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Abstract

Plant glycosyltransferases (UGTs) catalyze the transfer of a monosaccharide from an UDP-activated donor to an acceptor molecule thus forming a glycosidic linkage. The molecules that are glycosylated frequently are secondary metabolites involved in responses to biotic and abiotic stress, or phytohormones such as salicylic acid (SA). Our studies on the interaction between Arabidopsis thaliana and the obligate biotrophic oomycete pathogen, Hyaloperonospora arabidopsidis (Hpa) have identified the glycosyltransferase UGT76B1. This glycosyltransferase is transcriptionally activated during infection, and a knock-out mutation in its gene results in reduced plant susceptibility to downy mildew, while overexpression stimulates disease development. Compared to wild plants, infection with Hpa leads to a higher accumulation of SA in the ugt76B1 mutant and a faster and more intense stimulation of SA-dependent defenses. Mutant plants are thus in a constitutively "primed" state of defense, and we conclude that the oomycete pathogen stimulates synthesis of the host protein to attenuate immune responses. To identify further regulatory elements involved in UGT76B1-dependent SA homeostasis, we performed comparative full-genome transcriptome analyses between wild type and mutant plants. These analyses identified a gene, which is silent in wild-type plants but overexpressed in the ugt76B1 mutant. We will present the functional analyses of the genes encoding UGT76B1 and the candidate downstream regulatory element, and discuss our results in an hypothetical model.