New mechanisms of caspofungin tolerance in Cryptococcus neoformans

Fungal pathogens are responsible for a substantial disease burden among the increasing population of immunocompromised and immunosuppressed patients. There are relatively few antifungal drugs available to treat these pathogens. One of the most promising classes of drugs, the echinocandins, are not effective in treating Cryptococcus neoformans, which is responsible for hundreds of thousands of infections annually. This lack of efficacy is not well understood. The data deposited is derived from an msh1 deletion strain from a deletion collection of Cryptococcus neoformans. This strain is substantially more susceptible to the echinocandin drug caspofungin than wild-type Cryptococcus. In addition, sequence from the wild-type parent strain of the deletion collection is included as a control. Because Msh1 is a mismatch repair component and because an independent msh1 mutant failed to recapitulate the caspofungin susceptibility phenotype, this strain was sequenced to identify secondary mutations in the strain background that may contribute to the observed phenotype