Specific deletion of Cdc42 does not affect meiotic spindle organization/migration and homologous chromosome segregation but disrupts polarity establishment and cytokinesis in mouse oocytes

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 po...

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Bibliographic Details
Published in:Molecular biology of the cell 2013-12, Vol.24 (24), p.3832-3841
Main Authors: Wang, Zhen-Bo, Jiang, Zong-Zhe, Zhang, Qing-Hua, Hu, Meng-Wen, Huang, Lin, Ou, Xiang-Hong, Guo, Lei, Ouyang, Ying-Chun, Hou, Yi, Brakebusch, Cord, Schatten, Heide, Sun, Qing-Yuan
Format: Article
Language:English
Subjects:
Actin Capping Proteins - biosynthesis
Actin-Related Protein 2-3 Complex - biosynthesis
Animals
cdc42 GTP-Binding Protein - genetics
Cells, Cultured
Chromosome Segregation - genetics
Cytokinesis - genetics
Female
Infertility, Female - genetics
Meiosis - genetics
Mice
Mice, Inbred C57BL
Mice, Knockout
Oocytes - growth & development
Polar Bodies - cytology
Spindle Apparatus - genetics
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Summary: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.
ISSN:1059-1524
1939-4586
DOI:10.1091/mbc.E13-03-0123