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

Abstract

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