An activated form of NB-ARC protein RLS1 functions with cysteine-rich receptor-like protein RMC to trigger cell death in rice
Yiqin Wang, Zhenfeng Teng, Hua Li, Wei Wang, Fan Xu, Kai Sun, Jinfang Chu, Yangwen Qian, Gary J. Loake, Chengcai Chu, Jiuyou Tang
Abstract
A key event that follows pathogen recognition by a resistance (R) protein containing an NB-ARC (nucleotide-binding adaptor shared by Apaf-1, R proteins, and Ced-4) domain is hypersensitive response (HR)-type cell death accompanied by accumulation of reactive oxygen species and nitric oxide. However, the integral mechanisms that underlie this process remain relatively opaque. Here, we show that a gain-of-function mutation in the NB-ARC protein RLS1 (Rapid Leaf Senescence 1) triggers high-light-dependent HR-like cell death in rice. The RLS1-mediated defense response is largely independent of salicylic acid accumulation, NPR1 (Nonexpressor of Pathogenesis-Related Gene 1) activity, and RAR1 (Required for Mla12 Resistance 1) function. A screen for suppressors of RLS1 activation identified RMC (Root Meander Curling) as essential for the RLS1-activated defense response. RMC encodes a cysteine-rich receptor-like secreted protein (CRRSP) and functions as an RLS1-binding partner. Intriguingly, their co-expression resulted in a change in the pattern of subcellular localization and was sufficient to trigger cell death accompanied by a decrease in the activity of the antioxidant enzyme APX1. Collectively, our findings reveal an NB-ARC-CRRSP signaling module that modulates oxidative state, the cell death process, and associated immunity responses in rice.