Drought-triggered JA signaling promotes pathogen susceptibility by attenuating lignin defenses via UGT72BV9 in tea plants

Tea plants frequently encounter combined abiotic and biotic stresses, which severely threaten sustainable tea production. However, how plants integrate responses to multiple stresses remains unclear. Here, we demonstrate that short-term drought preconditioning enhances tea plant susceptibility to infection by the fungal pathogen Pseudopestalotiopsis camelliae-sinensis (Pcs). Transcriptome analysis identified a uridine-diphosphate (UDP)-dependent glycosyltransferase, CsUGT72BV9, that is co-induced under drought, Pcs infection, and combined stress. Biochemical assays showed that CsUGT72BV9 preferentially glycosylates 4-hydroxycoumarin, a key metabolite in the phenylpropanoid pathway. Silencing CsUGT72BV9 significantly promoted lignin accumulation and enhanced disease resistance, whereas its overexpression reduced resistance, indicating a negative role in defense. Furthermore, CsUGT72BV9 influences jasmonic acid (JA) accumulation, and we identified the transcription factor CsMYC2c, which directly binds to and activates CsUGT72BV9 expression, thereby forming a regulatory module that attenuates disease resistance. Collectively, our findings support a working model in which the CsMYC2c-CsUGT72BV9 module links drought-induced JA signaling to coumarin glycosylation, lignin remodeling, and increased susceptibility to Pcs. This study provides new insights into the molecular basis of plant adaptation to complex stress conditions and highlights potential targets for breeding stress-resistant tea varieties.