ArticleNature communications2016
Prevalent mutator genotype identified in fungal pathogen Candida glabrata promotes multi-drug resistance.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 170 papers, 1 of them a synthesis that pooled it.
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Who cites it
170 citing papers in PubMed, 1 synthesis or guideline pooled it, 273 citations in OpenAlex.
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- From Oral Candidiasis to Candidemia: A Review of Superficial to Invasive Progression.MicrobiologyOpen · 2026Review
- Insights on molecular drivers of phenotypic plasticity in Candidozyma auris.World journal of microbiology & biotechnology · 2026Review
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- Suppressed Protein Translation Caused by MSP-8 Deficiency Determines Fungal Multidrug Resistance with Fitness Cost.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Antifungal drug resistance in Candida glabrata: role of cellular signaling and gene regulatory networks.FEMS yeast research · 2025Review
- Comprehensive analysis of the mechanisms conferring resistance to phenamacril in theFrontiers in cellular and infection microbiology · 2025Review
- Article
110 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 8 institutions in 3 countries.
Funding
Abstract
The fungal pathogen Candida glabrata has emerged as a major health threat since it readily acquires resistance to multiple drug classes, including triazoles and/or echinocandins. Thus far, cellular mechanisms promoting the emergence of resistance to multiple drug classes have not been described in this organism. Here we demonstrate that a mutator phenotype caused by a mismatch repair defect is prevalent in C. glabrata clinical isolates. Strains carrying alterations in mismatch repair gene MSH2 exhibit a higher propensity to breakthrough antifungal treatment in vitro and in mouse models of colonization, and are recovered at a high rate (55% of all C. glabrata recovered) from patients. This genetic mechanism promotes the acquisition of resistance to multiple antifungals, at least partially explaining the elevated rates of triazole and multi-drug resistance associated with C. glabrata. We anticipate that identifying MSH2 defects in infecting strains may influence the management of patients on antifungal drug therapy.
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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.