Specific deletion of Cdc42 does not affect meiotic spindle organization/migration and homologous chromosome segregation but disrupts polarity establishment and cytokinesis in mouse oocytes |
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| Authors: | Zhen-Bo Wang Zong-Zhe Jiang Qing-Hua Zhang Meng-Wen Hu Lin Huang Xiang-Hong Ou Lei Guo Ying-Chun Ouyang Yi Hou Cord Brakebusch Heide Schatten Qing-Yuan Sun |
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| Affiliation: | Carnegie Institution;aState Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China;bUniversity of Chinese Academy of Sciences, Beijing 100049, China;cMolecular Pathology Section, Department of Biomedical Sciences, Biotech Research and Innovation Centre, University of Copenhagen, 2200 Copenhagen, Denmark;dDepartment of Veterinary Pathobiology, University of Missouri, Columbia, MO 65211 |
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| Abstract: | Mammalian oocyte maturation is distinguished by highly asymmetric meiotic divisions during which a haploid female gamete is produced and almost all the cytoplasm is maintained in the egg for embryo development. Actin-dependent meiosis I spindle positioning to the cortex induces the formation of a polarized actin cap and oocyte polarity, and it determines asymmetric divisions resulting in two polar bodies. Here we investigate the functions of Cdc42 in oocyte meiotic maturation by oocyte-specific deletion of Cdc42 through Cre-loxP conditional knockout technology. We find that Cdc42 deletion causes female infertility in mice. Cdc42 deletion has little effect on meiotic spindle organization and migration to the cortex but inhibits polar body emission, although homologous chromosome segregation occurs. The failure of cytokinesis is due to the loss of polarized Arp2/3 accumulation and actin cap formation; thus the defective contract ring. In addition, we correlate active Cdc42 dynamics with its function during polar body emission and find a relationship between Cdc42 and polarity, as well as polar body emission, in mouse oocytes. |
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