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<p>Nurse cell (NC) dumping, a process essential for oocyte development, involves the rapid cytoplasmic transfer from germline-derived NCs into the oocyte. However, its regulatory mechanism remains unclear. Here, we report that ecdysone signaling in stretch follicle cells (SFCs) regulates NC dumping through <i>dumpless1</i>, a ZAD-C<sub>2</sub>H<sub>2</sub> zinc finger transcription factor, in <i>Drosophila</i>. Ecdysone induced <i>dumpless1</i> expression in SFCs, and CRISPR/Cas9-mediated knockout of <i>dumpless1</i> or its functional domain ZAD suppresses NC dumping. Depletion of <i>dumpless1</i> upregulates integrin βPS expression in SFC plasma membrane, while reducing cortical enrichment of Rho1 signaling-dependent phosphorylated myosin light chain (p-MLC) and disrupting actin cables organization in NCs. SFC-specific overexpression of integrin βPS reduces p-MLC enrichment in the NC cortex, whereas its knockdown in SFCs of <i>dumpless1</i><sup>-/-</sup> mutants partially rescues NC dumping defect. Our findings identify <i>dumpless1</i> as a critical effector of ecdysone signaling, bridging somatic-germline communication through the integrin βPS-Rho1-p-MLC axis, revealing a multicellular regulatory mechanism in <i>Drosophila</i> oogenesis.</p>

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Ecdysone signaling-induced dumpless1 expression controls nurse cell dumping in Drosophila oogenesis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月7日

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  • Jingshan Li,
  • Zishan Pan,
  • Xiaoqi Peng,
  • Yu Feng,
  • Junfeng Wu,
  • Feiying Liang,
  • Qili Feng,
  • XiaoQiang Yu,
  • Huimin Deng

摘要

Nurse cell (NC) dumping, a process essential for oocyte development, involves the rapid cytoplasmic transfer from germline-derived NCs into the oocyte. However, its regulatory mechanism remains unclear. Here, we report that ecdysone signaling in stretch follicle cells (SFCs) regulates NC dumping through dumpless1, a ZAD-C2H2 zinc finger transcription factor, in Drosophila. Ecdysone induced dumpless1 expression in SFCs, and CRISPR/Cas9-mediated knockout of dumpless1 or its functional domain ZAD suppresses NC dumping. Depletion of dumpless1 upregulates integrin βPS expression in SFC plasma membrane, while reducing cortical enrichment of Rho1 signaling-dependent phosphorylated myosin light chain (p-MLC) and disrupting actin cables organization in NCs. SFC-specific overexpression of integrin βPS reduces p-MLC enrichment in the NC cortex, whereas its knockdown in SFCs of dumpless1-/- mutants partially rescues NC dumping defect. Our findings identify dumpless1 as a critical effector of ecdysone signaling, bridging somatic-germline communication through the integrin βPS-Rho1-p-MLC axis, revealing a multicellular regulatory mechanism in Drosophila oogenesis.