| Summary: | <i>Aspergillus flavus</i> produces carcinogenic and mutagenic aflatoxins, which cause economic losses and risk of food safety by contaminating grains, food and feed. In this study, we characterized two bZIP transcription factors, AflatfA and AflatfB, and their genetic interaction. Compared to the wild type (WT), <i>AflatfA</i> deletion and <i>AflatfA</i> and <i>AflatfB</i> double deletion both caused retarded vegetative growth of mycelia. Relative to WT, the <i>AflatfA</i> deletion strain (Δ<i>AflatfA</i>) and <i>AflatfA</i> and <i>AflatfB</i> double deletion strain (Δ<i>AflatfA</i>Δ<i>AflatfB</i>) produced more sclerotia, whereas the <i>AflatfB</i> deletion strain (Δ<i>AflatfB</i>) produced less sclerotia. After 4 °C preservation and incubation at 50 °C, conidia viability dramatically decreased in the Δ<i>AflatfA</i> and Δ<i>AflatfA</i>Δ<i>AflatfB</i> but Δ<i>AflatfB</i> mutants, whereas conidia viability of the Δ<i>AflatfA</i>Δ<i>AflatfB</i> strain was higher after storage at 4 °C than in <i>AflatfA</i> mutant. Conidia of Δ<i>AflatfA</i>, Δ<i>AflatfB</i> and Δ<i>AflatfA</i>Δ<i>AflatfB</i> strains significantly increased in sensitivity to H<sub>2</sub>O<sub>2</sub> in comparison with WT. Compared to WT, the mycelium of Δ<i>AflatfA</i> and Δ<i>AflatfB</i> strains were more sensitive to H<sub>2</sub>O<sub>2</sub>; conversely, the Δ<i>AflatfA</i>Δ<i>AflatfB</i> strain showed less sensitivity to H<sub>2</sub>O<sub>2</sub>. Δ<i>AflatfA</i> and Δ<i>AflatfA</i>Δ<i>AflatfB</i> strains displayed less sensitivity to the osmotic reagents NaCl, KCl and Sorbitol, in comparison with WT and Δ<i>AflatfB</i> strains. When on YES medium and hosts corn and peanut, Δ<i>AflatfA</i> and Δ<i>AflatfA</i>Δ<i>AflatfB</i> strains produced less aflatoxin B1 (AFB1) than Δ<i>AflatfB</i>, and the AFB1 yield of Δ<i>AflatfB</i> was higher than that of WT. When WT and mutants were inoculated on corn and peanut, the Δ<i>AflatfA</i> and Δ<i>AflatfA</i>Δ<i>AflatfB</i> but not Δ<i>AflatfB</i> mutants produced less conidia than did WT. Taken together, this study reveals that AflatfA controls more cellular processes, and the function of AflatfA is stronger than that of AflatfB when of the same process is regulated, except the response to H<sub>2</sub>O<sub>2</sub>, which might result from the effect of AflatfA on the transcriptional level of AflatfB.
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