ArticleMicrobiology (Reading, England)2017
A chromosome 4 trisomy contributes to increased fluconazole resistance in a clinical isolate of Candida albicans.
Article in Microbiology (Reading, England), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 58 citations in OpenAlex.
- Blood Cultures Contain Populations of Genetically Diverse Candida albicans Strains that May Differ in Echinocandin Tolerance and Fitness.The Journal of infectious diseases · 2026Article
- Parasex generates highly recombinant progeny in Candida albicans with increased virulence.Nature microbiology · 2026Article
- Strain background interacts with chromosome 7 aneuploidy to determine commensal and virulence phenotypes in Candida albicans.PLoS genetics · 2025Article
- Aneuploidy confers a unique transcriptional and phenotypic profile to Candida albicans.Nature communications · 2025Article
- The early transcriptional and post-transcriptional responses to fluconazole in sensitive and resistant Candida albicans.Scientific reports · 2024Article
- Candida albicans' inorganic phosphate transport and evolutionary adaptation to phosphate scarcity.PLoS genetics · 2024Article
- Review
- Article
- Strain background ofMicrobiology (Reading, England) · 2024Article
- Behind the scenes: Centromere-driven genomic innovations in fungal pathogens.PLoS pathogens · 2024Article
- Article
- Genomic epidemiology of antifungal resistance in human and avian isolates ofFrontiers in veterinary science · 2024Article
- Long-term stability of acquired drug resistance and resistance associated mutations in the fungal pathogenFrontiers in cellular and infection microbiology · 2024Article
- The Microevolution of Antifungal Drug Resistance in Pathogenic Fungi.Microorganisms · 2023Review
- Aneuploidy Formation in the Filamentous Fungus Aspergillus flavus in Response to Azole Stress.Microbiology spectrum · 2023Article
- Aneuploidy and gene dosage regulate filamentation and host colonization byProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Development and applications of a CRISPR activation system for facile genetic overexpression in Candida albicans.G3 (Bethesda, Md.) · 2023Article
- Stress combined with loss of the Candida albicans SUMO protease Ulp2 triggers selection of aneuploidy via a two-step process.PLoS genetics · 2022Article
- Karyon: a computational framework for the diagnosis of hybrids, aneuploids, and other nonstandard architectures in genome assemblies.GigaScience · 2022Article
- Acquisition of cross-azole tolerance and aneuploidy in Candida albicans strains evolved to posaconazole.G3 (Bethesda, Md.) · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Candida albicans is an important opportunistic fungal pathogen capable of causing both mucosal and disseminated disease. Infections are often treated with fluconazole, a front-line antifungal drug that targets the biosynthesis of ergosterol, a major component of the fungal cell membrane. Resistance to fluconazole can arise through a variety of mechanisms, including gain-of-function mutations, loss of heterozygosity events and aneuploidy. The clinical isolate P60002 was found to be highly resistant to azole-class drugs, yet lacked mutations or chromosomal rearrangements known to be associated with azole resistance. Transcription profiling suggested that increased expression of two putative drug efflux pumps, CDR11 and QDR1, might confer azole resistance. However, ectopic expression of the P60002 alleles of these genes in a drug-susceptible strain did not increase fluconazole resistance. We next examined whether the presence of three copies of chromosome 4 (Chr4) or chromosome 6 (Chr6) contributed to azole resistance in P60002. We established that Chr4 trisomy contributes significantly to fluconazole resistance, whereas Chr6 trisomy has no discernible effect on resistance. In contrast, a Chr4 trisomy did not increase fluconazole resistance when present in the standard SC5314 strain background. These results establish a link between Chr4 trisomy and elevated fluconazole resistance, and demonstrate the impact of genetic background on drug resistance phenotypes in C. albicans.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.