Objective Magnaporthe oryzae is a pathogen causing rice blast disease. The study on its functional genes can reveal the molecular mechanism of the disease and help to control the disease.

Methods The homologous proteins of Dock180 and ELMO in M. oryzae were identified by bioinformatics method, their coding genes were knocked out respectively, and the phenotype of the obtained gene deletion mutants were analyzed, and the interaction between the two proteins was analyzed by co-immunoprecipitation.

Results MoDOCK1 and MoELMO1 genes were identified in M. oryzae, and their respective gene deletion mutants were obtained successfully. The two mutants had almost the same phenotype. The absence of MoDock1 or MoElmo1 seriously affected the adhesion of conidia, resulting in longer bud tubes with septum and delayed appressoria formation. The addition of 8-Br-cAMP or IBMX can repair the defects in appressoria formation, suggesting that MoDock1 and MoElmo1 may play a role in the cAMP-PKA signaling pathway of M. oryzae. The infection of onion epidermis showed that the infection ability of gene deletion mutants was decreased. Rice infection assay showed that the absence of MoDOCK1 and MoELMO1 led to the weakening of the overall pathogenicity of M. oryzae. Finally, the interaction between MoDock1 and MoElmo1 was proved by co-immunoprecipitation.

Conclusion MoDock1 and MoElmo1 interact with each other, both of which are necessary for the adhesion of conidia, the normal formation of appressoria and the complete pathogenicity in M. oryzae.