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Updated: May 12, 2026

Inhibition of Aspergillus flavus Growth and Aflatoxin Production in Transgenic Maize Expressing the α-amylase Inhibitor from Lablab purpureus L.
Published on: February 15, 2019
Gene targets for fungal and mycotoxin control
J H Kim1, B C Campbell, R Molyneux
1Plant Mycotoxin Research, USDA-ARS Western Regional Research Center, 800 Buchanan St., 94710, Albany, CA, USA.
Gallic acid and other phenolics inhibit aflatoxin production in Aspergillus flavus by targeting antioxidative systems. Combining phenolics with mitochondrial respiration inhibitors offers a synergistic approach to control fungal growth.
Area of Science:
- Mycology
- Biochemistry
- Fungal Genetics
Background:
- Aflatoxin biosynthesis by Aspergillus flavus is a significant concern.
- Gallic acid, a phenolic compound, has demonstrated inhibitory effects on aflatoxin production.
- Antioxidative response systems in fungi represent potential targets for controlling aflatoxin biosynthesis.
Purpose of the Study:
- To investigate the mechanism by which gallic acid and other phenolics inhibit aflatoxin biosynthesis.
- To develop a high-throughput screening system for identifying fungal genes vulnerable to phenolic compounds.
- To explore the role of mitochondrial antioxidative stress systems in fungal response to antifungals and identify synergistic control strategies.
Main Methods:
- Utilized gallic acid and other antioxidant phenolics to study inhibition of aflatoxin biosynthesis in Aspergillus flavus.
- Developed a high-throughput screening system using Saccharomyces cerevisiae as a model fungus.
- Employed complementation analysis to verify stress responses in Aspergillus flavus, focusing on mitochondrial superoxide dismutase (Mn-SOD).
Main Results:
- Gallic acid and other phenolics inhibit aflatoxin biosynthesis upstream of the regulatory gene aflR.
- A yeast-based screening system successfully identified fungal genes sensitive to phenolic compounds.
- The sod2 mutant of Saccharomyces cerevisiae showed sensitivity to phenolics and mitochondrial respiration inhibitors, a response mirrored in Aspergillus flavus via its Mn-SOD gene (sodA).
Conclusions:
- Antioxidative response systems are viable molecular targets for controlling Aspergillus flavus.
- Phenolic compounds combined with inhibitors of mitochondrial respiration exhibit synergistic effects against Aspergillus flavus growth.
- Mitochondrial antioxidative stress systems are crucial for fungal adaptation to antifungal treatments.
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