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<p>Asymmetric division is crucial for oocyte and embryo development. During meiosis I, the spindle migrates to the subcortex, and F-actin accumulates to form the actin cap, which supports polar body extrusion. While the CDC42–NWASP–ARP2/3 pathway, regulated by Ran-GTP, is known to promote actin cap formation, how Ran-GTP controls cortical polarization and the precise function of the actin cap remain unclear. Here, we identify <i>Depdc7</i> as a novel actin cap–localized protein essential for actin cap formation and first polar body extrusion. DEPDC7 is recruited to the oocyte membrane by Ran-GTP and acts as a scaffold to promote cortical actin assembly. Strikingly, inhibiting CDK1 activity partially rescues the extrusion defect in <i>Depdc7</i>-depleted oocytes. These findings indicate that both CDK1 activity and actin cap formation are essential for polar body extrusion and function synergistically. Our study refines the molecular mechanism of actin cap assembly and highlights DEPDC7 as a key regulator of oocyte maturation and female fertility.</p>

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The mechanisms of DEPDC7-mediated actin cap establishment and meiosis progression in oocytes

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年6月22日

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  • Jian Mu,
  • Siyuan Xie,
  • Lin Zhao,
  • Yang Zeng,
  • Hao Gu,
  • Zhiqi Pan,
  • Ran Yu,
  • Zhihua Zhang,
  • Tianyu Wu,
  • Weijie Wang,
  • Lei Wang,
  • Qing Sang

摘要

Asymmetric division is crucial for oocyte and embryo development. During meiosis I, the spindle migrates to the subcortex, and F-actin accumulates to form the actin cap, which supports polar body extrusion. While the CDC42–NWASP–ARP2/3 pathway, regulated by Ran-GTP, is known to promote actin cap formation, how Ran-GTP controls cortical polarization and the precise function of the actin cap remain unclear. Here, we identify Depdc7 as a novel actin cap–localized protein essential for actin cap formation and first polar body extrusion. DEPDC7 is recruited to the oocyte membrane by Ran-GTP and acts as a scaffold to promote cortical actin assembly. Strikingly, inhibiting CDK1 activity partially rescues the extrusion defect in Depdc7-depleted oocytes. These findings indicate that both CDK1 activity and actin cap formation are essential for polar body extrusion and function synergistically. Our study refines the molecular mechanism of actin cap assembly and highlights DEPDC7 as a key regulator of oocyte maturation and female fertility.