Transcription factor AaSom1 regulates development and pathogenicity with AapksA as a key target in Alternaria alternata

Abstract Alternaria alternata tangerine pathotype causes Alternaria brown spot, a major fungal disease threatening citrus production in susceptible cultivars. This pathogen produces the host-specific toxin Alternaria citri toxin (ACT), which serves as the primary virulence factor. However, the regulatory mechanisms controlling ACT biosynthesis remain largely unclear. Here, we characterized the biological functions of the transcription factor AaSom1 and explored its target genes involved in ACT synthesis. Deletion of AaSom1 significantly reduced mycelial growth rate, abolished sporulation, suppressed ACT production, and eliminated pathogenicity. Both the LisH and Med15 domains of AaSom1 are essential for its complete biological function. RNA-seq, ChIP-seq, and DAP-seq analyses revealed that AaSom1 directly binds to the promoter of AapksA, which encodes a polyketide synthase involved in DHN-melanin biosynthesis, and subsequently activates AapksA transcription. AapksA deletion did not affect mycelial growth but significantly reduced conidiation, ACT production, lesion expansion rate, and pathogenicity. Collectively, AaSom1 functions as a multifunctional transcription factor that regulates development and pathogenicity, with AapksA as a key downstream target in A. alternata . These findings reveal a novel regulatory pathway that controls fungal pathogenesis through AaSom1-mediated transcriptional regulation.