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 pathogen...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.展开更多
基金This research was supported by the National Natural Science Foundation of China(NSFC)through grant numbers 31171935 and 31560551.
文摘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.
