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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 inter-molecular 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.

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