A NB-ARC-CRRSP Signaling Module Triggers HR-Like Cell Death and Associated Disease Resistance in Rice by Suppressing Antioxidant Defense Systems

Abstract

A key feature following pathogen recognition by resistance (R) proteins containing NB-ARC (nucleotide-binding adaptor shared by Apaf-1, R proteins, and Ced-4) domains is the hypersensitive response (HR). However, the underpinning mechanisms integral to this process remain relatively opaque. Here we show that a gain-of-function mutation in the NB-ARC protein, RLS1 (Rapid Leaf Senescence1), triggers high-light-dependent HR-like cell death in rice. The RLS1-mediated defense response is independent of SA (salicylic acid) accumulation, NPR1 (nonexpressor of pathogenesis-elated genes 1) activity and RAR1 (required for Mla12 resistance1) function. A screen for suppressors of RLS1 activation identified RMC (Root Meander Curling), a cysteine-rich receptor-like secreted protein (CRRSP). RMC is essential for the RLS1 activated defense response via functioning as a RLS1-binding partner and subsequently suppressing the activity of key antioxidant enzymes. Collectively, our findings reveal a NB-ARC-CRRSP signaling module that triggers HR-like cell death and associated disease resistance in rice.