Background: Tea-oil tree (Camellia oleifera) is a unique edible-oil tree in China, and anthracnose occurs in wherever it is cultivated, causing great economic losses each year. We have previously identified the Ascomycete fungus Colletotrichum fructicola as the major pathogen of anthracnose in Ca.oleifera. The purpose of this study was to characterize the biological function of Snf1 protein, a key component of the AMPK (AMP-activated protein kinase) pathway, for the molecular pathogenic-mechanisms of C. fructicola. Results: We characterized CfSnf1 as the homolog of Saccharomyces cerevisiae Snf1. Targeted CfSNF1 gene deletion revealed that CfSnf1 is involved in the utilization of specific carbon sources, conidiation, and stress responses. We further found that the ΔCfSnf1 mutant was not pathogenic to Ca.oleifera, resulting from its defect in appressorium formation. In addition, we provided evidence showing crosstalk between the AMPK and the cAMP/PKA pathways for the first time in filamentous fungi. Conclusion: This study indicate that CfSnf1 is a critical factor in the development and pathogenicity of C. fructicola and, therefore, a potential fungicide target for anthracnose control.

Camellia oleifera is one of the most valuable woody edible-oil crops, and anthracnose seriously afflicts its yield and quality. We recently showed that the CfSnt2 regulates the pathogenicity of Colletotrichum fructicola, the dominant causal agent of anthracnose on C. oleifera. However, the molecular mechanisms of CfSnt2-mediated pathogenesis remain largely unknown. Here, we found that CfSnt2 is localized to the nucleus to regulate the deacetylation of histone H3. The further transcriptomic analysis revealed that CfSnt2 mediates the expression of global genes, including most autophagy-related genes. Furthermore, we provided evidence showing that CfSnt2 negatively regulates autophagy and is involved in the responses to host-derived ROS and ER stresses. These combined functions contribute to the pivotal roles of CfSnt2 on pathogenicity. Taken together, our studies not only illustrate how CfSnt2 functions in the nucleus, but also link its roles on the autophagy and responses to host-derived stresses with pathogenicity in C. fructicola.

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.