The CfSnt2-Dependent Deacetylation of Histone H3 Mediates Autophagy and Pathogenicity of Colletotrichum fructicola.

Abstract

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.