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

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 phosphorylatio...

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Main Authors: Yingtang Ma, Hailiang Zheng, Ina Schmitz-Thom, Jiawen Wang, Fanglin Zhou, Chongyang Li, Yaling Zhang, Yiqiu Cheng, Daisuke Miki, Jörg Kudla, Chao-Feng Huang
Format: Article
Language:English
Published: Nature Portfolio 2025-06-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-025-60427-8
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author Yingtang Ma
Hailiang Zheng
Ina Schmitz-Thom
Jiawen Wang
Fanglin Zhou
Chongyang Li
Yaling Zhang
Yiqiu Cheng
Daisuke Miki
Jörg Kudla
Chao-Feng Huang
author_facet Yingtang Ma
Hailiang Zheng
Ina Schmitz-Thom
Jiawen Wang
Fanglin Zhou
Chongyang Li
Yaling Zhang
Yiqiu Cheng
Daisuke Miki
Jörg Kudla
Chao-Feng Huang
author_sort Yingtang Ma
collection DOAJ
description 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.
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issn 2041-1723
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spelling doaj-art-bbd663b8407d44edbd87491d4620a8b12025-08-20T03:10:34ZengNature PortfolioNature Communications2041-17232025-06-0116111810.1038/s41467-025-60427-8CPK28-mediated Ca2+ signaling regulates STOP1 localization and accumulation to facilitate plant aluminum resistanceYingtang Ma0Hailiang Zheng1Ina Schmitz-Thom2Jiawen Wang3Fanglin Zhou4Chongyang Li5Yaling Zhang6Yiqiu Cheng7Daisuke Miki8Jörg Kudla9Chao-Feng Huang10State Key Laboratory of Plant Trait Design, Shanghai Center for Plant Stress Biology, CAS Center for Excellence in Molecular Plant Sciences, Chinese Academy of SciencesState Key Laboratory of Plant Trait Design, Shanghai Center for Plant Stress Biology, CAS Center for Excellence in Molecular Plant Sciences, Chinese Academy of SciencesInstitut für Biologie und Biotechnologie der Pflanzen, Universität MünsterState Key Laboratory of Plant Trait Design, Shanghai Center for Plant Stress Biology, CAS Center for Excellence in Molecular Plant Sciences, Chinese Academy of SciencesState Key Laboratory of Plant Trait Design, Shanghai Center for Plant Stress Biology, CAS Center for Excellence in Molecular Plant Sciences, Chinese Academy of SciencesState Key Laboratory of Plant Trait Design, Shanghai Center for Plant Stress Biology, CAS Center for Excellence in Molecular Plant Sciences, Chinese Academy of SciencesState Key Laboratory of Plant Trait Design, Shanghai Center for Plant Stress Biology, CAS Center for Excellence in Molecular Plant Sciences, Chinese Academy of SciencesState Key Laboratory of Plant Trait Design, Shanghai Center for Plant Stress Biology, CAS Center for Excellence in Molecular Plant Sciences, Chinese Academy of SciencesState Key Laboratory of Plant Trait Design, Shanghai Center for Plant Stress Biology, CAS Center for Excellence in Molecular Plant Sciences, Chinese Academy of SciencesInstitut für Biologie und Biotechnologie der Pflanzen, Universität MünsterState Key Laboratory of Plant Trait Design, Shanghai Center for Plant Stress Biology, CAS Center for Excellence in Molecular Plant Sciences, Chinese Academy of SciencesAbstract 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.https://doi.org/10.1038/s41467-025-60427-8
spellingShingle Yingtang Ma
Hailiang Zheng
Ina Schmitz-Thom
Jiawen Wang
Fanglin Zhou
Chongyang Li
Yaling Zhang
Yiqiu Cheng
Daisuke Miki
Jörg Kudla
Chao-Feng Huang
CPK28-mediated Ca2+ signaling regulates STOP1 localization and accumulation to facilitate plant aluminum resistance
Nature Communications
title CPK28-mediated Ca2+ signaling regulates STOP1 localization and accumulation to facilitate plant aluminum resistance
title_full CPK28-mediated Ca2+ signaling regulates STOP1 localization and accumulation to facilitate plant aluminum resistance
title_fullStr CPK28-mediated Ca2+ signaling regulates STOP1 localization and accumulation to facilitate plant aluminum resistance
title_full_unstemmed CPK28-mediated Ca2+ signaling regulates STOP1 localization and accumulation to facilitate plant aluminum resistance
title_short CPK28-mediated Ca2+ signaling regulates STOP1 localization and accumulation to facilitate plant aluminum resistance
title_sort cpk28 mediated ca2 signaling regulates stop1 localization and accumulation to facilitate plant aluminum resistance
url https://doi.org/10.1038/s41467-025-60427-8
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