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To successfully colonize the plants, the pathogenic microbes secrete a mass of effector proteins which manipulate host immunity. Apple valsa canker is a destructive disease caused by the weakly parasitic fungus  Valsa mali . A previous study indicated that the  V. mali  effector protein 1 ( VmEP1 ) is an essential virulence factor. However, the pathogenic mechanism of  VmEP1  in  V .  mali  remains poorly understood. In this study, we found that the apple ( Malus domestica ) pathogenesis-related 10 proteins ( MdPR10 ) are the virulence target of  VmEP1  using a yeast two-hybrid screening. By bimolecular fluorescence (BiFC) and coimmunoprecipitation (Co-IP), we confirmed that the  VmEP1  interacts with  MdPR10 in vivo . Silencing of  MdPR10  notably enhanced the  V .  mali  infection, and overexpression of  MdPR10  markedly reduced its infection, which corroborates its positive role in plant immunity against  V .  mali . Furthermore, we showed that the co-expression of  VmEP1  with  MdPR10  compromised the  MdPR10 -mediated resistance to  V .  mali . Taken together, our results revealed a mechanism by which a  V .  mali  effector protein suppresses the host immune responses by interfering with the  MdPR10 -mediated resistance to  V .  mali  during the infection.

A Valsa mali Effector Protein 1 Targets Apple (Malus domestica) Pathogenesis-Related 10 Protein to Promote Virulence