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ABSTRACT Over the past decade, Candida auris has emerged as a highly transmissible human fungal pathogen. Because of its ability to transmit between patients in hospitals and its ability to rapidly develop drug resistance, C. auris presents unique challenges. However, at a genetic and genomic level we still understand relatively little about how drug resistance develops in this pathogen. Burrack et al. use experimental evolution and whole-genome sequencing to identify mutations correlated with fluconazole resistance in C. auris. They identify interesting genomic features, including highly plastic subtelomeric regions and whole chromosomal and segmental aneuploidies. Excitingly, they also identify the first example of a hypermutator strain in C. auris. In comparison with the model human fungal pathogen Candida albicans, C. auris is more likely to undergo mutation and less likely to undergo copy number variation in response to drug selection, which may be linked to differences in base ploidy level. |
