Abstract: Aflatoxin B1 （AFB1）, a highly carcinogenic secondary metabolite produced byAspergillus flavus, poses a serious threat to human health and agricultural economic development. CIT, a citrate synthase encoded by thecit1gene inA. flavus, catalyzes the condensation of acetyl-CoA and oxaloacetate to form citrate in the first step of the tricarboxylic acid （TCA） cycle, which is involved in the regulation of eukaryotic development, cell apoptosis, and cancer cell proliferation. To provide new insights for effective prevention and control ofA. flavus,the functions of Cit1 were explored in this study. Bioinformatics analysis indicated thatA. flavusCit1 displayed high similarity to orthologs from otherAspergillusspecies. The deletion ofcit1was constructed using homologous recombination methodology. Phenotypic assays and qRT-PCR analysis indicated that the deletion ofcit1affectedA. flavusdevelopment and pathogenicity. The colony diameter of the Δcit1strain was significantly reduced, and the conidial number and morphology in Δcit1differed from those of the wild type （WT） strain. Sclerotial formation was disrupted in Δcit1. Moreover, AFB1 production in Δcit1was decreased. Pathogenicity toward maize kernels in Δcit1was sharply attenuated compared with that of WT. Collectively, thecit1gene was crucial for sclerotial formation, and was also involved in various biological processes includingA. flavusvegetative growth, aflatoxin biosynthesis, and pathogenicity.

Key words: Aspergillus flavus, aflatoxin;cit1gene, citrate synthase