A pathogen-induced UGT genomic locus contributes to sinapic acid glycosylation and gray blight resistance in tea plant.

Abstract

UDP-glycosyltransferases (UGTs) are a superfamily essential for plant ecological adaptation, catalyzing the conversion of secondary metabolites into diverse bioactive glycosides. However, how UGTs efficiently modulate glycoside biosynthesis in response to environmental stresses remains unclear. Here, we characterized a pathogen-induced UGT genomic locus in the tea plant (Camellia sinensis) that responds to gray blight infection. Functional analyses showed that CsUGT84A22 converted sinapic acid into the antifungal compound sinapoyl-β-D-glucose (S-G). Suppression of CsUGT84A22 reduced S-G accumulation and impaired gray blight resistance in tea plants. In addition, CsMYB73, a transcription factor encoded within the genomic locus, negatively regulated CsUGT84A22 expression, and suppression of CsMYB73 enhanced both gray blight resistance and S-G biosynthesis. Furthermore, jasmonic acid (JA) biosynthesis was stimulated to improve gray blight resistance with accelerating CsUGT84A22 expression and S-G accumulation. Co-expression network analysis revealed that the JA signaling repressor CsJAZ14 negatively regulates gray blight resistance; specifically, in the absence of JA, it facilitates the CsMYB73-mediated suppression of CsUGT84A22 expression. Evolutionary trajectory analysis further indicated that the genomic locus was fully assembled from grasses to rosids, but diverged within the fabid lineage with loss of MYB73 homology. Together, these findings support a regulatory model in which JA signaling modulates a pathogen-induced genomic locus to promote disease resistance and provide a tractable route for engineering biosynthesis of natural antifungal compounds.

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