Preprint: Parallel FKS1 mutations drive echinocandin resistance in globally spreading Candida auris

A preprint posted to bioRxiv on 1 September 2026 presents a large-scale population genomic analysis of echinocandin resistance in Candida auris, a clonal fungal pathogen that has emerged as a global healthcare concern over the past decade.

Using genome-wide association across more than 600 isolates, the authors identified mutations in FKS1 — the gene encoding the enzyme β-1,3-glucan synthase, which is the molecular target of echinocandin antifungal drugs — as the dominant driver of resistance. Ancestral reconstruction of the population suggested that shared resistance mutations arose independently on multiple occasions in small outbreak clusters, a pattern the authors describe as parallel evolution operating under evolutionary constraint.

The findings have implications for understanding how resistance emerges and spreads in predominantly clonal pathogens, and may inform surveillance strategies for antifungal resistance. The work contributes to a growing literature on the genomic epidemiology of Candida auris, which has been designated a priority pathogen by several public health agencies.

This is a preprint that has not yet been peer-reviewed, and its findings should be interpreted accordingly. The study is primarily of interest to clinical and research mycologists, infectious disease specialists, and population geneticists working on antimicrobial resistance.