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. 2021 Jan 13;33(3):714–734. doi: 10.1093/plcell/koaa044

Figure 9.

Figure 9

Biochemistry and modulatory action of UGT76B1 in plant basal immunity and SAR. A, In addition to ILA, UGT76B1 glycosylates the two SAR-regulatory metabolites NHP and SA in parallel to form the respective O-β-glucosides NHP-H2 and SAG. The glucosyltransferases UGT74F1 and UGT74F2 also contribute to SA glucosylation. The enzyme catalyzing esterification of NHP to NHP-H1 is not yet characterized. B–E, Model for the function of UGT76B1 as a central hub in the regulation of plant basal immunity and SAR. The model illustrates the four major defense scenarios addressed in this study. Relative metabolite levels are depicted by the size of the letters of aglyca and glucosides, which also subsumes the enhanced or repressed biosynthetic activities. Increasing darkness of the central disc, sizes of letters, and widths of the dark red arrows symbolize the activity of UGT76B1 for each scenario. The strength of immune/SAR signaling is indicated by the sizes of purple arrows. B, Naïve Wt is in a state of contained basal defense. UGT76B1 provides a metabolic hub controlling the levels of the unconjugated, immune-stimulating NHP and SA. Both substrates can be alternatively glucosylated by UGT76B1 to the putatively inactive SAG and NHP-H2. Thereby, the mutual amplification loops of NHP and SA (+) and, consequently, basal defense are contained. ILA is an additional, competing substrate that inhibits SAG and NHP-H2 formation. C, The loss of UGT76B1 glucosylation releases this control. NHP and SA mutually enforce each other and promote a SAR-like, NHP- and SA-dependent enhanced basal immune status. The loss of UGT76B1 abolishes the formation of ILA glucoside and NHP-H2, whereas SAG and SGE are still produced due to the presence of other Arabidopsis SA glucosyltransferases. In addition, the elevated NHP level is accompanied by the enhanced formation of the UGT76B1-independent NHP-H1. D, The pathogen-induced activation of FMO1-mediated NHP biosynthesis and ICS1-regulated SA biosynthesis triggers SAR. In the Wt, UGT76B1 is transcriptionally induced as well. This inducible UGT76B1 expression modulates the levels of free NHP and SA and thereby dampens immune signaling once SAR is activated. E, In UGT76B1-OE plants, a constitutively de-regulated UGT76B1 expression shifts the basal und pathogen-inducible NHP and SA metabolic pools toward O-β-glucoside (NHP-H2, SAG) formation. This compromises NHP and SA accumulation, reduces basal immunity, and abrogates SAR.