The SNARE protein CfSnc1 of Colletotrichum fructicola is a key regulator in fungal pathogenicity and responses to hypovirulence-associated mycovirus infection

Abstract

Hypovirulence-associated mycoviruses not only provide new alternative for biological control, but also provide a model for studying the pathogenesis of fungal pathogens. Our previous study showed that the Colletotrichum alienum partitivirus 1 (CaPV1) is a hypovirulence-associated mycovirus which can affect vesicle transport in the host fungus. Soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) proteins play crucial roles in membrane fusion and vesicle trafficking in eukaryotes, which are essential in fungal development and virulence. Here, we identified and characterized CfSNC1 of Colletotrichum fructicola, an ortholog of yeast SNARE SNC1. CfSNC1 is down-regulated in response to infection with CaPV1. To elucidate the potential role of CfSNC1 and its involvement in the relationship between CaPV1 and C. fructicola, targeted gene deletion and complemented mutants were generated. Deletion of CfSNC1 affected vegetative growth and endocytosis pathway, reduced conidiation and appressorium formation, as well as the virulence. Upon CaPV1 infection, vegetative growth of the deletion mutant was more retarded when compared to the CaPV1-infected wild type (WT). Viral RNA accumulation was significantly increased in the deletion mutant compared to that in the virus-infected WT. Taken together, this study revealed that CfSnc1 is a host factor playing roles in development and virulence of C. fructicola and affecting the viral RNA accumulation of CaPV1, which might offer insights into the underlying mechanisms through which mycoviruses manipulate vesicle transport to influence fungal pathogenesis.