Gene deletion impacts conidiation and melanin production in Botrytis cinerea, suggesting Bcras1's role in virulence.
The fungal pathogen Botrytis cinerea causes gray mold disease, with Bcras1 serving as a key virulence factor. However, the role of Bcras1 in the environmental responses and its downstream signaling pathways remains unclear. This study investigated the function of Bcras1 and its regulatory network using gene deletion and transcriptomic analysis. Results showed that Δ Bcras1 mutants exhibited severe defects in conidiation, sclerotia formation, acid production, and virulence, along with increased sensitivity to stress and enhanced melanin production. Transcriptome profiling revealed 2236 downregulated and 2149 upregulated genes in Δ Bcras1 , including decreased expression of conidiation-related genes ( Bcbck1 , Bos5 , and Bcnop53 ), sclerotia-related gene ( Bcatf1 ), and MAPK pathway-related genes ( Bcsak1 , Bcmkk1 , Bcbck1 , and Bcste50 ), as well as altered ROS-related genes and upregulated melanin biosynthesis genes ( Bcsmr1 and Bcscd1 ). Functional characterization of the downregulated MAPK gene Bcste50 showed that it similarly affects growth, development, and virulence. Our results demonstrate that Bcras1 regulates multiple pathways controlling fungal development, virulence, and stress adaptation, with Bcste50 acting as a potential downstream component in this regulatory network.
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Zhang et al. (2025) studied this question.
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