ArticlePloS one2011
The transcription factor Ndt80 does not contribute to Mrr1-, Tac1-, and Upc2-mediated fluconazole resistance in Candida albicans.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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37 citing papers in PubMed, 58 citations in OpenAlex.
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- Investigation of fluconazole susceptibility to Candida albicans by MALDI-TOF MS and real-time PCR for CDR1, CDR2, MDR1 and ERG11.BMC microbiology · 2022Article
- The protein kinase Ire1 has a Hac1-independent essential role in iron uptake and virulence of Candida albicans.PLoS pathogens · 2022Article
- The zinc cluster transcription factor Rha1 is a positive filamentation regulator in Candida albicans.Genetics · 2022Article
- Imaging and Quantification of mRNA Molecules at Single-Cell Resolution in the Human Fungal Pathogen Candida albicans.mSphere · 2021Article
- Fructose Induces Fluconazole Resistance inInternational journal of molecular sciences · 2021Article
- Generation of Viable Candida albicans Mutants Lacking the "Essential" Protein Kinase Snf1 by Inducible Gene Deletion.mSphere · 2020Article
- Molecular and genetic basis of azole antifungal resistance in the opportunistic pathogenic fungus Candida albicans.The Journal of antimicrobial chemotherapy · 2020Review
- Lipid composition and cell surface hydrophobicity of Candida albicans influence the efficacy of fluconazole-gentamicin treatment.Yeast (Chichester, England) · 2020Article
- A Crucial Role for Ergosterol in Plasma Membrane Composition, Localisation, and Activity of Cdr1p and HMicroorganisms · 2019Article
- Linking Cellular Morphogenesis with Antifungal Treatment and Susceptibility inJournal of fungi (Basel, Switzerland) · 2019Review
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- Chemogenomic profiling to understand the antifungal action of a bioactive aurone compound.PloS one · 2019Article
- A Hyperactive Form of the Zinc Cluster Transcription Factor Stb5 CausesAntimicrobial agents and chemotherapy · 2018Article
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8 authors at 2 institutions in 3 countries.
Funding
Abstract
The pathogenic yeast Candida albicans can develop resistance to the widely used antifungal agent fluconazole, which inhibits ergosterol biosynthesis, by the overexpression of genes encoding multidrug efflux pumps or ergosterol biosynthesis enzymes. Zinc cluster transcription factors play a central role in the transcriptional regulation of drug resistance. Mrr1 regulates the expression of the major facilitator MDR1, Tac1 controls the expression of the ABC transporters CDR1 and CDR2, and Upc2 regulates ergosterol biosynthesis (ERG) genes. Gain-of-function mutations in these transcription factors result in constitutive overexpression of their target genes and are responsible for fluconazole resistance in many clinical C. albicans isolates. The transcription factor Ndt80 contributes to the drug-induced upregulation of CDR1 and ERG genes and also binds to the MDR1 and CDR2 promoters, suggesting that it is an important component of all major transcriptional mechanisms of fluconazole resistance. However, we found that Ndt80 is not required for the induction of MDR1 and CDR2 expression by inducing chemicals. CDR2 was even partially derepressed in ndt80Δ mutants, indicating that Ndt80 is a repressor of CDR2 expression. Hyperactive forms of Mrr1, Tac1, and Upc2 promoted overexpression of MDR1, CDR1/CDR2, and ERG11, respectively, with the same efficiency in the presence and absence of Ndt80. Mrr1- and Tac1-mediated fluconazole resistance was even slightly enhanced in ndt80Δ mutants compared to wild-type cells. These results demonstrate that Ndt80 is dispensable for the constitutive overexpression of Mrr1, Tac1, and Upc2 target genes and the increased fluconazole resistance of strains that have acquired activating mutations in these transcription factors.
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