The CfAtg5 Regulates the Autophagy and Pathogenicity of Colletotrichum fructicola on Camellia oleifera

Abstract

Camellia oleifera is the native economic edible oil tree in China and anthracnose occurs commonly in its producing areas. We previously found that ubiquitin-like CfAtg8-related autophagy is essential for the pathogenicity of Colletotrichum fructicola, the major pathogen of anthracnose on C. oleifera. The aim of this study is to further elucidate the roles of autophagy in the pathogenesis of C. fructicola. Based on BLAST_P analysis and reverse genetics, we identified the central hub of another ubiquitin-like system, CfAtg5, and characterized its functions in C. fructicola. As suspected, we found that CfAtg5 is required for autophagy, both in MM-N and H2O2 induction conditions. Targeted gene deletion of CfATG5 revealed that CfAtg5 is involved in growth and conidiation. We further found that the ∆Cfatg5 mutant is defective in appressorium formation and in responses to cell wall integrity and oxidative stresses. The combined effects, together with the abolished autophagy, result in the pathogenicity defects of the ∆Cfatg5 mutant. Our study further illustrates the importance of normal autophagy in the physiology and pathogenicity of C. fructicola, and offers a potential target in the development of new anthracnose control strategies.