Genetic analyses of autoimmune mutants uncover the MPK3/6-CHR5-SNC1 module in Arabidopsis.

Plant defense largely relies on an immune system that is induced by the binding of microbe-derived molecules to receptors at the plasma membrane, initiating the pattern-triggered immunity (PTI), and by the detection of pathogen effectors by intracellular nucleotide-binding leucine-rich repeat receptors (NLRs), eliciting the effector-triggered immunity (ETI). While PTI and ETI were initially thought to be independent, recent studies have revealed some interplay. Our group notably showed that the activity of mitogen-activated protein kinase 3 (MPK3) and MPK6 could link PTI and ETI responses by positively regulating the salicylic acid (SA)-dependent defense, through the up-regulation of some NLR genes. Here, we gained a better understanding of the relationship between these MAPKs and the key NLR suppressor of npr1-1, constitutive 1 (SNC1). By genetic analyses, we demonstrate that chromatin remodeling 5 (CHR5), a positive regulator of SNC1 expression, is downstream of MPK3 activity. We also provide evidence that CHR5 itself does not regulate immune MAPKs. We then show that plants expressing both MPK3 and SNC1 gain-of-function proteins synergistically exhibit a strong autoimmune phenotype. Finally, we report that MPK3 and MPK6 function redundantly upstream of SNC1. Overall, our results identified the MPK3/6-CHR5-SNC1 module, further refining the connection between PTI and ETI components.