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 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.
Highlights
The plants rely mainly on an innate complicated defense system to systematically counteract pathogen invasion
To resist the biotic and abiotic stress, the plants initiate a series of immune responses, such as reactive oxygen species (ROS) bursts, biosynthesis of phytohormones, the expression of a large number of defense-related genes, and callose deposition
The callose deposition at the cell wall is an early defense response (Jones and Dangl, 2006; Schwessinger and Ronald, 2012), which is associated with cell death (Han and Hwang, 2017)
Summary
The plants rely mainly on an innate complicated defense system to systematically counteract pathogen invasion. The ascomycete Valsa mali has been reported to produce 193 secretory proteins with unknown functions, 101 of which are V. mali-specific (Li et al, 2015). These EPs are divided into two classes based on their function, inducing cell death elicitors, such as VmE02 (Nie et al, 2019) and VmHEP1 (Zhang et al, 2019), and the cell death suppressors, such as VmEP1 (Li et al, 2015) and VmPxE1 (Zhang M. et al, 2018). How VmEP1 manipulates the host immunity is still not clear
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
