Key sugar transporters drive development and pathogenicity in Aspergillus flavus
- Author: mycolabadmin
- 9/8/2025
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Summary
Researchers studied how Aspergillus flavus fungus transports sugars, which is crucial for its growth, producing the toxic aflatoxin that contaminates crops like corn and peanuts. By removing genes responsible for sugar transport, they found that the fungus became weak, couldn’t infect plants or animals effectively, and stopped producing the dangerous aflatoxin. This discovery could help develop new strategies to prevent aflatoxin contamination in food and reduce serious fungal infections in humans.
Background
Aspergillus flavus is a ubiquitous filamentous fungus that causes invasive aspergillosis and produces aflatoxin B1 (AFB1), a carcinogenic toxin that contaminates crops. Sugar transporters (STPs) are essential for fungal metabolism, cell wall biosynthesis, and virulence, but remain largely uncharacterized in A. flavus.
Objective
This study systematically investigated three putative sugar transporter genes (G4B84_001982, G4B84_005374, and G4B84_009351) through functional characterization of gene deletion mutants to determine their roles in development, stress tolerance, and pathogenicity.
Results
G4B84_001982 and G4B84_005374 mediate uptake of diverse sugar substrates and are essential for growth, sporulation, germination, and sclerotium formation. Both mutants showed impaired growth, reduced conidiation, delayed germination, increased sensitivity to cell wall and osmotic stressors, and completely abolished sclerotium formation with attenuated virulence in infection models.
Conclusion
Two sugar transporters are essential for A. flavus development, stress tolerance, and pathogenicity. These findings highlight sugar-mediated pathogenicity mechanisms and suggest STPs represent promising antifungal targets for managing fungal diseases and aflatoxin contamination in agriculture.
- Published in:Frontiers in Cellular and Infection Microbiology,
- Study Type:Experimental Research,
- Source: 10.3389/fcimb.2025.1661799; PMID: 40989179