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Decoding resistance in Diutina catenulata by validating clinically relevant Erg11/Fks1 mutations.
Wei Zhang1,2,3, Na Wang1, Xin-Fei Chen3
1Hebei Key Laboratory of Pathogenic Mechanisms and Diagnosis & Treatment Technologies for Lung Microbiome, The First Affiliated Hospital of Hebei North University, Zhangjiakou, Hebei, China.
Frontiers in Cellular and Infection Microbiology
|March 5, 2026
Summary
Specific mutations in the ERG11 and FKS1 genes cause antifungal drug resistance in Diutina catenulata. This resistance is nutrient-dependent, impacting treatment strategies for this fungal pathogen.
Area of Science:
- Mycology
- Molecular Biology
- Drug Discovery
Background:
- Diutina catenulata is an emerging fungal pathogen.
- Antifungal drug resistance is a growing clinical concern.
- Understanding resistance mechanisms is crucial for effective treatment.
Purpose of the Study:
- To investigate the causal link between ERG11 and FKS1 gene mutations and antifungal drug resistance in Diutina catenulata.
- To elucidate the structural basis of resistance through molecular docking.
Main Methods:
- Constructed and validated recombinant plasmids with mutant ERG11 and FKS1 alleles in Saccharomyces cerevisiae.
- Performed antifungal susceptibility testing under varying nutrient conditions (SD-Ura, YPD).
- Utilized molecular docking to analyze drug-target interactions and resistance mechanisms.
Main Results:
- ERG11 (F126L) and FKS1 mutations conferred significant antifungal resistance in a nutrient-dependent manner.
- ERG11-F126L increased fluconazole MIC 21-fold in SD-Ura medium.
- FKS1 mutations increased echinocandin MICs by 1.4-2 fold; molecular docking revealed altered binding cavities and disrupted interactions.
Conclusions:
- Specific ERG11 and FKS1 mutations are key drivers of antifungal resistance in Chinese D. catenulata strains.
- Nutrient availability modulates the observed resistance phenotypes.
- Findings provide insights into resistance mechanisms for targeted antifungal therapy.
