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

中文翻译：

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水杨酸激活TGA3的BIN2磷酸化促进拟南芥PR基因表达和抗病性

植物防御激素水杨酸 (SA) 在免疫和系统获得性抗性中发挥着重要作用。病原体诱导的水杨酸被致病相关基因 1 (NPR1) 的非表达受体感知，TGA 转录因子会招募 NPR1 来诱导致病相关 (PR) 基因的表达。然而，翻译后修饰通过水杨酸信号传导/病原体感染影响 TGA 转录活性的机制尚未明确。在这里，我们报道油菜素类固醇不敏感2（BIN2）及其同源物bin2-3 bil1 bil2的功能丧失突变体会导致病原体抵抗力受损并对SA诱导的PR基因表达不敏感，而功能获得突变体bin2-1 表现出增强的 SA 信号传导和针对病原体的免疫力。我们的结果表明，水杨酸激活 BIN2 激酶，进而磷酸化 TGA3 Ser33，增强 TGA3 DNA 结合能力和 NPR1-TGA3 复合物形成，从而激活 PR 基因表达。这些发现表明 BIN2 是水杨酸信号传导的新成分，是平衡油菜素类固醇介导的植物生长和 SA 诱导的免疫的关键节点。