ArticleAntimicrobial agents and chemotherapy2009
Relative contributions of the Candida albicans ABC transporters Cdr1p and Cdr2p to clinical azole resistance.
Article in Antimicrobial agents and chemotherapy, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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69 citing papers in PubMed, 125 citations in OpenAlex.
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- Comparative functional analysis of a new CDR1-like ABC transporter gene in multidrug resistance and virulence between Magnaporthe oryzae and Trichophyton mentagrophytes.Cell communication and signaling : CCS · 2025Article
- Functional analysis of Candida albicans Cdr1 through homologous and heterologous expression studies.FEMS yeast research · 2025Review
- Adaptation of Candida albicans to specific host environments by gain-of-function mutations in transcription factors.PLoS pathogens · 2024Review
- Cryo-EM structures of Candida albicans Cdr1 reveal azole-substrate recognition and inhibitor blocking mechanisms.Nature communications · 2024Article
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- The evaluation of the overexpression of the ERG-11, MDR-1, CDR-1, and CDR-2 genes in fluconazole-resistant Candida albicans isolated from Ahvazian cancer patients with oral candidiasis.Journal of clinical laboratory analysis · 2022Article
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- Myriocin enhances the antifungal activity of fluconazole by blocking the membrane localization of the efflux pump Cdr1.Frontiers in pharmacology · 2022Article
- Antifungal Drug Resistance: Molecular Mechanisms inChemical reviews · 2021Review
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- Ketorolac-fluconazole: A New Combination Reverting Resistance inJournal of blood medicine · 2021Article
- Characterization of Three Pleiotropic Drug Resistance Transporter Genes and Their Participation in the Azole Resistance ofFrontiers in cellular and infection microbiology · 2021Article
- An oxindole efflux inhibitor potentiates azoles and impairs virulence in the fungal pathogen Candida auris.Nature communications · 2020Article
9 more citing papers are in PubMed but not listed here.
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3 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Candida albicans frequently develops resistance to treatment with azole drugs due to the acquisition of gain-of-function mutations in the transcription factor Tac1p. Tac1p hyperactivation in azole-resistant isolates results in the constitutive overexpression of several genes, including CDR1 and CDR2, which encode two homologous transporters of the ATP-binding cassette family. Functional studies of Cdr1p and Cdr2p have been carried out so far by heterologous expression in the budding yeast Saccharomyces cerevisiae and by gene deletion or overexpression in azole-sensitive C. albicans strains in which CDR1 expression is low and CDR2 expression is undetectable. Thus, the direct demonstration that CDR1 and CDR2 overexpression causes azole resistance in clinical strains is still lacking, as is our knowledge of the relative contribution of each transporter to clinical azole resistance. In the present study, we used the SAT1 flipper system to delete the CDR1 and CDR2 genes from clinical isolate 5674. This strain is resistant to several azole derivatives due to a strong hyperactive mutation in Tac1p and expresses high levels of Cdr1p and Cdr2p. We found that deleting CDR1 had a major effect, reducing resistance to fluconazole (FLC), ketoconazole (KTC), and itraconazole (ITC) by 6-, 4-, and 8-fold, respectively. Deleting CDR2 had a much weaker effect, reducing FLC or KTC resistance by 1.5-fold, and had no effect on ITC resistance. These results demonstrate that Cdr1p is a major determinant of azole resistance in strain 5674 and potentially in other clinical strains overexpressing Cdr1p and Cdr2p, while Cdr2p plays a more minor role.
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