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

Author

Listed:
  • Jingshan Li

    (South China Normal University)

  • Zishan Pan

    (South China Normal University)

  • Xiaoqi Peng

    (South China Normal University)

  • Yu Feng

    (South China Normal University)

  • Junfeng Wu

    (South China Normal University)

  • Feiying Liang

    (South China Normal University)

  • Qili Feng

    (South China Normal University)

  • XiaoQiang Yu

    (South China Normal University)

  • Huimin Deng

    (South China Normal University)

Abstract

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.

Suggested Citation

  • Jingshan Li & Zishan Pan & Xiaoqi Peng & Yu Feng & Junfeng Wu & Feiying Liang & Qili Feng & XiaoQiang Yu & Huimin Deng, 2025. "Ecdysone signaling-induced dumpless1 expression controls nurse cell dumping in Drosophila oogenesis," Nature Communications, Nature, vol. 16(1), pages 1-18, December.
    • Handle: RePEc:nat:natcom:v:16:y:2025:i:1:d:10.1038_s41467-025-63973-3
    DOI: 10.1038/s41467-025-63973-3
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