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Histone Acetyltransferase CfGcn5-Mediated Autophagy Governs the Pathogenicity of Colletotrichum fructicola

Camellia oleifera is a woody edible-oil plant in China, and anthracnose occurs wherever it is grown, causing serious losses each year. We previously identified that the histone acetyltransferase CfGcn5 orchestrates growth, development, and pathogenicity in Colletotrichum fructicola, the major causal...

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Detalles Bibliográficos
Autores principales: Zhang, Shengpei, Guo, Yuan, Li, Sizheng, Li, He
Formato: Online Artículo Texto
Lenguaje:English
Publicado: American Society for Microbiology 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9600425/
https://www.ncbi.nlm.nih.gov/pubmed/35975920
http://dx.doi.org/10.1128/mbio.01956-22
Descripción
Sumario:Camellia oleifera is a woody edible-oil plant in China, and anthracnose occurs wherever it is grown, causing serious losses each year. We previously identified that the histone acetyltransferase CfGcn5 orchestrates growth, development, and pathogenicity in Colletotrichum fructicola, the major causal agent of anthracnose on C. oleifera. To elucidate the underlying mechanism, we conducted a transcriptome analysis and found that CfGcn5 is mainly involved in ribosomes, catalytic and metabolic processes, primary metabolism, and autophagy. In addition, we provided evidence showing that CfGcn5 serves as an autophagy repressor to mediate the expression of many autophagy-related genes (ATG) and undergoes degradation during autophagy. Moreover, we found that the CfATG8 and CfATG9 gene-deletion mutants had defects in mitosis and autophagy, resulting in their decreased appressoria formation rates and lower turgor pressure. These combined effects caused the failure of their appressoria functions and caused defects on their pathogenicity, revealing the importance of autophagy in pathogenicity. Taken together, our study illustrates that the autophagy repressor CfGcn5 undergoes degradation in order to regulate autophagy-dependent pathogenicity in C. fructicola.