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Transcription factor RonA-driven GlcNAc catabolism is essential for growth, cell wall integrity, and pathogenicity in Aspergillus fumigatus

Summary

Researchers identified how a deadly fungus called Aspergillus fumigatus uses a special nutrient (GlcNAc) to survive and cause disease. They found that a protein called RonA controls this nutrient processing and also helps the fungus hide from the immune system by building a protective outer coating. When RonA is disabled, the fungus becomes much less dangerous because the immune system can recognize it better. This discovery suggests RonA could be a new target for developing antifungal drugs.

Background

Aspergillus fumigatus is a major human fungal pathogen causing invasive aspergillosis with high mortality rates. N-acetylglucosamine (GlcNAc) is an ubiquitous amino sugar serving as a structural component and signaling molecule. The GlcNAc catabolic pathway in A. fumigatus remains unexplored despite the organism’s metabolic versatility.

Objective

To identify and characterize the GlcNAc catabolic pathway components in A. fumigatus and determine their roles in fungal growth, cell wall integrity, and pathogenicity. The study focused on identifying key enzymes and transcription factors involved in GlcNAc metabolism.

Results

DacA and NagA were identified as essential enzymes for GlcNAc catabolism, while RonA functions as the critical transcription factor regulator. Δ ronA mutants showed severe growth defects, impaired cell wall integrity with reduced melanin (84.16% reduction) and increased surface proteins (145.27% increase), and significantly attenuated virulence in infection models.

Conclusion

RonA plays a pivotal role in GlcNAc catabolism, conidial cell wall integrity, and A. fumigatus pathogenesis. RonA represents a promising therapeutic target for antifungal drug development due to its dual role in metabolic regulation and immune evasion mechanisms.
  • Published in:Microbiology Spectrum,
  • Study Type:Experimental Research Study,
  • Source: PMID: 41059696, DOI: 10.1128/spectrum.00122-25
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