Salicylic acid‐activated BIN2 phosphorylation of TGA3 promotes Arabidopsis PR gene expression and disease resistance

Q Han, W Tan, Y Zhao, F Yang, X Yao, H Lin, D Zhang

The EMBO Journal

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‐ elated genes 1 (NPR1), which is recruited by TGA transcription factors to induce the expression of pathogenesis‐ elated (PR) genes. However, the mechanism by which post‐ ranslational 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.

水杨酸激活的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起着重要作用。由病原体诱导的水杨酸被NPR1受体感知，该受体被TGA转录因子招募以诱导病原体相关（PR）基因的表达。然而，翻译后修饰通过水杨酸信号/病原体感染影响TGA的转录活性的机制还没有得到很好的证实。在此，我们报告了功能缺失的brassinosteroid insensitive2（BIN2）及其同源物bin2-3 bil1 bil2的突变体导致病原体抵抗力受损，对SA诱导的PR基因表达不敏感，而功能增益的突变体bin2-1则表现出SA信号的增强和对病原体的免疫力。我们的研究结果表明，水杨酸激活了BIN2激酶，而BIN2激酶又在Ser33处磷酸化TGA3，增强TGA3的DNA结合能力和NPR1-TGA3复合物的形成，导致PR基因表达的激活。这些发现表明BIN2是水杨酸信号传导的一个新的组成部分，在平衡BR介导的植物生长和SA诱导的免疫方面起着关键的节点作用。

Note: 总体上BR到底是增强还是减弱抗病性，正如抗逆性一样，不同物种不同组织不同病有很多矛盾的报道，可能是物种或病原菌特异性的，又或者是实验条件的差异导致的？