| Summary: | <i>sfgA</i> is known as a key negative transcriptional regulator gene of asexual sporulation and sterigmatocystin production in <i>Aspergillus nidulans</i>. However, here, we found that the homolog <i>sfgA</i> gene shows a broad and complex regulatory role in governing growth, conidiation, sclerotia formation, secondary metabolism, and environmental stress responses in <i>Aspergillus flavus</i>. When <i>sfgA</i> was deleted in <i>A. flavus</i><i>,</i> the fungal growth was slowed, but the conidiation was significantly increased, and the sclerotia formation displayed different behavior at different temperatures, which increased at 30 °C but decreased at 36 °C. In addition, <i>sfgA</i> regulated aflatoxin biosynthesis in a complex way that was associated with the changes in cultured conditions, and the increased production of aflatoxin in the ∆<i>sfgA</i> mutant was associated with a decrease in sclerotia size. Furthermore, the ∆<i>sfgA</i> mutant exhibited sensitivity to osmotic, oxidative, and cell wall stresses but still produced dense conidia. Transcriptome data indicated that numerous development- and secondary-metabolism-related genes were expressed differently when <i>sfgA</i> was deleted. Additionally, we also found that <i>sfgA</i> functions downstream of <i>fluG</i> in <i>A. flavus</i>, which is consistent with the genetic position in FluG-mediated conidiation in <i>A. nidulans</i>. Collectively, <i>sfgA</i> plays a critical role in the development, secondary metabolism, and stress responses of <i>A. flavus,</i> and <i>sfgA</i> renders <i>A. flavus</i> more stable to the external environment.
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