Deciphering the Mrr1/Mdr1 Pathway in Azole Resistance of Candida auris
Open accessAbstract
Candida auris is an emerging yeast pathogen with a remarkable ability to develop antifungal resistance, in particular to fluconazole and other azoles. Azole resistance in C. auris was shown to result from different mechanisms, such as mutations in the target gene ERG11 or gain-of-function (GOF) mutations in the transcription factor TAC1b and overexpression of the drug transporter Cdr1.
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Cdr1, Mdr1 and Pdr16 cause clinical azole resistance.
“including the Cdr1 multidrug efflux ATP-binding cassette (ABC) transporter, the Mdr1 major facilitator and the putative phosphatidylinositol transfer protein Pdr16 (ref. 18), all of which cause clinical azole resistance16,19,20.”
From Candida auris skin tropism and antifungal resistance are mediated by carbonic anhydrase Nce103 (2025) · cites this paper as [19]
The Results and Discussion (pages unavailable) support roles for Cdr1 and the Mrr1–Mdr1 pathway in C. auris azole susceptibility. They do not address Pdr16, and the Discussion says the susceptibility change caused by Mrr1–Mdr1 alone remained below proposed clinical resistance breakpoints. Thus this source does not establish that all three cause clinical azole resistance. (LLM, conf=0.88)
Experimental — accuracy not yet measuredGain-of-function mutations in TAC1B and MRR1A contribute to clinical fluconazole resistance in C. auris.
“Likewise, gain-of-function mutations in TAC1B (C. auris homologue of C. albicans TAC1) and MRR1A (C. auris homologue of C. albicans MRR1) contribute to clinical fluconazole resistance in C. auris54,55.”
From Molecular mechanisms governing antifungal drug resistance (2023) · cites this paper as [55]
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References 34 · Cited by 59
Research works printed but not linked: 1
- [28]Clinical and Laboratory Standards Institute (CLSI). 2017. Reference method for broth dilution antifungal susceptibility testing of yeasts, 4th ed. Document M27. Wayne, PA. [Google Scholar]
- Authors
- Li, J., Coste, A. T., Bachmann, D., Sanglard, D., & Lamoth, F.
- Affiliations
- Centre Hospitalier Universitaire Vaudois (CH)
- Institute of Microbiology, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland
- Venue
- Antimicrobial Agents and Chemotherapy
- Publisher
- American Society for Microbiology
- Published
- 2022-04-19
- Volume
- 66
- Issue
- 4
- Pages
- e0006722-e0006722
- ISSN
- 0066-4804 (ISSN-L)
- 1098-6596
- PMC
- PMC9017311
- OpenAlex
- W4220984632
- Cited by
- 59
- References
- 34
- Citations by year
- 2026: 11 · 2025: 20 · 2024: 13 · 2023: 13 · 2022: 2
- FWCI
- 5.86
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Antimicrobial Agents and Chemotherapy (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- SERVAL (Université de Lausanne) (publishedVersion)
- IRIS (submittedVersion)
- Funders
- Swiss National Science Foundation (310030_192611)
- Fondation Santos-Suarez pour la Recherche Médicale
- Topics
- Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
- Life Sciences › Agricultural and Biological Sciences › Ecology, Evolution, Behavior and Systematics › Fungal Plant Pathogen Control
- Keywords
- Candida auris, azole resistance, fluconazole resistance, efflux pumps, CDR1, ERG11 mutations, antifungal resistance mechanisms
- MeSH terms
- Candida auris, Antifungal Agents, Azoles, Candida albicans, Fungal Proteins, Microbial Sensitivity Tests, Transcription Factors, Fluconazole, Drug Resistance, Fungal
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