论文题目：A BRI1-CNGC12 phosphorylation module links hormone signaling to manganese homeostasis in plants
论文作者：Zhenqian Zhang,Zhenghao Yu,Dixiang Xie,Ju Wang,Jingrong Li,Duoduo Lai,YaqiGao,JiaxinLi,Chuanfeng Ju,Yuzhou Zhang,Kun-Hsiang Liu, Cun Wang
论文摘要：
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.
酸性或淹水土壤中的锰（Mn）毒害会严重影响作物产量。高锰胁迫虽能触发调控锰稳态的钙离子（Ca²⁺）信号，但其信号产生机制尚未明确。本研究发现，环核苷酸门控通道 CNGC11/12 是植物耐受锰毒害的关键因子：cngc11/12双突变体对锰表现出高敏感性，cngc12单突变体的钙离子升高幅度显著降低。油菜素甾醇（BR）受体 BRI1 可与 CNGC12 发生物理互作，并对其 22 位丝氨酸残基进行磷酸化修饰，该修饰是激活 CNGC12 通道的关键步骤。与此一致，bri1突变体的锰诱导钙离子信号通路受损，且对锰毒害的敏感性显著增强。锰胁迫可快速激活 BRI1 激酶活性，数分钟内即达峰值；电生理实验证实，BRI1 介导的磷酸化作用可开启 CNGC12 依赖的钙离子电流。外源施加油菜素内酯可增强高锰诱导的钙离子信号、促进 BRI1 介导的 CNGC12 磷酸化，并提升植物的高锰耐受性。BRI1 或 CNGC12 的突变会导致 CPK5 对 MTP8 的磷酸化作用丧失，同时抑制 NRAMP1 的内吞过程。本研究证实，BRI1-CNGC12 模块是连接油菜素甾醇信号通路与钙离子依赖型锰解毒途径的核心节点，揭示了植物激素通路调控离子胁迫适应的分子机制。
论文链接：https://www.pnas.org/doi/10.1073/pnas.2514483123