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Fertilization-induced synergid cell death by RALF12-triggered ROS production and ethylene signaling

Author

Listed:
  • Junyi Chen

    (Central China Normal University)

  • Huan Wang

    (Central China Normal University)

  • Jinlin Wang

    (Central China Normal University)

  • Xixi Zheng

    (University of Regensburg)

  • Wantong Qu

    (Central China Normal University)

  • Huijian Fang

    (Central China Normal University)

  • Shuang Wang

    (Central China Normal University)

  • Le He

    (Central China Normal University)

  • Shuang Hao

    (Central China Normal University)

  • Thomas Dresselhaus

    (University of Regensburg)

Abstract

Fertilization-dependent elimination of the persistent synergid cell is essential to block supernumerary pollen tubes and thus to avoid polyspermy in flowering plants. Little is known about the molecular mechanisms ensuring timely induction and execution of synergid cell death. We analyzed manually isolated maize synergid cells along their degeneration and show that they are gland cells expressing batteries of genes encoding small secreted proteins under control of the MYB98 transcription factor. This network is down-regulated after fertilization, while genes involved in reactive oxygen species (ROS) production, ethylene biosynthesis and response, senescence, and oxidative stress regulation are induced before synergid elimination and its ultimate fusion with the endosperm. We further show that the fertilization-induced RALF12 peptide specifically triggers mitochondrial ROS and apoptosis, while ethylene promotes synergid degeneration. In conclusion, this study sheds light on developmental programmed cell death (dPCD) in plants and provides a unique resource to discover unknown PCD regulators.

Suggested Citation

  • Junyi Chen & Huan Wang & Jinlin Wang & Xixi Zheng & Wantong Qu & Huijian Fang & Shuang Wang & Le He & Shuang Hao & Thomas Dresselhaus, 2025. "Fertilization-induced synergid cell death by RALF12-triggered ROS production and ethylene signaling," Nature Communications, Nature, vol. 16(1), pages 1-18, December.
    • Handle: RePEc:nat:natcom:v:16:y:2025:i:1:d:10.1038_s41467-025-58246-y
    DOI: 10.1038/s41467-025-58246-y
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