Aurora kinase A is essential for meiosis in mouse oocytes
Language English Country United States Media electronic-ecollection
Document type Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't
Grant support
R01 GM112801
NIGMS NIH HHS - United States
PubMed
33901174
PubMed Central
PMC8102010
DOI
10.1371/journal.pgen.1009327
PII: PGENETICS-D-20-01877
Knihovny.cz E-resources
- MeSH
- Spindle Apparatus genetics MeSH
- Aurora Kinase A genetics MeSH
- Aurora Kinase B genetics MeSH
- Aurora Kinase C genetics MeSH
- Cell Nucleus Division genetics MeSH
- Fetal Proteins genetics MeSH
- Humans MeSH
- Meiosis genetics MeSH
- Mice MeSH
- Oocytes growth & development metabolism MeSH
- Microtubule-Organizing Center metabolism MeSH
- Polo-Like Kinase 1 MeSH
- Spindle Poles genetics MeSH
- Protein Serine-Threonine Kinases genetics MeSH
- Microtubule-Associated Proteins genetics MeSH
- Cell Cycle Proteins genetics MeSH
- Proto-Oncogene Proteins genetics MeSH
- Chromosome Segregation genetics MeSH
- Gene Expression Regulation, Developmental genetics MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Mice MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Research Support, N.I.H., Extramural MeSH
- Names of Substances
- Aurkb protein, mouse MeSH Browser
- Aurkc protein, mouse MeSH Browser
- Aurora Kinase A MeSH
- Aurora Kinase B MeSH
- Aurora Kinase C MeSH
- Fetal Proteins MeSH
- Protein Serine-Threonine Kinases MeSH
- Microtubule-Associated Proteins MeSH
- Cell Cycle Proteins MeSH
- Proto-Oncogene Proteins MeSH
- TACC3 protein, mouse MeSH Browser
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; Piscataway New Jersey United States of America
Institute of Animal Physiology and Genetics of the Czech Academy of Sciences Libechov Czech Republic
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