People with weakened immune systems - such as transplant recipients or cancer patients undergoing chemotherapy - are often plagued by fungal infections. Antifungal drugs do not always work because some organisms can pump them out of their cells before they do any damage. A paper in Nature reveals a mechanism of how such drugs have the unwanted effect of boosting the fungus' arsenal of pumps used to fight them off.
Anders Näär and colleagues have identified a crucial protein - known as Pdr1p - in fungi such as yeast (Saccharomyces cerevisiae) and the organism responsible for thrush-like infections (Candida glabrata) that directly binds the drug once it has gained entry into the cell. This binding stimulates the fungus to step up production of its defensive pumping gear, and the drug is ejected.
Pdr1p can bind different types of antifungal drug, giving rise to multidrug resistance. The authors hope that understanding the mechanism behind this resistance will help in the design of drugs to thwart it.
Anders Näär (Harvard Medical School, Charlestown, MA, USA)
Andre Goffeau (Universite de Louvain, Louvain-la-Neuve, Belgium)
(C) Nature press release.
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