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Arabidopsis thaliana ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1) controls defense activation and programmed cell death conditioned by intracellular Toll-related immune receptors that recognize specific pathogen effectors. EDS1 is also needed for basal resistance to invasive pathogens by restricting the progression of disease. In both responses, EDS1, assisted by its interacting partner, PHYTOALEXIN-DEFICIENT4 (PAD4), regulates accumulation of the phenolic defense molecule salicylic acid (SA) and other as yet unidentified signal intermediates. An Arabidopsis whole genome microarray experiment was designed to identify genes whose expression depends on EDS1 and PAD4, irrespective of local SA accumulation, and potential candidates of an SA-independent branch of EDS1 defense were found. We define two new immune regulators through analysis of corresponding Arabidopsis loss-of-function insertion mutants. FLAVIN-DEPENDENT MONOOXYGENASE1 (FMO1) positively regulates the EDS1 pathway, and one member (NUDT7) of a family of cytosolic Nudix hydrolases exerts negative control of EDS1 signaling. Analysis of fmo1 and nudt7 mutants alone or in combination with sid2-1, a mutation that severely depletes pathogen-induced SA production, points to SA-independent functions of FMO1 and NUDT7 in EDS1-conditioned disease resistance and cell death. We find instead that SA antagonizes initiation of cell death and stunting of growth in nudt7 mutants. [ABSTRACT FROM AUTHOR]

Plant nucleotide binding/leucine-rich repeat (NLR) immune receptors are activated by pathogen effectors to trigger host defenses and cell death. Toll-interleukin 1 receptor domain NLRs (TNLs) converge on the ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1) family of lipase-like proteins for all resistance outputs. In Arabidopsis ( Arabidopsis thaliana ) TNL-mediated immunity, At EDS1 heterodimers with PHYTOALEXIN DEFICIENT4 ( At PAD4) transcriptionally induced basal defenses. At EDS1 uses the same surface to interact with PAD4-related SENESCENCE-ASSOCIATED GENE101 ( At SAG101), but the role of At EDS1- At SAG101 heterodimers remains unclear. We show that At EDS1- At SAG101 functions together with N REQUIRED GENE1 ( At NRG1) coiled-coil domain helper NLRs as a coevolved TNL cell death-signaling module. At EDS1- At SAG101- At NRG1 cell death activity is transferable to the Solanaceous species Nicotiana benthamiana and cannot be substituted by At EDS1- At PAD4 with At NRG1 or At EDS1- At SAG101 with endogenous Nb NRG1. Analysis of EDS1-family evolutionary rate variation and heterodimer structure-guided phenotyping of At EDS1 variants and At PAD4- At SAG101 chimeras identify closely aligned ɑ-helical coil surfaces in the At EDS1- At SAG101 partner C-terminal domains that are necessary for reconstituted TNL cell death signaling. Our data suggest that TNL-triggered cell death and pathogen growth restriction are determined by distinctive features of EDS1-SAG101 and EDS1-PAD4 complexes and that these signaling machineries coevolved with other components within plant species or clades to regulate downstream pathways in TNL immunity., (© 2019 American Society of Plant Biologists. All rights reserved.)