BCB1, a member of the acyl-coenzyme A synthetase family, regulates the morphogenesis and pathogenicity of Botrytis cinerea

Botrytis cinerea is a non-host-specific phytopathogenic fungus capable of infecting numerous cash crops. Here, we analyzed the functions of the Bcb1 gene in B. cinerea , which encodes a membrane protein belonging to the acyl-coenzyme A synthase family. Compared to the wild type, Bcb1 -deletion mutants exhibited obvious morphological abnormalities, including slower vegetative growth and reduced melanin production. The absence of Bcb1 causes B. cinerea to form only small and incompletely developed infection cushions and fail to produce spores. The Bcb1 mutants displayed hypersensitivity to the membrane stressor SDS, the cell wall stressor Congo red, and the oxidative stressor H 2 O 2 and increased resistance to intracellular osmotic stress caused by KCl compared to the wild-type strain. However, there were no differences in tolerance to extracellular osmotic stress caused by NaCl. The deletion of Bcb1 also caused a reduction in pathogenicity. The qRT‒PCR results showed that the genes Bcpks12 and Bcpks13, which are related to melanin biosynthesis, and Bcpg2, BcBOT2, and cutA, which are related to virulence, were downregulated in ∆Bcb1 . These data suggest that BCB1 is important for conidial morphogenesis, and pathogenesis in B. cinerea .