Activation of NLR-Mediated Autoimmunity in Arabidopsis Mutant

From a reverse genetic screen using CRISPR/Cas9 gene editing tool, we unintentionally identified an autoimmune mutant. Map-based cloning and whole-genome sequencing revealed that it contains a deletion in SMALL UBIQUITIN-RELATED MODIFIER (SUMO) protease encoding gene (). Previous studies reported that mutants accumulate elevated levels of plant defense hormone salicylic acid (SA). However, upregulated () expression in only partly relies on SA level. In this study, we show that plant metabolite N-hydroxypipecolic acid (NHP) biosynthetic genes are upregulated in , and NHP biosynthesis mutant () partially suppresses the autoimmune phenotypes of , suggestive of a requirement of NHP signaling for the autoimmunity in . As activation of nucleotide-binding leucine-rich repeat immune receptors (NLRs) are associates with the biosynthesis of SA and NHP and lipase-like protein ENHANCED DISEASE SUSCEPTIBILITY 1 (EDS1) is a key component downstream of many NLRs, we examined the relationship between EDS1 and ESD4 by analyzing the double mutant. We found that largely suppresses autoimmunity and blocks the elevated expressions of SA and NHP biosynthesis-related genes in . Overall, our study provides evidence supporting the hypothesis that SUMO protease ESD4 likely targets a yet to be identified guardee of NLR by removing its SUMO modification to avoid recognition by the cognate NLR. Loss of ESD4 results in activation of NLR-mediated autoimmunity.