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CPK28-mediated Ca2+ signaling regulates STOP1 localization and accumulation to facilitate plant aluminum resistance

Author

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  • Yingtang Ma

    (Chinese Academy of Sciences
    University of the Chinese Academy of Sciences)

  • Hailiang Zheng

    (Chinese Academy of Sciences
    University of the Chinese Academy of Sciences)

  • Ina Schmitz-Thom

    (Universität Münster)

  • Jiawen Wang

    (Chinese Academy of Sciences)

  • Fanglin Zhou

    (Chinese Academy of Sciences)

  • Chongyang Li

    (Chinese Academy of Sciences)

  • Yaling Zhang

    (Chinese Academy of Sciences)

  • Yiqiu Cheng

    (Chinese Academy of Sciences)

  • Daisuke Miki

    (Chinese Academy of Sciences)

  • Jörg Kudla

    (Universität Münster)

  • Chao-Feng Huang

    (Chinese Academy of Sciences
    University of the Chinese Academy of Sciences)

Abstract

The transcription factor SENSITIVE TO PROTON RHIZOTOXICITY 1 (STOP1) functions as a crucial integrator of plant responses to various stresses, including aluminum (Al) stress. Its stability and accumulation are modulated by stress-specific post-translational mechanisms such as phosphorylation and ubiquitination. However, the upstream signaling mechanisms governing these modifications remain poorly understood. Here, we reveal that Ca2+ signaling and Ca2+-dependent phosphorylation are essential for Al stress-responsive regulation of STOP1. Al exposure specifically induces rapid, spatio-temporally defined biphasic Ca2+ signals in Arabidopsis roots and concomitantly activates the Ca2+-dependent kinase CPK28. Al-activated CPK28 phosphorylates STOP1 at Ser163, a modification that promotes the nuclear localization of STOP1 and prevents its degradation by inhibiting its interaction with the F-box protein RAE1. This phosphorylation enhances STOP1 accumulation and Al resistance. Our findings identify Ser163 phosphorylation as a key molecular switch and establish a Ca2+-CPK28-STOP1 signaling axis critical for plant adaptation to Al stress.

Suggested Citation

  • Yingtang Ma & Hailiang Zheng & Ina Schmitz-Thom & Jiawen Wang & Fanglin Zhou & Chongyang Li & Yaling Zhang & Yiqiu Cheng & Daisuke Miki & Jörg Kudla & Chao-Feng Huang, 2025. "CPK28-mediated Ca2+ signaling regulates STOP1 localization and accumulation to facilitate plant aluminum resistance," Nature Communications, Nature, vol. 16(1), pages 1-18, December.
    • Handle: RePEc:nat:natcom:v:16:y:2025:i:1:d:10.1038_s41467-025-60427-8
    DOI: 10.1038/s41467-025-60427-8
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    References listed on IDEAS

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    1. Kun-hsiang Liu & Yajie Niu & Mineko Konishi & Yue Wu & Hao Du & Hoo Sun Chung & Lei Li & Marie Boudsocq & Matthew McCormack & Shugo Maekawa & Tetsuya Ishida & Chao Zhang & Kevan Shokat & Shuichi Yanag, 2017. "Discovery of nitrate–CPK–NLP signalling in central nutrient–growth networks," Nature, Nature, vol. 545(7654), pages 311-316, May.
    2. Coline Balzergue & Thibault Dartevelle & Christian Godon & Edith Laugier & Claudia Meisrimler & Jean-Marie Teulon & Audrey Creff & Marie Bissler & Corinne Brouchoud & Agnès Hagège & Jens Müller & Serg, 2017. "Low phosphate activates STOP1-ALMT1 to rapidly inhibit root cell elongation," Nature Communications, Nature, vol. 8(1), pages 1-16, August.
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