Aurora kinase A is essential for meiosis in mouse oocytes.
Autor: | Blengini CS; Department of Genetics; Rutgers, The State University of New Jersey, Piscataway, New Jersey, United States of America.; Human Genetics Institute of New Jersey; Piscataway, New Jersey, United States of America., Ibrahimian P; Department of Genetics; Rutgers, The State University of New Jersey, Piscataway, New Jersey, United States of America., Vaskovicova M; Institute of Animal Physiology and Genetics of the Czech Academy of Sciences, Libechov, Czech Republic., Drutovic D; Institute of Animal Physiology and Genetics of the Czech Academy of Sciences, Libechov, Czech Republic., Solc P; Institute of Animal Physiology and Genetics of the Czech Academy of Sciences, Libechov, Czech Republic., Schindler K; Department of Genetics; Rutgers, The State University of New Jersey, Piscataway, New Jersey, United States of America.; Human Genetics Institute of New Jersey; Piscataway, New Jersey, United States of America. |
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Jazyk: | angličtina |
Zdroj: | PLoS genetics [PLoS Genet] 2021 Apr 26; Vol. 17 (4), pp. e1009327. Date of Electronic Publication: 2021 Apr 26 (Print Publication: 2021). |
DOI: | 10.1371/journal.pgen.1009327 |
Abstrakt: | 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. Competing Interests: The authors have declared that no competing interests exist. Author Petr Solc was unable to confirm their authorship contributions. On their behalf, the corresponding author has reported their contributions to the best of their knowledge. |
Databáze: | MEDLINE |
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