Cs WRKY30-initiates activation network of multi chemical defense events to confer resistance in tea plant to Colletotrichum camelliae
Tea anthracnose, caused by Colletotrichum camelliae, severely compromises tea yield and quality. However, the molecular mechanisms underlying tea plants resistance to C. camelliae remain poorly understood. In this study, multi-omics profiling revealed that C. camelliae infection triggers a series of resistance responses represented by H2O2 production, carbohydrates reallocation, and especially biosynthesis of defensive phenylpropanoids. Among these, dihydroquercetin, 3-O-methylquercetin, quercetin, and eriodictyol exerted observable antifungal activity. Genetic analysis of genes (CsPAL1 and CsPAL3) encoding phenylpropanoid biosynthesis confirmed the importance of defensive phenylpropanoids in conferring diseases resistance of tea plants to C. camelliae. Meanwhile, the mannitol content increased in tea leaves infected by C. camelliae. Furthermore, overexpression of CsMTD31 encoding mannitol dehydrogenase (MTD) reduced mannitol levels, enhancing ROS accumulation and tea resistance. Notably, we identified that CsWRKY30 directly transactivated CsMTD31, CsPAL1 and CsPAL3 expressions via binding to their promoters. This regulatory action simultaneously increases the content of phenylpropanoids and reduces mannitol levels, thereby enhancing disease resistance in tea plants. Moreover, CsWRKY30 was found to be a hub regulator in activating basal resistance responses, and its overexpression induced a general up-regulation of genes involved in defensive metabolisms and basal immunity. Collectively, this study elucidates a CsWRKY30-centered transcriptional network crucial for immunity activation, establishing an important theoretical and molecular foundation for breeding disease-resistant tea cultivars.