A Candida albicans Petite Mutant Strain with Uncoupled Oxidative Phosphorylation Overexpresses MDR1 and Has Diminished Susceptibility to Fluconazole and Voriconazole
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We showed that a Candida albicans petite mutant in which oxidative phosphorylation is uncoupled was eightfold more resistant to fluconazole and voriconazole than SC5314 but equally susceptible to ketoconazole, itraconazole, and amphotericin B. Strain P5 significantly overexpressed MDR1, which likely accounts for the decreased drug susceptibility.
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A petite C. albicans strain (J5) described by Cheng et al. showed decreased susceptibility to fluconazole and voriconazole but not itraconazole.
“Cheng et al. (14) described a petite C. albicans strain (J5) whose decrease in susceptibility to fluconazole and voriconazole but not itraconazole was noted.”
From Azole Susceptibility and Transcriptome Profiling in Candida albicans Mitochondrial Electron Transport Chain Complex I Mutants (2013) · cites this paper as [14]
The Abstract reports that the petite C. albicans strain had eightfold higher fluconazole and voriconazole MICs than SC5314, while its itraconazole MIC was unchanged. But the paper identifies the strain as P5, not J5; it also says the higher MICs remained within susceptible ranges. (LLM, conf=0.90)
Experimental — accuracy not yet measuredThe petite C. albicans strain J5 was isolated from wild-type SC5314 by serial passage through mouse spleens and shown to have uncoupled oxidative phosphorylation.
“The petite strain was originally isolated from wild-type C. albicans SC5314 by serial passage through mouse spleens and then shown to have uncoupled oxidative phosphorylation.”
From Azole Susceptibility and Transcriptome Profiling in Candida albicans Mitochondrial Electron Transport Chain Complex I Mutants (2013) · cites this paper as [14]
The Abstract says the authors serially passed SC5314 through mouse spleens and recovered a petite mutant with uncoupled oxidative phosphorylation. It identifies that mutant as P5, not J5, so the strain designation in the claim is unsupported. (LLM, conf=0.90)
Experimental — accuracy not yet measuredOne study reports a relationship between upregulation of the efflux pump gene MDR1, fluconazole resistance and uncoupled oxidative phosphorylation in C. albicans, while fluconazole hypersusceptibility has also been observed in C. albicans mitochondrial ETC complex I mutants.
“Interestingly, one study reports on a relationship between upregulation of the efflux pump gene MDR1, fluconazole resistance and uncoupled oxidative phosphorylation in C. albicans39, while fluconazole hypersusceptibility has also been observed in C. albicans mitochondrial ETC complex I mutants40.”
From Stimulation of superoxide production increases fungicidal action of miconazole against Candida albicans biofilms (2016) · cites this paper as [39]
Mdr1, part of the MFS of transporters, plays a role in fluconazole and voriconazole resistance, though it does not effect large MIC changes with other azole antifungals such as itraconazole, isavuconazole and posaconazole.
“Mdr1, part of the major facilitator superfamily (MFS) of transporters (Figure 1g), has also been shown to play a role in fluconazole and voriconazole resistance, though it does not effect large MIC changes with other azole antifungals such as itraconazole, isavuconazole and posaconazole.93–95”
From Molecular and genetic basis of azole antifungal resistance in the opportunistic pathogenic fungus<i>Candida albicans</i> (2020) · cites this paper as [95]
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References 43 · Cited by 62
Research works printed but not linked: 1
- [32]Sanglard, D., F. Ischer, M. Monod, and J. Bille. 1997. Cloning of Candida albicans genes conferring resistance to azole antifungal agents: characterization of CDR2, a new multidrug ABC transporter gene. Microbiology 143405-416. [DOI] [PubMed] [Google Scholar]
- Authors
- Cheng, S., Clancy, C. J., Nguyen, K. T., Clapp, W., & Nguyen, M. H.
- Affiliations
- University of Florida (US)
- Corresponding author
- Nguyen, M. Hong
- Venue
- Antimicrobial Agents and Chemotherapy
- Publisher
- American Society for Microbiology
- Published
- 2007-05
- Volume
- 51
- Issue
- 5
- Pages
- 1855-1858
- ISSN
- 0066-4804 (ISSN-L)
- 1098-6596
- PMC
- PMC1855545
- OpenAlex
- W2093100278
- Cited by
- 62
- References
- 43
- Citations by year
- 2026: 3 · 2025: 4 · 2024: 3 · 2021: 2 · 2020: 1 · 2019: 6 · 2018: 3 · 2017: 1 · 2016: 3 · 2015: 3 · 2014: 2 · 2013: 1 · 2012: 5
- FWCI
- 3.57
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Antimicrobial Agents and Chemotherapy (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Allergy and Infectious Diseases (P01AI061537)
- Topics
- Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
- Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
- Keywords
- Candida albicans, petite mutants, MDR1, fluconazole resistance, voriconazole resistance, antifungal susceptibility, ketoconazole, itraconazole, amphotericin B, SC5314
- MeSH terms
- Antifungal Agents, Candida albicans, Microbial Sensitivity Tests, Mutation, Oxidative Phosphorylation, Pyrimidines, Triazoles, Fluconazole, Reverse Transcriptase Polymerase Chain Reaction, ATP Binding Cassette Transporter, Subfamily B, Member 1, Drug Resistance, Fungal, Voriconazole
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