Prevalent mutator genotype identified in fungal pathogen Candida glabrata promotes multi-drug resistance.
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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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Among the more common Candida spp., C. glabrata probably poses the greatest risk with regard to the development of antifungal resistance, and this may be attributed to the prevalent mutator genotype promoting multi-drug resistance phenotypes.
“Among the more common Candida spp, C. glabrata probably poses the greatest risk with regard to the development of antifungal resistance and this may be attributed to the prevalent mutator genotype promoting multi-drug resistance phenotypes.110”
From Epidemiology of Invasive Candidiasis (2024) · cites this paper as [110]
Mutations in MSH2, a mismatch repair gene, can influence the capacity to acquire resistance to drugs.
“Additionally, it has been suggested that mutations in MSH2, a mismatch repair gene, can influence the capacity to acquire resistance to drugs (Healey et al., 2016).”
From Genome Comparisons of Candida glabrata Serial Clinical Isolates Reveal Patterns of Genetic Variation in Infecting Clonal Populations (2019) · cites this paper as Healey et al., 2016
Hypermutator phenotypes resulting from mutations in the DNA mismatch repair gene MSH2 have been suggested to enable fast adaptation to drugs in Cryptococcus neoformans and C. glabrata.
“Similarly, hypermutator phenotypes resulting from mutations in the DNA mismatch repair gene MSH2, have been suggested to enable fast adaptation to drugs in Cryptococcus neoformans and C. glabrata [134,135].”
From Evolutionary Emergence of Drug Resistance in Candida Opportunistic Pathogens (2018) · cites this paper as [135]
Specific mutations in the DNA mismatch repair gene MSH2 lead to a hyper-mutable phenotype and were found to be highly prevalent in clinical C. glabrata isolates.
“Specific mutations in the DNA mismatch repair gene MSH2 lead to a hyper-mutable phenotype and were found to be highly prevalent in clinical C. glabrata isolates [67].”
From Treatment of Invasive Candidiasis: A Narrative Review (2018) · cites this paper as [67]
MSH2 deletion significantly increases breakthrough infection and the emergence of resistance to all systemic antifungal drug classes in in vitro and animal experimental systems.
“MSH2 deletion significantly increases breakthrough infection and the emergence of resistance to all systemic antifungal drug classes in in vitro and animal experimental systems [67].”
From Treatment of Invasive Candidiasis: A Narrative Review (2018) · cites this paper as [67]
Analysis of serial clinical isolates demonstrated that msh2 mutations pre-date the emergence of antifungal resistance.
“analysis of serial clinical isolates demonstrated that msh2 mutations pre-date the emergence of antifungal resistance”
From Genetic Drivers of Multidrug Resistance in Candida glabrata (2016) · cites this paper as Healey et al., 2016
Deletion of MSH2 causes elevated propensity to breakthrough antifungal treatment in a mouse model of gastrointestinal colonization.
“deletion of MSH2 causes elevated propensity to breakthrough antifungal treatment in a mouse model of gastrointestinal (GI) colonization”
From Genetic Drivers of Multidrug Resistance in Candida glabrata (2016) · cites this paper as Healey et al., 2016
Complete loss of MMR function (msh2Δ) impacts fitness of C. glabrata in the host.
“we have demonstrated that complete loss of MMR function (msh2Δ) impacts fitness of C. glabrata in the host”
From Genetic Drivers of Multidrug Resistance in Candida glabrata (2016) · cites this paper as Healey et al., 2016
Strains with specific msh2 mutations exhibit a higher frequency of emergence of resistance in vitro.
“Strains with specific msh2 mutations exhibit a higher frequency of emergence of resistance in vitro”
From Genetic Drivers of Multidrug Resistance in Candida glabrata (2016) · cites this paper as Healey et al., 2016
msh2 mutation is a driver of the acquisition of antifungal resistance in C. glabrata.
“Our study suggests that msh2 mutation is a driver of the acquisition of antifungal resistance in C. glabrata.”
From Genetic Drivers of Multidrug Resistance in Candida glabrata (2016) · cites this paper as Healey et al., 2016
Over half (55%) of all C. glabrata isolates, susceptible and resistant, recovered from patients contain mutations within the MMR gene MSH2.
“We discovered that over half (55%) of all C. glabrata isolates (susceptible and resistant) recovered from patients contain mutations within the MMR gene MSH2.”
From Genetic Drivers of Multidrug Resistance in Candida glabrata (2016) · cites this paper as Healey et al., 2016
55% of clinical isolates of the fungus Candida glabrata contain a mutation in MSH2.
“In addition, 55% of clinical isolates of the fungus Candida glabrata contain a mutation in MSH2 (21).”
From Mismatch Repair of DNA Replication Errors Contributes to Microevolution in the Pathogenic Fungus <i>Cryptococcus neoformans</i> (2017) · cites this paper as [21]
Fifty-five percent of C. glabrata clinical isolates recovered from patients are msh2 mutants.
“Fifty-five percent of C. glabrata clinical isolates recovered from patients are msh2 mutants (other components of the MMR pathway were not sequenced) (21).”
From Mismatch Repair of DNA Replication Errors Contributes to Microevolution in the Pathogenic Fungus <i>Cryptococcus neoformans</i> (2017) · cites this paper as [21]
A comparison of paired or triplet isolates from the same patient showed that the MSH2 mutation predated the emergence of fluconazole resistance.
“In addition, a comparison of paired or triplet isolates from the same patient showed that the MSH2 mutation predated the emergence of fluconazole resistance (21).”
From Mismatch Repair of DNA Replication Errors Contributes to Microevolution in the Pathogenic Fungus <i>Cryptococcus neoformans</i> (2017) · cites this paper as [21]
Equivalent levels of mice colonization and infection were observed between the wild type and the msh2Δ mutant in a standard C. glabrata virulence assay.
“Similarly to C. neoformans, equivalent levels of mice colonization and infection were also observed between the wild type and the msh2Δ mutant in a standard C. glabrata virulence assay (21).”
From Mismatch Repair of DNA Replication Errors Contributes to Microevolution in the Pathogenic Fungus <i>Cryptococcus neoformans</i> (2017) · cites this paper as [21]
MSH2 mutations are present in a higher percentage in fluconazole-resistant clinical isolates than in susceptible strains in C. glabrata.
“MSH2 mutations are present in a higher percentage in fluconazole-resistant clinical isolates than in susceptible strains in C. glabrata (21).”
From Mismatch Repair of DNA Replication Errors Contributes to Microevolution in the Pathogenic Fungus <i>Cryptococcus neoformans</i> (2017) · cites this paper as [21]
Deletions of MSH2 in C. glabrata result in high levels of spontaneous antifungal resistance in vitro, in addition to an increase in the occurrence of resistance to caspofungin arising during in vivo growth.
“Deletions of MSH2 in C. glabrata also result in high levels of spontaneous antifungal resistance in vitro, in addition to an increase in the occurrence of resistance to caspofungin arising during in vivo growth (21).”
From Mismatch Repair of DNA Replication Errors Contributes to Microevolution in the Pathogenic Fungus <i>Cryptococcus neoformans</i> (2017) · cites this paper as [21]
The genetic mechanism involved in this process supports the acquisition of resistance to multiple antifungals, partially explaining the higher rates of triazole and multidrug resistance associated with C. glabrata.
“The genetic mechanism involved in this process supports the acquisition of resistance to multiple antifungals, partially explaining the higher rates of triazole and multidrug resistance associated with C. glabrata [201].”
From Candida glabrata Biofilms: How Far Have We Come? (2017) · cites this paper as [201]
Healey and colleagues showed a mutator phenotype caused by a mismatch repair defect that is prevalent in C. glabrata clinical isolates.
“Recently, Healey and colleagues [201] showed a mutator phenotype caused by a mismatch repair defect which is prevalent in C. glabrata clinical isolates.”
From Candida glabrata Biofilms: How Far Have We Come? (2017) · cites this paper as [201]
55% of all C. glabrata recovered from patients have these genetic characteristics.
“Also, the authors found that 55% of all C. glabrata that are recovered from patients have these genetic characteristics, which is clinically very concerning.”
From Candida glabrata Biofilms: How Far Have We Come? (2017) · cites this paper as [201]
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- Authors
- Healey, K. R., Zhao, Y., Perez, W. B., Lockhart, S. R., Sobel, J. D., Farmakiotis, D., Kontoyiannis, D. P., Sanglard, D., Taj-Aldeen, S. J., Alexander, B. D., Jimenez-Ortigosa, C., Shor, E., & Perlin, D. S.
- Affiliations
- Rutgers Health (US)
- Centers for Disease Control and Prevention (US)
- Wayne State University (US)
- The University of Texas MD Anderson Cancer Center (US)
- Centre Hospitalier Universitaire Vaudois (CH)
- Duke University (US)
- Corresponding author
- Perlin, David S.
- ORCID
- Venue
- Nature Communications
- Published
- 2016-03-29
- Volume
- 7
- Issue
- 1
- Pages
- 11128-11128
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC5603725
- OpenAlex
- W2314754341
- Cited by
- 276
- References
- 35
- Citations by year
- 2026: 12 · 2025: 21 · 2024: 27 · 2023: 18 · 2022: 29 · 2021: 26 · 2020: 23 · 2019: 36 · 2018: 33 · 2017: 38 · 2016: 13
- FWCI
- 36.94
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- IRIS (submittedVersion, cc-by)
- RePEc: Research Papers in Economics (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- SERVAL (Université de Lausanne) (submittedVersion, other-oa)
- Funders
- Arnold and Mabel Beckman Foundation
- National Institutes of Health (2r01ai109025-11, AI109025)
- National Institute of Allergy and Infectious Diseases (AI109025, R01AI-109025)
- Topics
- Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
- Life Sciences › Agricultural and Biological Sciences › Ecology, Evolution, Behavior and Systematics › Fungal Plant Pathogen Control
- Keywords
- Candida glabrata, mutator phenotype, DNA mismatch repair, MSH2, multidrug resistance, antifungal resistance, triazole resistance, echinocandin resistance, clinical isolates, fungal pathogens
- MeSH terms
- Animals, Antifungal Agents, Candidiasis, Disease Models, Animal, Genes, Fungal, Genotype, Humans, Kidney, Mutation, Phenotype, Colony Count, Microbial, Gene Deletion, Drug Resistance, Multiple, Drug Resistance, Fungal, Candida glabrata, Mice, Echinocandins
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