Abstract
Aflatoxin biosynthesis is correlated with oxidative stress and is proposed to function as a secondary defense mechanism to redundant intracellular reactive oxygen species (ROS). We find that the antioxidant gallic acid inhibits aflatoxin formation and growth in Aspergillus flavus in a dose-dependent manner. Global expression analysis (RNA-Seq) of gallic acid-treated A. flavus showed that 0.8% (w/v) gallic acid revealed two possible routes of aflatoxin inhibition. Gallic acid significantly inhibited the expression of farB, encoding a transcription factor that participates in peroxisomal fatty acid β-oxidation, a fundamental contributor to aflatoxin production. Secondly, the carbon repression regulator encoding gene, creA, was significantly down regulated by gallic acid treatment. CreA is necessary for aflatoxin synthesis, and aflatoxin biosynthesis genes were significantly downregulated in ∆creA mutants. In addition, the results of antioxidant enzyme activities and the lipid oxidation levels coupled with RNA-Seq data of antioxidant genes indicated that gallic acid may reduce oxidative stress through the glutathione- and thioredoxin-dependent systems in A. flavus.
Highlights
Aspergillus flavus is a saprotrophic and plant pathogenic fungus and an opportunistic human and animal pathogen [1]
We present here our finding that Gallic acid (GA) significantly inhibited the expression of the farB gene, which controls the activity of peroxisomal fatty acid β-oxidation [17], and of the carbon repression regulator encoding gene, creA, which has recently been found involved in aflatoxin synthesis [18]
The cluster #54, responsible for the aflatoxin biosynthesis, was one of these 16 clusters, and almost all the assigned genes expression were significantly downregulated in the 0.8% (w/v) GA treated samples compared with the untreated samples (Figure 4, Table S3)
Summary
Aspergillus flavus is a saprotrophic and plant pathogenic fungus and an opportunistic human and animal pathogen [1]. In addition to a requirement for adequate acyl-CoA pools to synthesize aflatoxin, several groups have proposed that oxidative stress is a prerequisite for aflatoxin biosynthesis in Aspergillus parasiticus [8,9,10] This observation is tied in with the hypothesis that aflatoxin is a secondary defense system protecting the fungus from excess ROS [11]. Piperine inhibited aflatoxin production in A. flavus concurrently with positive regulation of genes belonging to superoxide dismutase and catalase families, as well as genes encoding the basic leucine zipper (bZIP) transcription factors AtfA, AtfB, and Ap-1 [15] These bZIP transcription factors and MsnA are thought to participate in a regulatory network that mediates both the oxidative stress and aflatoxin pathways in A. parasiticus [11].
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