A Phytophthora sojae effector PsCRN63 forms homo-/heterodimers to suppress plant immunity via an inverted association manner

作者：Li, Qi; Zhang, Meixiang; Shen, Danyu; Liu, Tingli; Chen, Yanyu; Zhou, Jian-Min^*; Dou, Daolong^*

来源：Scientific Reports, 2016, 6(1): 26951.

DOI：10.1038/srep26951

• PSEUDOMONAS-SYRINGAE EFFECTOR
• INF1-INDUCED CELL-DEATH
• INNATE IMMUNITY
• NICOTIANA-BENTHAMIANA
• TRANSCRIPTION FACTOR
• PATHOGEN PHYTOPHTHORA
• CYTOPLASMIC EFFECTORS
• NEP1-LIKE PROTEINS
• MOLECULAR-PATTERNS
• ARABIDOPSIS

Oomycete pathogens produce a large number of effectors to promote infection. Their mode of action are largely unknown. Here we show that a Phytophthora sojae effector, PsCRN63, suppresses flg22-induced expression of FRK1 gene, a molecular marker in pathogen-associated molecular patterns (PAMP)-triggered immunity (PTI). However, PsCRN63 does not suppress upstream signaling events including flg22-induced MAPK activation and BIK1 phosphorylation, indicating that it acts downstream of MAPK cascades. The PsCRN63-transgenic Arabidopsis plants showed increased susceptibility to bacterial pathogen Pseudomonas syringae pathovar tomato (Pst) DC3000 and oomycete pathogen Phytophthora capsici. The callose deposition were suppressed in PsCRN63-transgenic plants compared with the wild-type control plants. Genes involved in PTI were also down-regulated in PsCRN63-transgenic plants. Interestingly, we found that PsCRN63 forms an dimer that is mediated by intermolecular interactions between N-terminal and C-terminal domains in an inverted association manner. Furthermore, the N-terminal and C-terminal domains required for the dimerization are widely conserved among CRN effectors, suggesting that homo-/hetero-dimerization of Phytophthora CRN effectors is required to exert biological functions. Indeed, the dimerization was required for PTI suppression and cell death-induction activities of PsCRN63.

• 出版日期2016-5-31
• 单位植物基因组学国家重点实验室; 南京农业大学; 中国科学院遗传与发育生物学研究所