ArticlePLoS pathogens2014
Systematic phenotyping of a large-scale Candida glabrata deletion collection reveals novel antifungal tolerance genes.
Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers.
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Who cites it
118 citing papers in PubMed, 190 citations in OpenAlex.
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- Candida auris skin tropism and antifungal resistance are mediated by carbonic anhydrase Nce103.Nature microbiology · 2026Article
- Leveraging synthetic genetic array screening to identify therapeutic targets and inhibitors for combatting azole resistance inMicrobiology spectrum · 2025Article
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- Induction of Antifungal Tolerance Reveals Genetic and Phenotypic Changes inJournal of fungi (Basel, Switzerland) · 2025Article
- The stress-protectant molecule trehalose mediates fluconazole tolerance inAntimicrobial agents and chemotherapy · 2025Article
- Antifungal drug resistance in Candida glabrata: role of cellular signaling and gene regulatory networks.FEMS yeast research · 2025Review
- The transcription factor CgHaa1 plays a role in virulence of the pathogenic yeast Candida glabrata.FEMS yeast research · 2025Article
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- Transposon-sequencing (Tn-seq) of the Candida glabrata reference strain CBS138 reveals epigenetic plasticity, structural variation, and intrinsic mechanisms of resistance to micafungin.G3 (Bethesda, Md.) · 2024Article
- Systematic analysis of themBio · 2024Article
- Lysosomal diacylglycerol pyrophosphate phosphatase is not essential in Trypanosoma brucei.Molecular biology reports · 2024Article
- Improving homology-directed repair by small molecule agents for genetic engineering in unconventional yeast?-Learning from the engineering of mammalian systems.Microbial biotechnology · 2024Review
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- An expanded toolkit of drug resistance cassettes formSphere · 2023Article
58 more citing papers are in PubMed but not listed here.
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Authors and funding
28 authors at 14 institutions in 6 countries.
Funding
Abstract
The opportunistic fungal pathogen Candida glabrata is a frequent cause of candidiasis, causing infections ranging from superficial to life-threatening disseminated disease. The inherent tolerance of C. glabrata to azole drugs makes this pathogen a serious clinical threat. To identify novel genes implicated in antifungal drug tolerance, we have constructed a large-scale C. glabrata deletion library consisting of 619 unique, individually bar-coded mutant strains, each lacking one specific gene, all together representing almost 12% of the genome. Functional analysis of this library in a series of phenotypic and fitness assays identified numerous genes required for growth of C. glabrata under normal or specific stress conditions, as well as a number of novel genes involved in tolerance to clinically important antifungal drugs such as azoles and echinocandins. We identified 38 deletion strains displaying strongly increased susceptibility to caspofungin, 28 of which encoding proteins that have not previously been linked to echinocandin tolerance. Our results demonstrate the potential of the C. glabrata mutant collection as a valuable resource in functional genomics studies of this important fungal pathogen of humans, and to facilitate the identification of putative novel antifungal drug target and virulence genes.
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