ArticleEukaryotic cell2014
UPC2 is universally essential for azole antifungal resistance in Candida albicans.
Article in Eukaryotic cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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40 citing papers in PubMed, 73 citations in OpenAlex.
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- Galactose Inhibits the Translation of Erg1 that Enhances the Antifungal Activities of Azoles AgainstAntibiotics (Basel, Switzerland) · 2025Article
- Regulation of Ergosterol Biosynthesis in Pathogenic Fungi: Opportunities for Therapeutic Development.Microorganisms · 2025Review
- Distinguishing mutants that resist drugs via different mechanisms by examining fitness tradeoffs.eLife · 2024Article
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- Distinguishing mutants that resist drugs via different mechanisms by examining fitness tradeoffs.bioRxiv : the preprint server for biology · 2024Article
- Pitavastatin Calcium Confers Fungicidal Properties to Fluconazole by Inhibiting Ubiquinone Biosynthesis and Generating Reactive Oxygen Species.Antioxidants (Basel, Switzerland) · 2024Article
- The atypical antipsychotic aripiprazole alters the outcome of disseminatedbioRxiv : the preprint server for biology · 2024Article
- Upc2-mediated mechanisms of azole resistance inMicrobiology spectrum · 2024Article
- Insights into the structure, function, and impact ofCurrent medical mycology · 2024Review
- The Microevolution of Antifungal Drug Resistance in Pathogenic Fungi.Microorganisms · 2023Review
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- SAGA Complex Subunits inFrontiers in cellular and infection microbiology · 2022Article
- Sterol Composition Modulates the Response ofJournal of fungi (Basel, Switzerland) · 2021Article
- Antifungal Drug Resistance: Molecular Mechanisms inChemical reviews · 2021Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
In Candida albicans, the transcription factor Upc2 is central to the regulation of ergosterol biosynthesis. UPC2-activating mutations contribute to azole resistance, whereas disruption increases azole susceptibility. In the present study, we investigated the relationship of UPC2 to fluconazole susceptibility, particularly in azole-resistant strains. In addition to the reduced fluconazole MIC previously observed with UPC2 disruption, we observed a lower minimum fungicidal concentration (MFC) for a upc2Δ/Δ mutant than for its azole-susceptible parent, SC5314. Moreover, the upc2Δ/Δ mutant was unable to grow on a solid medium containing 10 μg/ml fluconazole and exhibited increased susceptibility and a clear zone of inhibition by Etest. Time-kill analysis showed higher fungistatic activity against the upc2Δ/Δ mutant than against SC5314. UPC2 disruption in strains carrying specific resistance mutations also resulted in reduced MICs and MFCs. UPC2 disruption in a highly azole resistant clinical isolate containing multiple resistance mechanisms likewise resulted in a reduced MIC and MFC. This mutant was unable to grow on a solid medium containing 10 μg/ml fluconazole and exhibited increased susceptibility and a clear zone of inhibition by Etest. Time-kill analysis showed increased fungistatic activity against the upc2Δ/Δ mutant in the resistant background. Microarray analysis showed attenuated induction by fluconazole of genes involved in sterol biosynthesis, iron transport, or iron homeostasis in the absence of UPC2. Taken together, these data demonstrate that the UPC2 transcriptional network is universally essential for azole resistance in C. albicans and represents an attractive target for enhancing azole antifungal activity.
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