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Multiple requirements of PLK1 during mouse oocyte maturation
P. Solc, TS. Kitajima, S. Yoshida, A. Brzakova, M. Kaido, V. Baran, A. Mayer, P. Samalova, J. Motlik, J. Ellenberg,
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články, práce podpořená grantem
NLK
Directory of Open Access Journals
od 2006
Free Medical Journals
od 2006
Public Library of Science (PLoS)
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PubMed Central
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od 2006-12-01
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od 2006-10-01
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od 2006-01-01
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od 2006-01-01
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od 2008-01-01
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od 2006-12-01
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od 2006-12-01
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od 2006-12-01
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od 2006
- MeSH
- anafázi podporující komplex metabolismus MeSH
- jaderný obal metabolismus MeSH
- kinetochory metabolismus MeSH
- konfokální mikroskopie MeSH
- meióza fyziologie MeSH
- myši MeSH
- oocyty růst a vývoj MeSH
- organizační centrum mikrotubulů metabolismus MeSH
- počítačové zpracování obrazu MeSH
- protein-serin-threoninkinasy metabolismus MeSH
- proteiny buněčného cyklu metabolismus MeSH
- protoonkogenní proteiny metabolismus MeSH
- segregace chromozomů fyziologie MeSH
- western blotting MeSH
- zvířata MeSH
- Check Tag
- myši MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Polo-like kinase 1 (PLK1) orchestrates multiple events of cell division. Although PLK1 function has been intensively studied in centriole-containing and rapidly cycling somatic cells, much less is known about its function in the meiotic divisions of mammalian oocytes, which arrest for a long period of time in prophase before meiotic resumption and lack centrioles for spindle assembly. Here, using specific small molecule inhibition combined with live mouse oocyte imaging, we comprehensively characterize meiotic PLK1's functions. We show that PLK1 becomes activated at meiotic resumption on microtubule organizing centers (MTOCs) and later at kinetochores. PLK1 is required for efficient meiotic resumption by promoting nuclear envelope breakdown. PLK1 is also needed to recruit centrosomal proteins to acentriolar MTOCs to promote normal spindle formation, as well as for stable kinetochore-microtubule attachment. Consequently, PLK1 inhibition leads to metaphase I arrest with misaligned chromosomes activating the spindle assembly checkpoint (SAC). Unlike in mitosis, the metaphase I arrest is not bypassed by the inactivation of the SAC. We show that PLK1 is required for the full activation of the anaphase promoting complex/cyclosome (APC/C) by promoting the degradation of the APC/C inhibitor EMI1 and is therefore essential for entry into anaphase I. Moreover, our data suggest that PLK1 is required for proper chromosome segregation and the maintenance of chromosome condensation during the meiosis I-II transition, independently of the APC/C. Thus, our results define the meiotic roles of PLK1 in oocytes and reveal interesting differential requirements of PLK1 between mitosis and oocyte meiosis in mammals.
Cell Biology and Biophysics Unit European Molecular Biology Laboratory Heidelberg Germany
Institute of Animal Physiology and Genetics Libechov Czech Republic
Institute of Animal Physiology Kosice Slovakia
Laboratory for Chromosome Segregation RIKEN Center for Developmental Biology Kobe Japan
Citace poskytuje Crossref.org
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