A novel pathogen-responsive glycosyltransferase UGT73C7 mediates the redirection of phenylpropanoid metabolism and promotes SNC1-dependent Arabidopsis immunity.

Recent studies have shown that global metabolic reprogramming is a common event in plant innate immunity, however, the relevant molecular mechanisms remain largely unknown. Here, we identified a pathogen-induced glycosyltransferase UGT73C7 that plays a critical role in Arabidopsis disease resistance through mediating redirection of the phenylpropanoid pathway. Loss of UGT73C7 function resulted in significantly decreased resistance to Pst DC3000, whereas constitutive overexpression of UGT73C7 led to enhanced defense response. UGT73C7-activated immunity was demonstrated to be dependent on the upregulated expression of SNC1, a TIR-type NLR gene. Further, in vitro and in vivo assays indicated that UGT73C7 could glycosylate p-coumaric acid and ferulic acid, the upstream metabolites in phenylpropanoid pathway. Mutations that lead to the loss of UGT73C7 enzyme activities resulted in the failure of inducing SNC1. Moreover, glycosylation activity of UGT73C7 resulted in the redirection of phenylpropanoid metabolic flux to biosynthesis of hydroxycinnamic acids and coumarins. The disruption of phenylpropanoid pathway suppressed UGT73C7-promoted SNC1 expression and immune response. Together, this study not only identified UGT73C7 as an important regulator that adjusts phenylpropanoid metabolism upon pathogen challenge, but also provided a link between phenylpropanoid metabolism and an NLR gene. Supporting Information.