アスペルギルス・フラバスにおけるスプライシング因子スキップのベンゾイル化は、発生、酸化ストレス応答、および病原性にとって重要である
Xuan Chen1,2, Yuqi Zhang1, Wenxin Luo1
1State Key Laboratory of Agricultural and Forestry Biosecurity, Key Laboratory of Pathogenic Fungi and Mycotoxins of Fujian Province, and School of Life Sciences, Fujian Agriculture and Forestry University, Fuzhou 350002, China.
Abstract:
Alternative splicing of pre-mRNA is a crucial mechanism in gene expression regulation. As a core component of the spliceosome, the biological function of the Skip protein in Aspergillus flavus remains unknown. Quantitative real-time PCR (qPCR) analysis revealed the presence of two skip gene copies in A. flavus. Single-copy deletion of Skip resulted in slowed growth, reduced conidiation, abolished sclerotial formation, increased aflatoxin biosynthesis, and diminished crop colonization. Meanwhile, Skip was found to regulate the oxidative stress response by modulating the alternative splicing of yapA. Subsequently, immunoprecipitation and Western blot analyses identified lysine 325 (K325) as the benzoylated site on the Skip protein, which catalyzed by the acyltransferase EsaA. Mutation of benzoylated site K325 directly impaired fungal morphogenesis, pathogenicity, and stress adaptation. These findings established the crucial role of Skip and its benzoylation in A. flavus and suggested a potential target for controlling its infection in important crops.
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