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Aurora kinase A is essential for meiosis in mouse oocytes
Authors:Cecilia S. Blengini  Patricia Ibrahimian  Michaela Vaskovicova  David Drutovic  Petr Solc  Karen Schindler
Affiliation:1. Department of Genetics; Rutgers, The State University of New Jersey, Piscataway, New Jersey, United States of America;2. Human Genetics Institute of New Jersey; Piscataway, New Jersey, United States of America;3. Institute of Animal Physiology and Genetics of the Czech Academy of Sciences, Libechov, Czech Republic;Cornell University, UNITED STATES
Abstract: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.
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