The Arabidopsis Protein RIN13 Enhances Plant Immunity Through The SNC1-EDS1/PAD4 Signaling Pathway

In the process of growth and development,plants will be attacked by a variety of pathogens.In order to protect themselves,plants have evolved a complex and effective immune system.This immune system includes two layers:pathogen-associated molecular pattern-triggered immunity,named PTI and effector-triggered immunity,referred to as ETI.The plasma-membrane localized pattern recognition receptors(PRRs)can recognize the conservative Pathogen-associated molecular patterns(PAMPs)of pathogens to trigger PTI,and inhibit the infection of pathogens.To enhance pathogenicity,pathogens have evolved virulence proteins(“effectors”)to suppress PTI.In response,plants have adapted by obtaining multiple intracellular nucleotide-binding leucine-rich repeat receptors(NB-LRRs,NLRs)to detect effectors,and stimulate ETI.ETI activation usually results in a faster and stronger immune response than PTI,which induces programmed cell death at the site of infection,also known as hypersensitivity response(HR).Resistance to Pseudomonas syringae pv.Maculicola 1(RPM1)is a typical NLR receptor which can confer resistance to pathogenic bacteria in plants.RPM1 interaction protein 13(RIN13)was first identified by yeast two-hybrid screening experiments using an extended NB-ARC domain(amino acids 28-553)of RPM1 as a bait.Overexpression of RIN13 was previously reported to enhance disease resistance,and suppress RPM1-mediated hypersensitive response in Arabidopsis via a yet unknown mechanism.Therefore,we constructed RIN13 overexpressing plants to further study the function of RIN13.Here,we showed that RIN13 is a nucleus-localized protein,and functions in the nucleus.Overexpression of RIN13 leads to autoimmunity with high accumulation of salicylic acid(SA),constitutive expressions of pathogenesis-related genes,dwarfism,and enhanced resistance to virulent pathogen.Further research showed that both SA-dependent and SA-independent signaling pathways are involved in RIN13-mediated immune responses.RIN13-induced dwarfism was rescued completely by either mutant pad4-1or eds1-2 but partially by snc1-r1,a mutant of the TNL gene SNC1,suggesting the involvement of EDS1/PAD4 and SNC1 in RIN13 functioning.Further research showed that overexpression of RIN13 can block the invasion of pathogenic bacteria by promoting stomata closure,suggesting that stomatal immunity also participates in RIN13-mediated immune processes.We found that RIN13-mediated stomatal closure depends on PAD4,but not SA.Collectively,our study uncovered a signalling pathway whereby SNC1 and EDS1/PAD4 act together to modulate RIN13-triggered plant defense responses.