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Background  There is a pressing need to identify novel antifungal drug targets to aid in the therapy of life-threatening mycoses and overcome increasing drug resistance. Identifying specific mechanisms of action of membrane-interacting antimicrobial drugs on the model fungus  Saccharomyces cerevisiae  is one avenue towards addressing this issue. The  S. cerevisiae  deletion mutants  Δizh2 ,  Δizh3 ,  Δaif1  and  Δstm1  were demonstrated to be resistant to amphibian-derived antimicrobial peptides (AMPs). The purpose of this study was to examine whether AMPs and polyene antifungals have a similar mode of action; this was done by comparing the relative tolerance of the mutants listed above to both classes of antifungal.    Findings  In support of previous findings on solid media it was shown that  Δizh2  and  Δizh3  mutants had increased resistance to both amphotericin B (1–2 μg ml −1 ) and nystatin (2.5 – 5 μg ml −1 ) in liquid culture, after acute exposure. However,  Δaif1  and  Δstm1  had wild-type levels of susceptibility to these polyenes. The generation of reactive oxygen species (ROS) after exposure to amphotericin B was also reduced in  Δizh2  and  Δizh3 . These data indicated that polyene antifungal and AMPs may act via distinct mechanisms of inducing cell death in  S. cerevisiae .    Conclusions  Further understanding of the mechanism(s) involved in causing cell death and the roles of  IZH2  and  IZH3  in drug susceptibility may help to inform improved drug design and treatment of fungal pathogens.

annals of clinical microbiology and antimicrobials

The polyene antifungals, amphotericin B and nystatin, cause cell death in Saccharomyces cerevisiae by a distinct mechanism to amphibian-derived antimicrobial peptides