ArticleJournal of bacteriology1999
Specific chromosome alterations in fluconazole-resistant mutants of Candida albicans.
Article in Journal of bacteriology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
What it found
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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.
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Who cites it
72 citing papers in PubMed, 142 citations in OpenAlex.
- Fungal DNA damage repair: from model to driver of virulence and AMR.Bioscience reports · 2026Review
- Aneuploidy promotes transient stress adaptation and metabolic flexibility in the human fungal pathogen Aspergillus fumigatus.Current biology : CB · 2026Article
- Whole-chromosome duplications drive antimicrobial resistance inbioRxiv : the preprint server for biology · 2025Article
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- The role of gene copy number variation in antimicrobial resistance in human fungal pathogens.npj antimicrobials and resistance · 2025Review
- Hsp90-Mediated Multi-Drug Resistance in DNA Polymerase-Defective Strains ofJournal of fungi (Basel, Switzerland) · 2024Article
- Long-term stability of acquired drug resistance and resistance associated mutations in the fungal pathogenFrontiers in cellular and infection microbiology · 2024Article
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- Review
- Selection of Ethanol Tolerant Strains ofbioRxiv : the preprint server for biology · 2023Article
- Post-transcriptional control of antifungal resistance in human fungal pathogens.Critical reviews in microbiology · 2023Review
- Review
- Acquisition of cross-azole tolerance and aneuploidy in Candida albicans strains evolved to posaconazole.G3 (Bethesda, Md.) · 2022Article
- Article
- Systematic truncations of chromosome 4 and their responses to antifungals in Candida albicans.Journal, genetic engineering & biotechnology · 2021Article
- The role of aneuploidy in the emergence of echinocandin resistance in human fungal pathogen Candida albicans.PLoS pathogens · 2021Article
- Article
- Review
- Host-Induced Genome Instability Rapidly Generates Phenotypic Variation across Candida albicans Strains and Ploidy States.mSphere · 2020Article
- Molecular and genetic basis of azole antifungal resistance in the opportunistic pathogenic fungus Candida albicans.The Journal of antimicrobial chemotherapy · 2020Review
12 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
The exposure of Candida albicans to fluconazole resulted in the nondisjunction of two specific chromosomes in 17 drug-resistant mutants, each obtained by an independent mutational event. The chromosomal changes occurred at high frequencies and were related to the duration of the drug exposure. The loss of one homologue of chromosome 4 occurred after incubation on a fluconazole medium for 7 days. A second change, the gain of one copy of chromosome 3, was observed after exposure for 35 or 40 days. We found that the mRNA levels of ERG11, CDR1, CDR2, and MDR1, the candidate fluconazole resistance genes, remained either the same or were diminished. The lack of overexpression of putative drug pumps or the drug target indicated that some other mechanism(s) may be operating. The fluconazole resistance phenotype, electrophoretic karyotypes, and transcript levels of mutants were stable after growth for 112 generations in the absence of fluconazole. This is the first report to demonstrate that resistance to fluconazole can be dependent on chromosomal nondisjunction. Furthermore, we suggest that a low-level resistance to fluconazole arising during the early stages of clinical treatment may occur by this mechanism. These results support our earlier hypothesis that changes in C. albicans chromosome number is a common means to control a resource of potentially beneficial genes that are related to important cellular functions.
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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.