ArticleNature microbiology2024
Most azole resistance mutations in the Candida albicans drug target confer cross-resistance without intrinsic fitness cost.
Article in Nature microbiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed.
- Phylogenetic and Structural Analysis of Miconazole Susceptibility in Malassezia pachydermatis Isolates From Dogs With Otitis Externa.Veterinary dermatology · 2026Article
- The shape of fitness functions and the distribution of mutational effect sizes jointly limit adaptation by regulatory mutations.Nature ecology & evolution · 2026Article
- Integrative computational-experimental discovery of α-hederin as a multi-mechanistic, low-toxicity antifungal agent targeting Candida albicans CYP51.Journal of advanced research · 2026Article
- Generation of antifungals to combat drug resistance using language models and diffusion models.Journal of advanced research · 2026Article
- CYP51C Y319H and H349R substitutions cannot confer azole resistance inMicrobiology spectrum · 2026Article
- Micafungin exposure drives multidrug resistance inbioRxiv : the preprint server for biology · 2026Article
- Predicting antifolate resistance in the unculturable fungal pathogen Pneumocystis jirovecii.PLoS genetics · 2026Article
- Machine learning identifies novel signatures of antifungal drug resistance in Saccharomycotina yeasts.PLoS genetics · 2026Article
- Genetic variation and mutational determinants of azole resistance in Candida albicans strains of oropharyngeal colonization in HIV patients and bloodstream infections.Journal of biomedical science · 2026Article
- A cost-effective and scalable barcoded library construction method for deep mutational scanning studies.PLoS biology · 2026Article
- Article
- Analysis of the genome of a Pseudomonas monsensis isolate that produces the antifungal dipeptide maculosin.Access microbiology · 2026Article
- Decoding resistance inFrontiers in cellular and infection microbiology · 2026Article
- Clinical characteristics and etiological analysis of deep fungal infections in a general hospital in Southwest China (2020-2024).Frontiers in public health · 2026Article
- Emerging antifungal resistance in Candida parapsilosis: the end of the innocence.npj antimicrobials and resistance · 2025Review
- Antifungal treatment strategies and their impact on resistance development in clinical settings.The Journal of antimicrobial chemotherapy · 2025Review
- EnhancedDrug delivery · 2025Article
- Targeted loss of heterozygosity in Candida albicans using CRISPR-Cas9 reveals the functional impact of allelic variation.Genetics · 2025Article
- Osh2 mediatesAntimicrobial agents and chemotherapy · 2025Article
- FungAMR: a comprehensive database for investigating fungal mutations associated with antimicrobial resistance.Nature microbiology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Azole antifungals are the main drugs used to treat fungal infections. Amino acid substitutions in the drug target Erg11 (Cyp51) are a common resistance mechanism in pathogenic yeasts. How many and which mutations confer resistance is, however, largely unknown. Here we measure the impact of nearly 4,000 amino acid variants of Candida albicans Erg11 on the susceptibility to six clinical azoles. This was achieved by deep mutational scanning of CaErg11 expressed in Saccharomyces cerevisiae. We find that a large fraction of mutations lead to resistance (33%), most resistance mutations confer cross-resistance (88%) and only a handful of resistance mutations show a significant fitness cost (9%). Our results reveal that resistance to azoles can arise through a large set of mutations and this will probably lead to azole pan-resistance, with little evolutionary compromise. This resource will help inform treatment choices in clinical settings and guide the development of new drugs.
Indexed as
Identifiers
39379635What 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.