ArticleCell communication and signaling : CCS2026
DEPDC7 couples homologous chromosome segregation to asymmetric cytokinesis through recruiting ARP2/3 complex in oocyte meiosis.
Article in Cell communication and signaling : CCS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
During mammal meiosis, proper cytokinesis is essential for oocyte maturation. This process depends on actin cap formation and cortical polarity establishment. In this study, we reported that DEP domain-containing protein 7 (DEPDC7) functioned as a regulator of oocyte cytokinesis. Conditional knockout of DEPDC7 in oocytes resulted in triploid zygotes, impaired early embryo development, and ultimately led to female subfertility. Chromosome spread analysis showed that superovulated oocytes lacking DEPDC7 were diploid. Although the assembly and migration of the spindles were normal in DEPDC7-deleted oocytes during meiosis I, actin cap assembly and first polar body extrusion were severely disrupted. Furthermore, we found that DEPDC7 colocalized and interacted with ARP2/3 complex, regulating its subcortical enrichment. Taken together, our findings reveal the function of DEPDC7 is required for polarity establishment and coupling chromosome segregation to cytokinesis during mouse oocyte meiosis.
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