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Insights into the structure, function, and impact of Candida albicans UPC2 gene on azole resistance; a mini-review

Summary

Candida albicans is a common fungal infection that doctors treat with azole medications, but the fungus is increasingly developing resistance to these drugs. Scientists have discovered that a gene called UPC2 plays a key role in this resistance by controlling the production of enzymes that help the fungus survive azole treatment. Understanding how UPC2 works could help develop new strategies to overcome drug-resistant fungal infections.

Background

Candidiasis is a prevalent fungal infection caused by Candida species, particularly C. albicans, with rising global incidence of invasive fungal infections. The emergence of resistance to azole medications, which are frequently prescribed for treatment, presents a significant clinical challenge.

Objective

This mini-review summarizes findings on the structure, function, and role of the UPC2 gene in azole resistance mechanisms in C. albicans. The review examines how UPC2 mutations contribute to antifungal drug resistance development.

Results

The UPC2 gene encodes a zinc(II)-Cys(6) transcription factor of 712 amino acids located on chromosome 1 of C. albicans. Gain-of-function mutations in UPC2 (such as G648D, A643V, Y642F) lead to upregulation of ERG11 gene expression and increased ergosterol biosynthesis, resulting in azole resistance. Exposure to azoles triggers UPC2 overexpression, enhancing production of lanosterol 14α-demethylase, the primary azole target enzyme.

Conclusion

The UPC2 gene plays a crucial role in regulating azole resistance in C. albicans through control of ergosterol biosynthesis pathways. Understanding UPC2-mediated resistance mechanisms is essential for developing effective antifungal therapies and diagnostic strategies to combat emerging drug-resistant Candida infections.
  • Published in:Current Medical Mycology,
  • Study Type:Mini-review,
  • Source: PMID: 40662146, DOI: 10.22034/cmm.2024.345248.1595
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