ArticleCommunications biology2022
Genomic evolution towards azole resistance in Candida glabrata clinical isolates unveils the importance of CgHxt4/6/7 in azole accumulation.
Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 8 citations in OpenAlex.
- Alkylamidobetaines Induced Changes in Multidrug-Resistant, BiofilmingInternational journal of molecular sciences · 2026Article
- Recent Outbreaks, Resistance Trends, and Control Measures inJournal of fungi (Basel, Switzerland) · 2026Review
- Azole-Driven Cross-Resistance and Transporter Gene Expression inMicroorganisms · 2026Article
- Article
- Gim3 buffers and potentiates de novo mutations that affect fluconazole susceptibility in yeast.EMBO reports · 2026Article
- Comprehensive Insights into Sugar Transporters ofJournal of fungi (Basel, Switzerland) · 2026Article
- Experimental Evolution of PathogenicMicroorganisms · 2026Review
- Community-Onset Fungemias: Epidemiology and Genomic Characterization at a Tertiary-Care Hospital in Barcelona, Spain.Journal of fungi (Basel, Switzerland) · 2025Article
- Beyond Conventional Antifungals: Combating Resistance Through Novel Therapeutic Pathways.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Antifungal drug resistance in Candida glabrata: role of cellular signaling and gene regulatory networks.FEMS yeast research · 2025Review
- Fungal Drug Response and Antimicrobial Resistance.Journal of fungi (Basel, Switzerland) · 2023Review
- Multiple genome analysis ofMicrobial cell (Graz, Austria) · 2022Article
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The increasing prevalence of candidosis caused by Candida glabrata is related to its ability to acquire azole resistance. Although azole resistance mechanisms are well known, the mechanisms for azole import into fungal cells have remained obscure. In this work, we have characterized two hexose transporters in C. glabrata and further investigate their role as potential azole importers. Three azole susceptible C. glabrata clinical isolates were evolved towards azole resistance and the acquired resistance phenotype was found to be independent of CgPDR1 or CgERG11 mutations. Through whole-genome sequencing, CgHXT4/6/7 was found to be mutated in the three evolved strains, when compared to their susceptible parents. CgHxt4/6/7 and the 96% identical CgHxt6/7 were found to confer azole susceptibility and increase azole accumulation in C. glabrata cells, strikingly rescuing the susceptibility phenotype imposed by CgPDR1 deletion, while the identified loss-of-function mutation in CgHXT4/6/7, leads to increased azole resistance. In silico docking analysis shows that azoles display a strong predicted affinity for the glucose binding site of CgHxt4/6/7. Altogether, we hypothesize that hexose transporters, such as CgHxt4/6/7 and CgHxt6/7, may constitute a family of azole importers, involved in clinical drug resistance in fungal pathogens, and constituting promising targets for improved antifungal therapy.
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