ArticleEukaryotic cell2011
Functional dissection of a Candida albicans zinc cluster transcription factor, the multidrug resistance regulator Mrr1.
Article in Eukaryotic cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 38 citations in OpenAlex.
- Advances in vulvovaginal candidiasis research: a comprehensive review from epidemiology, diagnosis, treatment to resistance mechanisms.Frontiers in microbiology · 2026Review
- Article
- Regulatory insight for a Zn2Cys6 transcription factor controlling effector-mediated virulence in a fungal pathogen of wheat.PLoS pathogens · 2024Article
- Transcriptional Response of Candida auris to the Mrr1 Inducers Methylglyoxal and Benomyl.mSphere · 2022Article
- Transcriptomic Analysis of Resistant and Wild-Type Isolates Revealed Fludioxonil as a Candidate for Controlling the Emerging Isoprothiolane Resistant Populations ofFrontiers in microbiology · 2022Article
- Participation of the ABC TransporterJournal of fungi (Basel, Switzerland) · 2021Article
- Balancing Positive and Negative Selection:mBio · 2021Article
- Molecular and genetic basis of azole antifungal resistance in the opportunistic pathogenic fungus Candida albicans.The Journal of antimicrobial chemotherapy · 2020Review
- Review
- Research of Mrr1, Cap1 and MDR1 inExperimental and therapeutic medicine · 2018Article
- A Putative ZnFrontiers in microbiology · 2018Article
- Candida albicans Swi/Snf and Mediator Complexes Differentially Regulate Mrr1-InducedAntimicrobial agents and chemotherapy · 2017Article
- Quinone derivatives isolated from the endolichenic fungus Phialocephala fortinii are Mdr1 modulators that combat azole resistance in Candida albicans.Scientific reports · 2016Article
- Article
- Induction of Candida albicans drug resistance genes by hybrid zinc cluster transcription factors.Antimicrobial agents and chemotherapy · 2015Article
- Disruption of the transcriptional regulator Cas5 results in enhanced killing of Candida albicans by Fluconazole.Antimicrobial agents and chemotherapy · 2014Article
- SAGA/ADA complex subunit Ada2 is required for Cap1- but not Mrr1-mediated upregulation of the Candida albicans multidrug efflux pump MDR1.Antimicrobial agents and chemotherapy · 2014Article
- UPC2 is universally essential for azole antifungal resistance in Candida albicans.Eukaryotic cell · 2014Article
- Multidrug resistance in fungi: regulation of transporter-encoding gene expression.Frontiers in physiology · 2014Review
- Inducible and constitutive activation of two polymorphic promoter alleles of the Candida albicans multidrug efflux pump MDR1.Antimicrobial agents and chemotherapy · 2012Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
The overexpression of the MDR1 gene, which encodes a multidrug efflux pump of the major facilitator superfamily, is a frequent cause of resistance to the widely used antimycotic agent fluconazole and other toxic compounds in the pathogenic yeast Candida albicans. The zinc cluster transcription factor Mrr1 controls MDR1 expression in response to inducing chemicals, and gain-of-function mutations in MRR1 are responsible for the constitutive MDR1 upregulation in fluconazole-resistant C. albicans strains. To understand how Mrr1 activity is regulated, we identified functional domains of this transcription factor. A hybrid protein consisting of the N-terminal 106 amino acids of Mrr1 and the transcriptional activation domain of Gal4 from Saccharomyces cerevisiae constitutively induced MDR1 expression, demonstrating that the DNA binding domain is sufficient to target Mrr1 to the MDR1 promoter. Using a series of C-terminal truncations and systematic internal deletions, we could show that Mrr1 contains multiple activation and inhibitory domains. One activation domain (AD1) is located in the C terminus of Mrr1. When fused to the tetracycline repressor TetR, this distal activation domain induced gene expression from a TetR-dependent promoter. The deletion of an inhibitory region (ID1) located near the distal activation domain resulted in constitutive activity of Mrr1. The additional removal of AD1 abolished the constitutive activity, but the truncated Mrr1 still could activate the MDR1 promoter in response to the inducer benomyl. These results demonstrate that the activity of Mrr1 is regulated in multiple ways and provide insights into the function of an important mediator of drug resistance in C. albicans.
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