Abstract
Aspergillus flavus colonizes oil-seed crops, contaminating them with aflatoxins; highly carcinogenic mycotoxins that cause severe health and economic losses. Genetic studies may reveal new targets for effective control strategies. Here, we characterized a putative WOPR transcription factor gene, osaA, in A. flavus. Our results revealed that osaA regulates conidiation and sclerotial formation. Importantly, deletion of osaA reduces aflatoxin B(1) production, while, unexpectedly, transcriptome analysis indicated upregulation of aflatoxin biosynthetic genes, suggesting post-transcriptional or cofactor-mediated regulation. Cyclopiazonic acid production also decreased in the absence of osaA. In addition, the osaA mutant exhibited upregulation of genes in the imizoquin and aspirochlorine clusters. Moreover, osaA is indispensable for normal seed colonization; deletion of osaA significantly reduced fungal burden in corn kernels. Aflatoxin content in seeds also decreased in the absence of osaA. Furthermore, deletion of osaA caused a reduction in cell-wall chitin content, as well as alterations in oxidative stress sensitivity, which could in part contribute to the observed reduction in pathogenicity. Additionally, promoter analysis of osaA-dependent genes indicated potential interactions with stress-responsive regulators, indicated by an enrichment in Sko1 and Cst6 binding motifs. Understanding the osaA regulatory scope provides insight into fungal biology and identifies potential targets for controlling aflatoxin contamination and pathogenicity.