein, Drosophila)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170617
[St] Status:MEDLINE
[do] DOI:10.1242/dev.148171


  8 / 261 MEDLINE  
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[PMID]:28503907
[Au] Autor:Okada M; Kusunoki S; Ishibashi Y; Kito K
[Ad] Endereço:Department of Life Sciences, School of Agriculture, Meiji University, Kawasaki, 214-8571, Japan.
[Ti] Título:Proteomics analysis for asymmetric inheritance of preexisting proteins between mother and daughter cells in budding yeast.
[So] Source:Genes Cells;22(6):591-601, 2017 Jun.
[Is] ISSN:1365-2443
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In budding yeast, a mother cell can produce a finite number of daughter cells over its life. The accumulation of a variety of types of damaged components has an impact on the aging process. Asymmetrical inheritance during cell division causes these aberrant intracellular constituents to be retained in mother cells and prevents them from segregating to daughter cells. However, the understanding of asymmetrical inheritance of individual proteins that are damaged or old age, and their relevance to the aging process, has been limited. The aim of this study is to propose a proteomics strategy for asymmetrical inheritance of preexisting proteins between mother and daughter cells. During synchronous culture for one generation, newly synthesized proteins were labeled with stable isotope amino acids to discriminate preexisting proteins originally expressed in mother cells, followed by separation of mother and daughter cells using a conventional method based on biotin labeling. Isotope incorporation ratios for individual proteins were quantified using mass spectrometry. We successfully identified 21 proteins whose preexisting versions were asymmetrically inherited in mother cells, including plasma membrane transporter involved in the aging process and organelle-anchoring proteins related to the stress response to misfolded proteins. Thus, our approach would be useful for making catalog of asymmetrically inherited proteins.
[Mh] Termos MeSH primário: Proteoma/análise
Proteômica/métodos
Proteínas de Saccharomyces cerevisiae/metabolismo
Saccharomyces cerevisiae/citologia
Saccharomyces cerevisiae/metabolismo
[Mh] Termos MeSH secundário: Divisão Celular Assimétrica
Cromatografia Líquida
Saccharomyces cerevisiae/crescimento & desenvolvimento
Espectrometria de Massas em Tandem
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Proteome); 0 (Saccharomyces cerevisiae Proteins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170516
[St] Status:MEDLINE
[do] DOI:10.1111/gtc.12497


  9 / 261 MEDLINE  
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[PMID]:28441530
[Au] Autor:Ma X; Zhu X; Han Y; Story B; Do T; Song X; Wang S; Zhang Y; Blanchette M; Gogol M; Hall K; Peak A; Anoja P; Xie T
[Ad] Endereço:Stowers Institute for Medical Research, 1000 East 50th Street, Kansas City, MO 64110, USA; Department of Cell Biology and Anatomy, University of Kansas Medical Center, Kansas City, KS 66160, USA.
[Ti] Título:Aubergine Controls Germline Stem Cell Self-Renewal and Progeny Differentiation via Distinct Mechanisms.
[So] Source:Dev Cell;41(2):157-169.e5, 2017 Apr 24.
[Is] ISSN:1878-1551
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Piwi family protein Aubergine (Aub) maintains genome integrity in late germ cells of the Drosophila ovary through Piwi-associated RNA-mediated repression of transposon activities. Although it is highly expressed in germline stem cells (GSCs) and early progeny, it remains unclear whether it plays any roles in early GSC lineage development. Here we report that Aub promotes GSC self-renewal and GSC progeny differentiation. RNA-iCLIP results show that Aub binds the mRNAs encoding self-renewal and differentiation factors in cultured GSCs. Aub controls GSC self-renewal by preventing DNA-damage-induced Chk2 activation and by translationally controlling the expression of self-renewal factors. It promotes GSC progeny differentiation by translationally controlling the expression of differentiation factors, including Bam. Therefore, this study reveals a function of Aub in GSCs and their progeny, which promotes translation of self-renewal and differentiation factors by directly binding to its target mRNAs and interacting with translational initiation factors.
[Mh] Termos MeSH primário: Divisão Celular Assimétrica/fisiologia
Diferenciação Celular/fisiologia
Autorrenovação Celular/fisiologia
Proteínas de Drosophila/metabolismo
Drosophila melanogaster/metabolismo
Células Germinativas/metabolismo
Fatores de Iniciação de Peptídeos/metabolismo
Células-Tronco/citologia
[Mh] Termos MeSH secundário: Animais
Quinase do Ponto de Checagem 2/metabolismo
Drosophila melanogaster/citologia
Feminino
Ovário/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Drosophila Proteins); 0 (Peptide Initiation Factors); 0 (aubergine protein, Drosophila); EC 2.7.1.11 (Checkpoint Kinase 2); EC 2.7.11.1 (lok protein, Drosophila)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170915
[Lr] Data última revisão:
170915
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170426
[St] Status:MEDLINE


  10 / 261 MEDLINE  
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[PMID]:28409314
[Au] Autor:Daynac M; Petritsch CK
[Ad] Endereço:Department of Neurological Surgery, Brain Tumor Research Center, University of California, San Francisco, CA, USA.
[Ti] Título:Regulation of Asymmetric Cell Division in Mammalian Neural Stem and Cancer Precursor Cells.
[So] Source:Results Probl Cell Differ;61:375-399, 2017.
[Is] ISSN:0080-1844
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Stem and progenitor cells are characterized by their abilities to self-renew and produce differentiated progeny. The balance between self-renewal and differentiation is achieved through control of cell division mode, which can be either asymmetric or symmetric. Failure to properly control cell division mode may result in premature depletion of the stem/progenitor cell pool or abnormal growth and impaired differentiation. In many tissues, including the brain, stem cells and progenitor cells undergo asymmetric cell division through the establishment of cell polarity. Cell polarity proteins are therefore potentially critical regulators of asymmetric cell division. Decrease or loss of asymmetric cell division can be associated with reduced differentiation common during aging or impaired remyelination as seen in demyelinating diseases. Progenitor-like glioma precursor cells show decreased asymmetric cell division rates and increased symmetric divisions, which suggests that asymmetric cell division suppresses brain tumor formation. Cancer stem cells, on the other hand, still undergo low rates of asymmetric cell division, which may provide them with a survival advantage during therapy. These findings led to the hypotheses that asymmetric cell divisions are not always tumor suppressive but can also be utilized to maintain a cancer stem cell population. Proper control of cell division mode is therefore not only deemed necessary to generate cellular diversity during development and to maintain adult tissue homeostasis but may also prevent disease and determine disease progression. Since brain cancer is most common in the adult and aging population, we review here the current knowledge on molecular mechanisms that regulate asymmetric cell divisions in the neural and oligodendroglial lineage during development and in the adult brain.
[Mh] Termos MeSH primário: Divisão Celular Assimétrica/fisiologia
Células-Tronco Neoplásicas/citologia
Células-Tronco Neurais/citologia
[Mh] Termos MeSH secundário: Animais
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170726
[Lr] Data última revisão:
170726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170415
[St] Status:MEDLINE
[do] DOI:10.1007/978-3-319-53150-2_17



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