The Transcription Factor FgSge1 Harnesses the SAGA Complex to Activate Mycotoxin Biosynthesis and Fungal Virulence

Understanding how fungi regulate mycotoxin production is critical for managing crop diseases and reducing contamination in food systems. Here, we elucidate the mechanism of the transcription factor FgSge1 in Fusarium graminearum, a significant fungal pathogen responsible for Fusarium head blight in cereal crops, in regulating mycotoxin biosynthesis and pathogenicity. FgSge1 specifically binds to the 8-bp cis-element TAARGTTT. Under mycotoxin-induced conditions, FgSge1 binds to this cis-element within its own promoter, activating its own transcription. Additionally, FgSge1 connects with this cis-element within the promoters of mycotoxin biosynthesis genes and interacts directly with the scaffold protein FgAda2 of the Spt-Ada-Gcn5-Acetyltransferase (SAGA) complex. This interaction recruits the histone acetyltransferase FgGcn5 to the promoters of DON biosynthetic genes, promoting histone acetylation and facilitating jet-like chromatin architecture, thereby activating transcription. In contrast, the FgSge1 mutant fails to recruit the SAGA complex, leading to reduced histone acetylation, disrupted chromatin structure, and impaired DON biosynthesis. Together, these findings establish FgSge1 as a critical self-activating regulatory factor that links histone acetylation to higher-order chromatin remodeling, orchestrating mycotoxin gene activation, and providing a framework for understanding epigenetic control of mycotoxin biosynthesis and virulence in fungi.