Fig. 10

Model of WRKY1 regulating PR1-mediated immune balance in defense against powdery mildew (PM). Upon PM attack, plants activate salicylic acid (SA)-mediated defense mechanisms. WRKY1 promotes SA biosynthesis by positively regulating the SA biosynthetic gene EPS1, which in turn initiates PR1 protein production. As PM infection progresses, SA accumulates, leading to excessive PR1 protein accumulation, which can be detrimental to plant growth and development. To balance defense and growth, WRKY1 initiates the WRKY40-NPR3g module to suppress PR1 expression in an SA-dependent manner. WRKY40 positively regulates NPR3g expression. NPR3g interacts with NPR1 in an SA-dependent manner. Two TGA2c transcripts, TGA2c-1 and TGA2c-2, both interact with NPR1 to activate PR1 expression, with the distinction that the interaction between TGA2c-2 and NPR1 is SA-dependent. NPR3g inhibits PR1 expression by disrupting the TGA2c-2-NPR1 interaction. Mechanistically, the BTB-POZ domain of NPR1 is essential for its binding to both NPR3g and TGA2c-2. In other words, NPR3g competes with TGA2c-2 for binding to the BTB-POZ domain of NPR1. The red line represents protein-protein interaction