Abstract
Aspergillus flavus is a globally distributed filamentous fungus of major agricultural and medical importance, capable of producing carcinogenic aflatoxins and forming two specialized developmental structures, conidia and sclerotia. While the molecular framework governing conidiation has been well characterized in Aspergillus nidulans, the corresponding mechanisms in A. flavus remain somewhat unelucidated. In this study, we identified and functionally characterized AfldrnA, a gene encoding a basic helix-loop-helix (bHLH) transcription factor. Targeted deletion of AfldrnA resulted in an aconidial phenotype accompanied by a significant increase in sclerotia formation, whereas complementation with the intact AfldrnA gene restored conidiation and reduced sclerotia development. Phenotypic assays revealed that the ΔAfldrnA mutant exhibited normal vegetative growth, unchanged antifungal susceptibility, and unaffected aflatoxin B(1) production, indicating that AfldrnA primarily regulates developmental rather than metabolic differentiation. Additionally, observed differences between standard and dark incubation conditions suggest that AfldrnA may be involved in environmentally responsive regulation of fungal development. Overall, this study identifies AfldrnA as a pivotal transcriptional regulator essential for coordinating conidiation and sclerotia formation in A. flavus, providing new insights into the genetic and environmental regulation of fungal developmental programs.