Arabidopsis NIMIN1, 2 mediate redox homeostasis and JA/ET pathways to modulate Botrytis cinerea resistance

摘要

Arabidopsis NIM1-INTERACTING1 (NIMIN1) and NIMIN2 are required for salicylic acid (SA)-dependent resistance against biotrophic pathogens.In this study,we have demonstrated that NIMIN1,2 are also essential for plant defense response to necrotrophic pathogen Botrytis cinerea.The nimin1 and nimin2 mutants displayed a higher susceptibility against B.cinerea than the wild type,which correlated with a decrease in B.cinerea-induced PDF1.2 expression.Mutation in NIMIN1 or NIMIN2 enhanced accumulation of hydrogen peroxide (H2O2) with reductions in the activities of three main antioxidant enzymes superoxide dismutase (SOD),catalase (CAT),and peroxidase (POD) at the early time (24h) of upon B.cinerea infection.These mutations also resulted in a visible decrease in B.cinerea-induced Ethylene Responsive Factor 1 (ERF1),Octadecanoid-Responsive Arabidopsis AP2/ERF 59 (ORA59),Allene Oxide Cyclase (AOC3),Opda Reductase 3 (OPR3),ACC Synthesis 2 (ACS2) and ACS6 expression,but an advance in MYC2 expression,indicating that NIMIN1,2 are essential for B.cinerea-activated jasmonic acid (JA)/ethylene (ET) biosynthesis and signaling.However,mutation in NIMIN1 or NIMIN2 drastically suppressed JA-,but not ET-activated PDF1.2 expression.Together,these results suggest that NIMIN1,2 may positively control the B.cinerea resistance by mediating redox homeostasis and JA/ET pathways in Arabidopsis.