DEPDC7 couples homologous chromosome segregation to asymmetric cytokinesis through recruiting ARP2/3 complex in oocyte meiosis.

IF 11.6 2区生物学 Q1 CELL BIOLOGY

Cell Communication and Signaling Pub Date : 2026-07-14 DOI:10.1186/s12964-026-03068-8

Jia-Ni Guo, Si-Min Sun, Xue-Mei Yang, Chao Jiang, Yi-Ke Lu, Yuan-Hong Xu, Bing-Wang Zhao, Zhen-Bo Wang

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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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在卵母细胞减数分裂中，DEPDC7通过募集ARP2/3复合体将同源染色体分离与不对称胞质分裂结合。

在哺乳动物减数分裂过程中，适当的细胞分裂对卵母细胞成熟至关重要。这一过程取决于肌动蛋白帽的形成和皮层极性的建立。在本研究中，我们报道了DEP结构域蛋白7 （DEPDC7）作为卵母细胞胞质分裂的调节因子。条件敲除卵母细胞中的DEPDC7导致三倍体受精卵，损害早期胚胎发育，最终导致女性生育能力低下。染色体扩散分析表明，缺乏DEPDC7的超排卵卵母细胞为二倍体。虽然在减数分裂I中缺失depdc7的卵母细胞纺锤体的组装和迁移是正常的，但肌动蛋白帽组装和第一极体挤压严重中断。此外，我们发现DEPDC7与ARP2/3复合物共定位并相互作用，调节其皮质下富集。综上所述，我们的研究结果表明，在小鼠卵母细胞减数分裂过程中，DEPDC7的功能是极性建立和染色体分离耦合到细胞分裂所必需的。

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来源期刊

Cell Communication and Signaling CELL BIOLOGY-

CiteScore

11.00

自引率

0.00%

发文量

180

期刊介绍： Cell Communication and Signaling (CCS) is a peer-reviewed, open-access scientific journal that focuses on cellular signaling pathways in both normal and pathological conditions. It publishes original research, reviews, and commentaries, welcoming studies that utilize molecular, morphological, biochemical, structural, and cell biology approaches. CCS also encourages interdisciplinary work and innovative models, including in silico, in vitro, and in vivo approaches, to facilitate investigations of cell signaling pathways, networks, and behavior. Starting from January 2019, CCS is proud to announce its affiliation with the International Cell Death Society. The journal now encourages submissions covering all aspects of cell death, including apoptotic and non-apoptotic mechanisms, cell death in model systems, autophagy, clearance of dying cells, and the immunological and pathological consequences of dying cells in the tissue microenvironment.