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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


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[PMID]:29261648
[Au] Autor:Zuin J; Casa V; Pozojevic J; Kolovos P; van den Hout MCGN; van Ijcken WFJ; Parenti I; Braunholz D; Baron Y; Watrin E; Kaiser FJ; Wendt KS
[Ad] Endereço:Department of Cell Biology, Erasmus MC, Rotterdam, The Netherlands.
[Ti] Título:Regulation of the cohesin-loading factor NIPBL: Role of the lncRNA NIPBL-AS1 and identification of a distal enhancer element.
[So] Source:PLoS Genet;13(12):e1007137, 2017 12.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cohesin is crucial for genome stability, cell division, transcription and chromatin organization. Its functions critically depend on NIPBL, the cohesin-loader protein that is found to be mutated in >60% of the cases of Cornelia de Lange syndrome (CdLS). Other mutations are described in the cohesin subunits SMC1A, RAD21, SMC3 and the HDAC8 protein. In 25-30% of CdLS cases no mutation in the known CdLS genes is detected. Until now, functional elements in the noncoding genome were not characterized in the molecular etiology of CdLS and therefore are excluded from mutation screening, although the impact of such mutations has now been recognized for a wide range of diseases. We have identified different elements of the noncoding genome involved in regulation of the NIPBL gene. NIPBL-AS1 is a long non-coding RNA transcribed upstream and antisense to NIPBL. By knockdown and transcription blocking experiments, we could show that not the NIPBL-AS1 gene product, but its actual transcription is important to regulate NIPBL expression levels. This reveals a possibility to boost the transcriptional activity of the NIPBL gene by interfering with the NIPBL-AS1 lncRNA. Further, we have identified a novel distal enhancer regulating both NIPBL and NIPBL-AS1. Deletion of the enhancer using CRISPR genome editing in HEK293T cells reduces expression of NIPBL, NIPBL-AS1 as well as genes found to be dysregulated in CdLS.
[Mh] Termos MeSH primário: Elementos Facilitadores Genéticos
Oligonucleotídeos Antissenso/genética
Oligonucleotídeos Antissenso/metabolismo
Proteínas/genética
Proteínas/metabolismo
[Mh] Termos MeSH secundário: Proteínas de Ciclo Celular/genética
Proteínas de Ciclo Celular/metabolismo
Proteínas Cromossômicas não Histona/genética
Proteínas Cromossômicas não Histona/metabolismo
Segregação de Cromossomos
Síndrome de Lange/genética
Regulação da Expressão Gênica
Genoma Humano
Células HEK293
Seres Humanos
Mutação
Fenótipo
Regiões Promotoras Genéticas
RNA Longo não Codificante/genética
RNA Longo não Codificante/metabolismo
Análise de Sequência de DNA
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cell Cycle Proteins); 0 (Chromosomal Proteins, Non-Histone); 0 (NIPBL protein, human); 0 (Oligonucleotides, Antisense); 0 (Proteins); 0 (RNA, Long Noncoding); 0 (cohesins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1007137


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[PMID]:29208645
[Au] Autor:Mariezcurrena A; Uhlmann F
[Ad] Endereço:Chromosome Segregation Laboratory, The Francis Crick Institute, London NW1 1AT, United Kingdom.
[Ti] Título:Observation of DNA intertwining along authentic budding yeast chromosomes.
[So] Source:Genes Dev;31(21):2151-2161, 2017 11 01.
[Is] ISSN:1549-5477
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:DNA replication of circular genomes generates physically interlinked or catenated sister DNAs. These are resolved through transient DNA fracture by type II topoisomerases to permit chromosome segregation during cell division. Topoisomerase II is similarly required for linear chromosome segregation, suggesting that linear chromosomes also remain intertwined following DNA replication. Indeed, chromosome resolution defects are a frequent cause of chromosome segregation failure and consequent aneuploidies. When and where intertwines arise and persist along linear chromosomes are not known, owing to the difficulty of demonstrating intertwining of linear DNAs. Here, we used excision of chromosomal regions as circular "loop outs" to convert sister chromatid intertwines into catenated circles. This revealed intertwining at replication termination and cohesin-binding sites, where intertwines are thought to arise and persist but not to a greater extent than elsewhere in the genome. Intertwining appears to spread evenly along chromosomes but is excluded from heterochromatin. We found that intertwines arise before replication termination, suggesting that replication forks rotate during replication elongation to dissipate torsion ahead of the forks. Our approach provides previously inaccessible insight into the topology of eukaryotic chromosomes and illuminates a process critical for successful chromosome segregation.
[Mh] Termos MeSH primário: Cromossomos Fúngicos/metabolismo
Replicação do DNA
DNA Fúngico/metabolismo
Saccharomyces cerevisiae/genética
Saccharomyces cerevisiae/metabolismo
[Mh] Termos MeSH secundário: Proteínas de Ciclo Celular/metabolismo
Proteínas Cromossômicas não Histona/metabolismo
Segregação de Cromossomos
Estruturas Genéticas
Genoma Fúngico
Heterocromatina/metabolismo
Origem de Replicação/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cell Cycle Proteins); 0 (Chromosomal Proteins, Non-Histone); 0 (DNA, Fungal); 0 (Heterochromatin); 0 (cohesins)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180130
[Lr] Data última revisão:
180130
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171207
[St] Status:MEDLINE
[do] DOI:10.1101/gad.305557.117


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[PMID]:29261713
[Au] Autor:Coll M; Striano P; Ferrer-Costa C; Campuzano O; Matés J; Del Olmo B; Iglesias A; Pérez-Serra A; Mademont I; Picó F; Oliva A; Brugada R
[Ad] Endereço:Cardiovascular Genetics Center, IDIBGI, Dr. Trueta University Hospital, Parc Hospitalari Martí i Julià, Edifici, Salt (Spain).
[Ti] Título:Targeted next-generation sequencing provides novel clues for associated epilepsy and cardiac conduction disorder/SUDEP.
[So] Source:PLoS One;12(12):e0189618, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sudden unexpected death in epilepsy is an unpredicted condition in patients with a diagnosis of epilepsy, and autopsy does not conclusively identify cause of death. Although the pathophysiological mechanisms that underlie this entity remain unknown, the fact that epilepsy can affect cardiac function is not surprising. The genetic factors involving ion channels co-expressed in the heart and brain and other candidate genes have been previously described. In the present study, 20 epilepsy patients with personal or family history of heart rhythm disturbance/cardiac arrhythmias/sudden death were sequenced using a custom re-sequencing panel. Twenty-six relatives were genetically analysed to ascertain the family segregation in ten individuals. Four subjects revealed variants with positive genotype-phenotype segregation: four missense variants in the CDKL5, CNTNAP2, GRIN2A and ADGRV1 genes and one copy number variant in KCNQ1. The potential pathogenic role of variants in new candidate genes will need further studies in larger cohorts, and the evaluation of the potential pathogenic role in the cardio-cerebral mechanisms requires in vivo/in vitro studies. In addition to family segregation, evaluation of the potential pathogenic roles of these variants in cardio-cerebral mechanisms by in vivo/in vitro studies should also be performed. The potential pathogenic role of variants in new candidate genes will need further studies in larger cohorts.
[Mh] Termos MeSH primário: Doença do Sistema de Condução Cardíaco/complicações
Doença do Sistema de Condução Cardíaco/genética
Morte Súbita/etiologia
Epilepsia/complicações
Epilepsia/genética
Sequenciamento de Nucleotídeos em Larga Escala/métodos
[Mh] Termos MeSH secundário: Adolescente
Adulto
Criança
Segregação de Cromossomos
Estudos de Coortes
Éxons/genética
Feminino
Variação Genética
Seres Humanos
Padrões de Herança/genética
Masculino
Meia-Idade
Linhagem
Deleção de Sequência/genética
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189618


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[PMID]:28455374
[Au] Autor:Greenwood JR; Finnegan EJ; Watanabe N; Trevaskis B; Swain SM
[Ad] Endereço:CSIRO Agriculture and Food, Black Mountain Science and Innovation Park, GPO Box 1700, Canberra, Australian Capital Territory 2601, Australia.
[Ti] Título:New alleles of the wheat domestication gene reveal multiple roles in growth and reproductive development.
[So] Source:Development;144(11):1959-1965, 2017 06 01.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The advantages of free threshing in wheat led to the selection of the domesticated allele, which is now present in almost all modern wheat varieties. and the pre-domestication allele, , encode an AP2 transcription factor, with the domesticated allele conferring a free-threshing character and a subcompact (i.e. partially compact) inflorescence (spike). We demonstrate that mutations in the miR172 binding site of the gene are sufficient to increase transcript levels via a reduction in miRNA-dependent degradation, consistent with the conclusion that a single nucleotide polymorphism in the miRNA binding site of relative to was essential in defining the modern allele. We describe novel gain- and loss-of-function alleles of and use these to define new roles for this gene in spike development. is required for the suppression of 'sham ramification', and increased Q expression can lead to the formation of ectopic florets and spikelets (specialized inflorescence branches that bear florets and grains), resulting in a deviation from the canonical spike and spikelet structures of domesticated wheat.
[Mh] Termos MeSH primário: Alelos
Genes de Plantas
Desenvolvimento Vegetal/genética
Triticum/crescimento & desenvolvimento
Triticum/genética
[Mh] Termos MeSH secundário: Sequência de Bases
Sítios de Ligação/genética
Segregação de Cromossomos/genética
Regulação da Expressão Gênica no Desenvolvimento
Regulação da Expressão Gênica de Plantas
Inflorescência/genética
Mutação/genética
Fenótipo
Polimorfismo de Nucleotídeo Único/genética
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Reprodução/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (RNA, Messenger)
[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:170430
[St] Status:MEDLINE
[do] DOI:10.1242/dev.146407


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[PMID]:29046344
[Au] Autor:Thomas GE; Renjith MR; Manna TK
[Ad] Endereço:School of Biology, Indian Institute of Science Education and Research Thiruvananthapuram, CET Campus, Thiruvananthapuram, Kerala 695016, India.
[Ti] Título:Kinetochore-microtubule interactions in chromosome segregation: lessons from yeast and mammalian cells.
[So] Source:Biochem J;474(21):3559-3577, 2017 Oct 18.
[Is] ISSN:1470-8728
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Chromosome congression and segregation require robust yet dynamic attachment of the kinetochore with the spindle microtubules. Force generated at the kinetochore-microtubule interface plays a vital role to drive the attachment, as it is required to move chromosomes and to provide signal to sense correct attachments. To understand the mechanisms underlying these processes, it is critical to describe how the force is generated and how the molecules at the kinetochore-microtubule interface are organized and assembled to withstand the force and respond to it. Research in the past few years or so has revealed interesting insights into the structural organization and architecture of kinetochore proteins that couple kinetochore attachment to the spindle microtubules. Interestingly, despite diversities in the molecular players and their modes of action, there appears to be architectural similarity of the kinetochore-coupling machines in lower to higher eukaryotes. The present review focuses on the most recent advances in understanding of the molecular and structural aspects of kinetochore-microtubule interaction based on the studies in yeast and vertebrate cells.
[Mh] Termos MeSH primário: Fenômenos Fisiológicos Celulares/fisiologia
Segregação de Cromossomos/fisiologia
Cinetocoros/metabolismo
Microtúbulos/metabolismo
Leveduras/metabolismo
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Cinetocoros/química
Microtúbulos/química
Ligação Proteica/fisiologia
Saccharomyces cerevisiae/química
Saccharomyces cerevisiae/metabolismo
Leveduras/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171020
[St] Status:MEDLINE
[do] DOI:10.1042/BCJ20170518


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[PMID]:29017027
[Au] Autor:Vukusic K; Buda R; Bosilj A; Milas A; Pavin N; Tolic IM
[Ad] Endereço:Division of Molecular Biology, Ruder Boskovic Institute, Bijenicka cesta 54, 10000 Zagreb, Croatia.
[Ti] Título:Microtubule Sliding within the Bridging Fiber Pushes Kinetochore Fibers Apart to Segregate Chromosomes.
[So] Source:Dev Cell;43(1):11-23.e6, 2017 Oct 09.
[Is] ISSN:1878-1551
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:During cell division, mitotic spindle microtubules segregate chromosomes by exerting forces on kinetochores. What forces drive chromosome segregation in anaphase remains a central question. The current model for anaphase in human cells includes shortening of kinetochore fibers and separation of spindle poles. Both processes require kinetochores to be linked with the poles. Here we show, by combining laser ablation, photoactivation, and theoretical modeling, that kinetochores can separate without any attachment to one spindle pole. This separation requires the bridging fiber, a microtubule bundle that connects sister kinetochore fibers. Bridging fiber microtubules in intact spindles slide apart with kinetochore fibers, indicating strong crosslinks between them. We conclude that sliding of microtubules within the bridging fibers drives pole separation and pushes kinetochore fibers poleward by the friction of passive crosslinks between these fibers. Thus, sliding within the bridging fiber works together with the shortening of kinetochore fibers to segregate chromosomes.
[Mh] Termos MeSH primário: Anáfase/fisiologia
Segregação de Cromossomos/fisiologia
Cinetocoros/metabolismo
Metáfase/fisiologia
Microtúbulos/metabolismo
[Mh] Termos MeSH secundário: Células Cultivadas
Seres Humanos
Modelos Biológicos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171011
[St] Status:MEDLINE


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[PMID]:28942922
[Au] Autor:Zelazowski MJ; Sandoval M; Paniker L; Hamilton HM; Han J; Gribbell MA; Kang R; Cole F
[Ad] Endereço:Department of Epigenetics and Molecular Carcinogenesis, University of Texas MD Anderson Cancer Center, Smithville, TX 78957, USA.
[Ti] Título:Age-Dependent Alterations in Meiotic Recombination Cause Chromosome Segregation Errors in Spermatocytes.
[So] Source:Cell;171(3):601-614.e13, 2017 Oct 19.
[Is] ISSN:1097-4172
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Faithful chromosome segregation in meiosis requires crossover (CO) recombination, which is regulated to ensure at least one CO per homolog pair. We investigate the failure to ensure COs in juvenile male mice. By monitoring recombination genome-wide using cytological assays and at hotspots using molecular assays, we show that juvenile mouse spermatocytes have fewer COs relative to adults. Analysis of recombination in the absence of MLH3 provides evidence for greater utilization in juveniles of pathways involving structure-selective nucleases and alternative complexes, which can act upon precursors to generate noncrossovers (NCOs) at the expense of COs. We propose that some designated CO sites fail to mature efficiently in juveniles owing to inappropriate activity of these alternative repair pathways, leading to chromosome mis-segregation. We also find lower MutLγ focus density in juvenile human spermatocytes, suggesting that weaker CO maturation efficiency may explain why younger men have a higher risk of fathering children with Down syndrome.
[Mh] Termos MeSH primário: Envelhecimento
Segregação de Cromossomos
Meiose
Recombinação Genética
Espermatócitos/metabolismo
[Mh] Termos MeSH secundário: Animais
Aberrações Cromossômicas
Reparo do DNA
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Endogâmicos DBA
Espermatócitos/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170926
[St] Status:MEDLINE


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[PMID]:28942021
[Au] Autor:Ifuji A; Kuga T; Kaibori Y; Saito Y; Nakayama Y
[Ad] Endereço:Department of Biochemistry & Molecular Biology, Kyoto Pharmaceutical University, Kyoto 607-8414, Japan.
[Ti] Título:A novel immunofluorescence method to visualize microtubules in the antiparallel overlaps of microtubule-plus ends in the anaphase and telophase midzone.
[So] Source:Exp Cell Res;360(2):347-357, 2017 Nov 15.
[Is] ISSN:1090-2422
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cell division, in which duplicated chromosomes are separated into two daughter cells, is the most dynamic event during cell proliferation. Chromosome movement is powered mainly by microtubules, which vary in morphology and are organized into characteristic structures according to mitotic progression. During the later stages of mitosis, antiparallel microtubules form the spindle midzone, and the irregular formation of the midzone often leads to failure of cytokinesis, giving rise to the unequal segregation of chromosomes. However, it is difficult to analyze the morphology of these microtubules because microtubules in the antiparallel overlaps of microtubule-plus ends in the midzone are embedded in highly electron-dense matrices, impeding the access of anti-tubulin antibodies to their epitopes during immunofluorescence staining. Here, we developed a novel method to visualize selectively antiparallel microtubule overlaps in the midzone. When cells are air-dried before fixation, aligned α-tubulin staining is observed and colocalized with PRC1 in the center of the midzone of anaphase and telophase cells, suggesting that antiparallel microtubule overlaps can be visualized by this method. In air-dried cells, mCherry-α-tubulin fluorescence and ß-tubulin staining show almost the same pattern as α-tubulin staining in the midzone, suggesting that the selective visualization of antiparallel microtubule overlaps in air-dried cells is not attributed to an alteration of the antigenicity of α-tubulin. Taxol treatment extends the microtubule filaments of the midzone in air-dried cells, and nocodazole treatment conversely decreases the number of microtubules, suggesting that unstable microtubules are depolymerized during the air-drying method. It is of note that the air-drying method enables the detection of the disruption of the midzone and premature midzone formation upon Aurora B and Plk1 inhibition, respectively. These results suggest that the air-drying method is suitable for visualizing microtubules in the antiparallel overlaps of microtubule-plus ends of the midzone and for detecting their effects on midzone formation.
[Mh] Termos MeSH primário: Anáfase
Imunofluorescência/métodos
Microtúbulos/metabolismo
Fuso Acromático/metabolismo
Telófase
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Segregação de Cromossomos/fisiologia
Citocinese/fisiologia
Células HeLa
Seres Humanos
Microtúbulos/ultraestrutura
Mitose
Fuso Acromático/ultraestrutura
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170925
[St] Status:MEDLINE


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[PMID]:28935709
[Au] Autor:Wang H; Choe MH; Lee IW; Namgoong S; Kim JS; Kim NH; Oh JS
[Ad] Endereço:Department of Animal Sciences, Chungbuk National University, Cheongju 28644, Korea.
[Ti] Título:CIP2A acts as a scaffold for CEP192-mediated microtubule organizing center assembly by recruiting Plk1 and aurora A during meiotic maturation.
[So] Source:Development;144(20):3829-3839, 2017 10 15.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In somatic cells spindle microtubules are nucleated from centrosomes that act as major microtubule organizing centers (MTOCs), whereas oocytes form meiotic spindles by assembling multiple acentriolar MTOCs without canonical centrosomes. Aurora A and Plk1 are required for these events, but the underlying mechanisms remain largely unknown. Here we show that CIP2A regulates MTOC organization by recruiting aurora A and Plk1 at spindle poles during meiotic maturation. CIP2A colocalized with pericentrin at spindle poles with a few distinct cytoplasmic foci. Although CIP2A has been identified as an endogenous inhibitor of protein phosphatase 2A (PP2A), overexpression of CIP2A had no effect on meiotic maturation. Depletion of CIP2A perturbed normal spindle organization and chromosome alignment by impairing MTOC organization. Importantly, CIP2A was reciprocally associated with CEP192, promoting recruitment of aurora A and Plk1 at MTOCs. CIP2A was phosphorylated by Plk1 at S904, which targets CIP2A to MTOCs and facilitates MTOC organization with CEP192. Our results suggest that CIP2A acts as a scaffold for CEP192-mediated MTOC assembly by recruiting Plk1 and aurora A during meiotic maturation in mouse oocytes.
[Mh] Termos MeSH primário: Aurora Quinase A/genética
Autoantígenos/fisiologia
Proteínas de Ciclo Celular/fisiologia
Proteínas Cromossômicas não Histona/fisiologia
Proteínas de Membrana/fisiologia
Centro Organizador dos Microtúbulos
Proteínas Serina-Treonina Quinases/fisiologia
Proteínas Proto-Oncogênicas/fisiologia
[Mh] Termos MeSH secundário: Animais
Antígenos/metabolismo
Autoantígenos/genética
Proteínas de Ciclo Celular/genética
Centrossomo/metabolismo
Proteínas Cromossômicas não Histona/genética
Segregação de Cromossomos
Citoplasma/metabolismo
Feminino
Regulação da Expressão Gênica no Desenvolvimento
Meiose
Proteínas de Membrana/genética
Camundongos
Microtúbulos/metabolismo
Oócitos/metabolismo
Ovário/metabolismo
Fosforilação
Proteínas Serina-Treonina Quinases/genética
Proteínas Proto-Oncogênicas/genética
RNA Interferente Pequeno/metabolismo
Fuso Acromático/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens); 0 (Autoantigens); 0 (CEP192 protein, mouse); 0 (Cell Cycle Proteins); 0 (Chromosomal Proteins, Non-Histone); 0 (KIAA1524 protein, mouse); 0 (Membrane Proteins); 0 (Proto-Oncogene Proteins); 0 (RNA, Small Interfering); 0 (pericentrin); EC 2.7.11.1 (Aurka protein, mouse); EC 2.7.11.1 (Aurora Kinase A); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (polo-like kinase 1)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE
[do] DOI:10.1242/dev.158584



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