背景回顾：The plant defense hormone, salicylic acid (SA), plays essential roles in immunity and systemic acquired resistance. Salicylic acid induced by the pathogen is perceived by the receptor nonexpressor of pathogenesis-related genes 1 (NPR1), which is recruited by TGA transcription factors to induce the expression of pathogenesis-related (PR) genes. 

提出问题：However, the mechanism by which post-translational modifications affect TGA's transcriptional activity by salicylic acid signaling/pathogen infection is not well-established.  

结果-功能缺失和获得突变体表型：Here, we report that the loss-of-function mutant of brassinosteroid insensitive2 (BIN2) and its homologs, bin2-3 bil1 bil2, causes impaired pathogen resistance and insensitivity to SA-induced PR gene expression, whereas the gain-of-function mutant, bin2-1, exhibited enhanced SA signaling and immunity against the pathogen. 

结果-作用机制：Our results demonstrate that salicylic acid activates BIN2 kinase, which in turn phosphorylates TGA3 at Ser33 to enhance TGA3 DNA binding ability and NPR1–TGA3 complex formation, leading to the activation of PR gene expression.

结论：These findings implicate BIN2 as a new component of salicylic acid signaling, functioning as a key node in balancing brassinosteroid-mediated plant growth and SA-induced immunity.

 摘 要 

植物防御激素水杨酸（SA）在植物免疫和系统获得性抗性中发挥重要作用。由病原菌侵染诱导产生的水杨酸会被受体NPR1所感知，进而被TGA转录因子招募以诱导病原相关（PR）基因的表达。但是，水杨酸信号转导/病原菌侵染通过哪些翻译后修饰影响TGA的转录活性还不清楚。本文中，作者发现BIN2基因及其同源基因的功能缺失突变体bin2-3 bil1 bil2表现出抗病性缺陷以及对SA诱导的PR基因表达的不敏感，同时功能获得突变体bin2-1表现出SA信号转导和对病原菌抗性的增强。本文的结果揭示了水杨酸激活BIN2激酶，进而磷酸化TGA3蛋白的Ser33以增强TGA3的DNA结合能力和NPR1–TGA3复合物形成，最终激活PR基因的表达。这些发现暗示了BIN2作为一个水杨酸信号转导的组分，在平衡油菜素内酯介导的植物生长和SA诱导的免疫之间的关键节点发挥功能。

 张大伟