A BRI1-CNGC12 phosphorylation module links hormone signaling to manganese homeostasis in plants.

作者：Zhenqian Zhang, Zhenghao Yu, Dixiang Xie, Ju Wang, Jingrong Li, Duoduo Lai, Yaqi Gao, Jiaxin Li, Chuanfeng Ju, Yuzhou Zhang, Kun-hsiang Liu, Cun Wang · 发表于：Proceedings of the National Academy of Sciences of the United States of America · 年份：2026 · DOI：10.1073/pnas.2514483123 · 研究领域：Medicine

Manganese (Mn) toxicity in acidic or waterlogged soils severely impacts crop productivity. Although high-Mn stress triggers Ca2+ signals that regulate Mn homeostasis, the mechanism generating these signals remains unclear. Here, we show that the cyclic nucleotide-gated channel CNGC11/12 are essential for Mn tolerance, as cngc11/12 mutants exhibited hypersensitivity to Mn and cngc12 mutant showed reduced Ca2+ elevations. The brassinosteroid (BR) receptor BRI1 physically interacted with CNGC12 and phosphorylated Ser22 residue, a modification critical for channel activation. Accordingly, bri1 mutants displayed impaired Mn-induced Ca2+ signaling and heightened Mn sensitivity. Mn stress rapidly activated BRI1 kinase, peaking within minutes, and electrophysiological assays confirmed that BRI1-mediated phosphorylation gates CNGC12-dependent Ca2+ currents. Exogenous brassinolide treatment augmented high-Mn-induced Ca2+ signaling, BRI1-mediated CNGC12 phosphorylation, and high-Mn tolerance. Mutations in either BRI1 or CNGC12 abolished CPK5-dependent phosphorylation of MTP8 and impaired NRAMP1 endocytosis. Our study identifies the BRI1-CNGC12 module as a key node linking BR signaling to Ca2+-dependent Mn detoxification, revealing how phytohormone pathways regulate ion stress adaptation.