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Aurora kinase A is essential for meiosis in mouse oocytes
CS. Blengini, P. Ibrahimian, M. Vaskovicova, D. Drutovic, P. Solc, K. Schindler
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články, Research Support, N.I.H., Extramural, práce podpořená grantem
Grantová podpora
R01 GM112801
NIGMS NIH HHS - United States
NLK
Directory of Open Access Journals
od 2005
Free Medical Journals
od 2005
Public Library of Science (PLoS)
od 2005-07-01
PubMed Central
od 2005
Europe PubMed Central
od 2005
ProQuest Central
od 2005-07-01
Open Access Digital Library
od 2005-01-01
Open Access Digital Library
od 2005-01-01
Open Access Digital Library
od 2005-07-01
Medline Complete (EBSCOhost)
od 2005-07-01
Health & Medicine (ProQuest)
od 2005-07-01
- MeSH
- aparát dělícího vřeténka genetika MeSH
- aurora kinasa A genetika MeSH
- aurora kinasa B genetika MeSH
- aurora kinasa C genetika MeSH
- dělení bunečného jádra genetika MeSH
- fetální proteiny genetika MeSH
- lidé MeSH
- meióza genetika MeSH
- myši MeSH
- oocyty růst a vývoj metabolismus MeSH
- organizační centrum mikrotubulů metabolismus MeSH
- póly dělícího vřeténka genetika MeSH
- protein-serin-threoninkinasy genetika MeSH
- proteiny asociované s mikrotubuly genetika MeSH
- proteiny buněčného cyklu genetika MeSH
- protoonkogenní proteiny genetika MeSH
- segregace chromozomů genetika MeSH
- vývojová regulace genové exprese genetika MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- myši MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Research Support, N.I.H., Extramural MeSH
The Aurora protein kinases are well-established regulators of spindle building and chromosome segregation in mitotic and meiotic cells. In mouse oocytes, there is significant Aurora kinase A (AURKA) compensatory abilities when the other Aurora kinase homologs are deleted. Whether the other homologs, AURKB or AURKC can compensate for loss of AURKA is not known. Using a conditional mouse oocyte knockout model, we demonstrate that this compensation is not reciprocal because female oocyte-specific knockout mice are sterile, and their oocytes fail to complete meiosis I. In determining AURKA-specific functions, we demonstrate that its first meiotic requirement is to activate Polo-like kinase 1 at acentriolar microtubule organizing centers (aMTOCs; meiotic spindle poles). This activation induces fragmentation of the aMTOCs, a step essential for building a bipolar spindle. We also show that AURKA is required for regulating localization of TACC3, another protein required for spindle building. We conclude that AURKA has multiple functions essential to completing MI that are distinct from AURKB and AURKC.
Human Genetics Institute of New Jersey
Institute of Animal Physiology and Genetics of the Czech Academy of Sciences Libechov Czech Republic
Piscataway New Jersey United States of America
Rutgers The State University of New Jersey Piscataway New Jersey United States of America
Citace poskytuje Crossref.org
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