RIN13-mediated disease resistance depends on SNC1-EDS1/PAD4 signaling pathway in Arabidopsis.

Liu, Xiaoxiao; Liu, Hui; He, Jingjing; Zhang, Siyuan; Han, Hui; Wang, Zhangying; Liu, Wen-Cheng; Liang, Yun-Kuan; Gao, Zhiyong

Plants have evolved an innate immune system to protect themselves from pathogen invasion with the help of intracellular NB-LRR (NLR) receptors though the mechanisms remain largely undefined. RIN13 (RPM1-interacting protein 13) was previously reported to enhance disease resistance, and suppress RPM1 (a CNL type NLR)-mediated hypersensitive response in Arabidopsis via a yet unknown mechanism. Here, we show 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, enhanced resistance to virulent pathogen, and dwarfism. In addition, genetic and transcriptome analysis show that SA-dependent and SA-independent pathways are both required for RIN13-mediated disease resistance with EDS1/PAD4 complex as an integration point. RIN13-induced dwarfism was rescued completely by either mutant pad4-1 or 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. Furthermore, transient expression assays indicated that RIN13 promotes the nuclear accumulation of PAD4. Collectively, our study uncovered a signalling pathway whereby SNC1 and EDS1/PAD4 act together to modulate RIN13-triggered plant defense responses.