Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

The Antioxidant Gallic Acid Inhibits Aflatoxin Formation in Aspergillus flavus by Modulating Transcription Factors FarB and CreA

Version 1 : Received: 12 June 2018 / Approved: 13 June 2018 / Online: 13 June 2018 (09:59:49 CEST)

A peer-reviewed article of this Preprint also exists.

Zhao, X.; Zhi, Q.-Q.; Li, J.-Y.; Keller, N.P.; He, Z.-M. The Antioxidant Gallic Acid Inhibits Aflatoxin Formation in Aspergillus flavus by Modulating Transcription Factors FarB and CreA. Toxins 2018, 10, 270. Zhao, X.; Zhi, Q.-Q.; Li, J.-Y.; Keller, N.P.; He, Z.-M. The Antioxidant Gallic Acid Inhibits Aflatoxin Formation in Aspergillus flavus by Modulating Transcription Factors FarB and CreA. Toxins 2018, 10, 270.

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 A. 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 DcreA 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.

Keywords

Aspergillus flavus; antioxidant gallic acid; aflatoxin; farB; creA

Subject

Biology and Life Sciences, Immunology and Microbiology

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