A novel mode of WRKY1 regulating PR1-mediated immune balance to defend against powdery mildew in apple
文献类型： 外文期刊
作者： Lan, Liming 1 ; Cao, Lifang 1 ; Zhang, Lulu 1 ; Fu, Weihong 1 ; Luo, Changguo 2 ; Wu, Chao 1 ; Zeng, Xianqi 1 ; Qu, Shenchun 1 ; Yu, Xinyi 1 ; Deng, Wenyi 1 ; Xu, Xu 1 ; Cai, Binhua 1 ; Wang, Sanhong 1 ;
作者机构： 1.Nanjing Agr Univ, Coll Hort, Nanjing 210095, Peoples R China
2.Guizhou Acad Agr Sci, Inst Pomol, Guiyang 550006, Peoples R China
关键词： Apple powdery mildew; Salicylic acid; PR1; Plant immunity; Immune balance; WRKY40-NPR3g module; NPR1; TGA2c variants; Alternative splicing; BTB-POZ domain; EPS1; WRKY1; Immune defense mechanism
期刊名称：MOLECULAR HORTICULTURE （ 影响因子：8.1； 五年影响因子：11.0 ）
ISSN： 2730-9401
年卷期： 2025 年 5 卷 1 期
页码：
收录情况： SCI
摘要： Powdery mildew (PM), caused by the biotrophic fungus Podospharea leucotricha, poses a significant threat to apple production. Salicylic acid (SA) signaling plays a crucial role in enhancing resistance to biotrophic pathogens. While PR1, a defense protein induced by SA, is essential for plant immunity, its excessive accumulation can be detrimental. However, the mechanism of PR1-mediated immune balance remains unclear. This study identified a key transcription factor, WRKY1, which enhances the SA accumulation by modulating the SA biosynthesis gene EPS1, while simultaneously regulating the WRKY40-NPR3g module to prevent sustained PR1 expression caused by continuous SA accumulation. Specifically, the transcription factor WRKY40 upregulates NPR3g expression, and NPR3g interacts with NPR1 in an SA-dependent manner. Then, two TGA2c variants that interact with NPR1 to activate PR1 expression were identified: canonical TGA2c-1 and alternative splicing of TGA2c-2 with an exon deletion. SA does not influence the NPR1-TGA2c-1 interaction but is essential for the NPR1-TGA2c-2 interaction. Notably, NPR3g reduces PR1 levels by selectively disrupting the NPR1-TGA2c-2 complex through competition for the BTB-POZ domain of NPR1. In conclusion, this study identifies a novel mechanism by which WRKY1 modulates PR1-mediated immune balance to defend against PM.
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