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Roles of the Sec2p Gene in the Growth and Pathogenicity Regulation of Aspergillus fumigatus

Summary

Scientists studied a gene called Sec2p in a harmful fungus that causes serious lung infections in people with weak immune systems. When they removed this gene, the fungus grew more slowly and was much less dangerous to infected mice, with 67% of mice surviving compared to only 22% with normal fungus. The gene controls how the fungus breaks down its own cell parts for nutrition and repairs its cell wall, so blocking it weakens the fungus significantly.

Background

Aspergillus fumigatus is a filamentous fungus causing invasive aspergillosis in immunocompromised individuals. The Sec2p gene encodes a guanine nucleotide exchange factor that activates the Rab protein Sec4, but its specific function in A. fumigatus remains unclear. Understanding genes regulating fungal growth is crucial for identifying potential therapeutic targets.

Objective

This study investigated the roles of the Sec2p gene in A. fumigatus growth and pathogenicity regulation. The researchers examined how Sec2p deletion affects fungal growth, autophagy pathways, cell wall integrity responses, and virulence in infected mice.

Results

Sec2p deletion resulted in slower A. fumigatus growth (42% reduction in colony diameter) and reduced virulence, increasing mouse survival rate from 22-33% to 67%. The mutant strain showed accumulated autophagosomes indicating inhibited autophagosome degradation, reduced autophagy activity, thinner cell walls, and enhanced resistance to cell wall stressors while maintaining stronger cell wall integrity pathway signaling under stress.

Conclusion

Sec2p positively regulates the autophagy pathway and negatively regulates the cell wall integrity pathway during cell wall stress, coordinating A. fumigatus growth and pathogenicity. The gene represents a potential target for treating fungal infections through disruption of nutrient homeostasis and autophagy.
  • Published in:Journal of Fungi (Basel),
  • Study Type:Original Research,
  • Source: PMID: 39852455
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