Abstract
Colletotrichum fructicola is a fungal pathogen that causes Camellia oleifera anthracnose. Mitogen-activated protein kinase cascade signaling regulates plants defenses and is modulated by Ste50, a scaffold protein that mediates the interaction of Ste11 and Ste7. In this study, the Saccharomyces cerevisiae STE50 homolog CfSTE50 in C. fructicola was identified and disrupted. CfSTE50 encodes a 482 amino acid protein. The mutants showed significant differences in conidial yields and appressorium failed to form. Vegetative growth also decreased compared to wild-type strains. Inoculation with conidial suspensions showed that the virulence of the mutant on wounded leaves was significantly impaired. Further analysis showed that the targeted deletion of CfSTE50 resulted in enhanced sensitivity to external peroxide stress, but reduced sensitivity to cell wall stress. These results provide evidence that CfSte50 regulates the growth and development of C. fructicola and regulates asexual reproduction, appressorium formation, pathogenicity and the response to external stresses.
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