ArticleEukaryotic cell2007
cis-Acting elements within the Candida albicans ERG11 promoter mediate the azole response through transcription factor Upc2p.
Article in Eukaryotic cell, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 52 citations in OpenAlex.
- Advances in vulvovaginal candidiasis research: a comprehensive review from epidemiology, diagnosis, treatment to resistance mechanisms.Frontiers in microbiology · 2026Review
- K143R Amino Acid Substitution in 14-α-Demethylase (Erg11p) Changes Plasma Membrane and Cell Wall Structure ofInternational journal of molecular sciences · 2022Article
- The role of non-standard translation in Candida albicans pathogenesis.FEMS yeast research · 2021Review
- Molecular and genetic basis of azole antifungal resistance in the opportunistic pathogenic fungus Candida albicans.The Journal of antimicrobial chemotherapy · 2020Review
- Review
- A Crucial Role for Ergosterol in Plasma Membrane Composition, Localisation, and Activity of Cdr1p and HMicroorganisms · 2019Article
- Loss of Upc2p-InduciblemBio · 2018Article
- The Role of UPC2 Gene in Azole-Resistant Candida tropicalis.Mycopathologia · 2016Article
- Stepwise emergence of azole, echinocandin and amphotericin B multidrug resistance in vivo in Candida albicans orchestrated by multiple genetic alterations.The Journal of antimicrobial chemotherapy · 2015Article
- Transcription factor ADS-4 regulates adaptive responses and resistance to antifungal azole stress.Antimicrobial agents and chemotherapy · 2015Article
- Article
- Ascorbic acid inhibition of Candida albicans Hsp90-mediated morphogenesis occurs via the transcriptional regulator Upc2.Eukaryotic cell · 2014Article
- UPC2A is required for high-level azole antifungal resistance in Candida glabrata.Antimicrobial agents and chemotherapy · 2014Article
- UPC2 is universally essential for azole antifungal resistance in Candida albicans.Eukaryotic cell · 2014Article
- Improvement of experimental testing and network training conditions with genome-wide microarrays for more accurate predictions of drug gene targets.BMC systems biology · 2014Article
- Novel antifungal drug discovery based on targeting pathways regulating the fungus-conserved Upc2 transcription factor.Antimicrobial agents and chemotherapy · 2014Article
- Antifungal resistance and new strategies to control fungal infections.International journal of microbiology · 2012Article
- Using RNA-seq to determine the transcriptional landscape and the hypoxic response of the pathogenic yeast Candida parapsilosis.BMC genomics · 2011Article
- Regulatory circuitry governing fungal development, drug resistance, and disease.Microbiology and molecular biology reviews : MMBR · 2011Review
- Regulation of the hypoxic response in Candida albicans.Eukaryotic cell · 2010Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The azole antifungal drugs are used to treat infections caused by Candida albicans and other fungi. These drugs interfere with the biosynthesis of ergosterol, the major sterol in fungal cells, by inhibiting an ergosterol biosynthetic enzyme, lanosterol 14 alpha-demethylase, encoded by the ERG11 gene. In vitro, these drugs as well as other ergosterol biosynthesis inhibitors increase ERG11 mRNA expression by activation of the ERG11 promoter. The signal for this activation most likely is the depletion of ergosterol, the end product of the pathway. To identify cis-acting regulatory elements that mediate this activation, ERG11 promoter fragments have been fused to the luciferase reporter gene from Renilla reniformis. Promoter deletions and linker scan mutations localized the region important for azole induction to a segment from bp -224 to -251 upstream of the start codon, specifically two 7-bp sequences separated by 13 bp. These sequences form an imperfect inverted repeat. The region is recognized by the transcription factor Upc2p and functions as an enhancer of transcription, as it can be placed upstream of a heterologous promoter in either direction, resulting in the azole induction of that promoter. The promoter constructs are not azole inducible in the upc2/upc2 homozygous deletion, demonstrating that Upc2p controls the azole induction of ERG11. These results identify an azole-responsive enhancer element (ARE) in the ERG11 promoter that is controlled by the Upc2p transcription factor. No other ARE is present in the promoter. Thus, this ARE and Upc2p are necessary and sufficient for azole induction of ERG11.
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