Ca2+-dependent cytoplasmic and nuclear phosphorylation of STOP1 by CPK21 and CPK23 confers ALMT1-dependent aluminum resistance
Hongrui Cao,
Rongxiu Cui,
Huan Guo,
Qiuchen Xia,
Jianing Zhang,
Wenxin Liu and
Zhong-Bao Yang ()
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Hongrui Cao: Shandong University (Qingdao)
Rongxiu Cui: Shandong University (Qingdao)
Huan Guo: Shandong University (Qingdao)
Qiuchen Xia: Shandong University (Qingdao)
Jianing Zhang: Shandong University (Qingdao)
Wenxin Liu: Shandong University (Qingdao)
Zhong-Bao Yang: Shandong University (Qingdao)
Nature Communications, 2025, vol. 16, issue 1, 1-19
Abstract:
Abstract Calcium (Ca) signalling is critical for plant responses to aluminum (Al) stress, with STOP1-mediated ALMT1 expression playing a crucial role in Arabidopsis Al resistance. However, the specific intracellular Ca2+ sensors responsible for transducing Al signals in this process remain unclear. In this study, we identified CPK21 and CPK23, members of the CPK family, as key regulators promoting STOP1-mediated ALMT1 expression under Al stress, significantly influencing malate exudation from roots to limit Al accumulation in root tips. Al stress triggers rapid Ca2+-dependent accumulation of CPK21 and CPK23 in the plasma membrane, cytoplasm and nucleus of root apical cells. The Al-activated CPK21 and CPK23 subsequently phosphorylate STOP1 in both the cytoplasm and nucleus of root apical cells, stabilizing STOP1 by preventing its interaction with RAE1, ultimately enhancing Al resistance. This entire process is Ca2+-dependent. The study unveils a previously undisclosed regulatory network in which CPKs integrate Al-evoked Ca2+ signals and transcriptional reprogramming through the Ca2+-CPK21/23-STOP1 cascade to effectively respond to and adapt to Al stress in plants.
Date: 2025
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:16:y:2025:i:1:d:10.1038_s41467-025-60426-9
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DOI: 10.1038/s41467-025-60426-9
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