Overexpression of the receptor-like cytoplasmic kinase SZE1 positively regulates the PTI signaling pathway in Arabidopsis

Abstract

Plants resist pathogen attacks through innate immune responses. RLCK (Receptor-like cytoplasmic kinase) is essential for plant innate immunity, but only a few RLCK functions have been discovered. SZE1 (Suppressor of ZED1-D1) was reported to be involved in the ETI (Effector-triggered Immunity) signaling pathway, but by analyzing the transcriptome data, we found that SZE1 was upregulated under flg22 (22 amino acids at flagellin's N-terminus) and Pseudomonas syringae treatment. The function of the SZE1 gene in the PTI signaling pathway was studied using SZE1 overexpression and mutant plants. While overexpression of the SZE1 gene enhanced PTI (PAMP-triggered immunity) signal transduction and the ability of Arabidopsis to resist P.s.t. DC3000 (Pseudomonas syringae pv tomato DC3000), sze1 mutants were more sensitive to pathogen infection. We also found that SZE1 could interact with BAK1 (BRI1-associated receptor kinase 1) by yeast two-hybrid and Co-IP (Co-immunoprecipitation) assays. Our results demonstrate that SZE1 positively regulates the PTI signaling pathway, which may enhance flg22-triggered PTI signal transduction by interacting with BAK1 to form a complex. Although PTI and ETI immune responses involve different activation mechanisms, eventually, they converge into many similar downstream responses. Our results provide evidence that SZE1 is a signaling element that participates in both PTI and ETI.