Evidence map›Paper›PMID 34699784›Full record

ArticleCurrent biology : CB2021

Narrow mutational signatures drive acquisition of multidrug resistance in the fungal pathogen Candida glabrata.

Ewa Ksiezopolska, Miquel Àngel Schikora-Tamarit, Reinhard Beyer, Juan Carlos Nunez-Rodriguez, Christoph Schüller, Toni Gabaldón

Open access · bronzeAbstract read
In one paragraph

Article in Current biology : CB, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
5.5field-weighted citation impact, top 3% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

63 citing papers in PubMed, 110 citations in OpenAlex.

  1. Article
  2. Micafungin exposure drives multidrug resistance inbioRxiv : the preprint server for biology · 2026
    Article
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  5. Journal of medical microbiology · 2026
    Review
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  14. Tn-seq screens inmSphere · 2025
    Article
  15. Article
  16. International journal of molecular sciences · 2025
    Article
  17. Article
  18. Article
  19. Article
  20. Article

3 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Ewa KsiezopolskaBarcelona Supercomputing Centre (BSC-CNS), Life Sciences Department, Jordi Girona 29, 08034 Barcelona, Spain; Institute for Research in Biomedicine (IRB Barcelona), Mechanisms of Disease Program, The Barcelona Institute of Science and Technology, Baldiri Reixac 10, 08028 Barcelona, Spain.
Miquel Àngel Schikora-TamaritBarcelona Supercomputing Centre (BSC-CNS), Life Sciences Department, Jordi Girona 29, 08034 Barcelona, Spain; Institute for Research in Biomedicine (IRB Barcelona), Mechanisms of Disease Program, The Barcelona Institute of Science and Technology, Baldiri Reixac 10, 08028 Barcelona, Spain.
Reinhard BeyerInstitute of Microbial Genetics and Core Facility Bioactive Substances: Screening and Analysis, University of Natural Resources and Life Sciences, Vienna (BOKU), Konrad Lorenz Strasse 24, 3430 Tulln an der Donau, Austria.
Juan Carlos Nunez-RodriguezBarcelona Supercomputing Centre (BSC-CNS), Life Sciences Department, Jordi Girona 29, 08034 Barcelona, Spain; Institute for Research in Biomedicine (IRB Barcelona), Mechanisms of Disease Program, The Barcelona Institute of Science and Technology, Baldiri Reixac 10, 08028 Barcelona, Spain.
Christoph SchüllerInstitute of Microbial Genetics and Core Facility Bioactive Substances: Screening and Analysis, University of Natural Resources and Life Sciences, Vienna (BOKU), Konrad Lorenz Strasse 24, 3430 Tulln an der Donau, Austria.
Toni GabaldónBarcelona Supercomputing Centre (BSC-CNS), Life Sciences Department, Jordi Girona 29, 08034 Barcelona, Spain; Institute for Research in Biomedicine (IRB Barcelona), Mechanisms of Disease Program, The Barcelona Institute of Science and Technology, Baldiri Reixac 10, 08028 Barcelona, Spain; Catalan Institution for Research and Advanced Studies (ICREA), Passeig Lluis Companys 23, 08010 Barcelona, Spain. Electronic address: toni.gabaldon@bsc.es.
Barcelona Supercomputing Center · ESBOKU University · ATInstitució Catalana de Recerca i Estudis Avançats · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fungal infections are a growing medical concern, in part due to increased resistance to one or multiple antifungal drugs. However, the evolutionary processes underpinning the acquisition of antifungal drug resistance are poorly understood. Here, we used experimental microevolution to study the adaptation of the yeast pathogen Candida glabrata to fluconazole and anidulafungin, two widely used antifungal drugs with different modes of action. Our results show widespread ability of rapid adaptation to one or both drugs. Resistance, including multidrug resistance, is often acquired at moderate fitness costs and mediated by mutations in a limited set of genes that are recurrently and specifically mutated in strains adapted to each of the drugs. Importantly, we uncover a dual role of ERG3 mutations in resistance to anidulafungin and cross-resistance to fluconazole in a subset of anidulafungin-adapted strains. Our results shed light on the mutational paths leading to resistance and cross-resistance to antifungal drugs.

Indexed as

Candida glabrataFluconazoleAnidulafunginAntifungal AgentsDrug Resistance, FungalDrug Resistance, MultipleMicrobial Sensitivity TestsMutationAnidulafunginAntifungal AgentsFluconazoleantifungalCandida glabratacross-resistancedrug resistanceexperimental evolutionmultidrug resistance

Identifiers

PMID34699784
PMCPMC8660101
OpenAlexW3209188300

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.