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Our goal is to understand the mechanisms regulating biofilm formation by the model organism Candida albicans, and to develop new ways to inhibit biofilm formation on abiotic surfaces such as maple sap tubing. C. albicans is the model organism of choice when studying yeast biofilm formation, since the yeast Saccharomyces cerevisiae does not form significant biofilms. C. albicans biofilm formation depends on cells switching between budded and hyphal growth (budded-to-hyphal transition; BHT). Previously, we discovered 21 molecules that inhibited the BHT without killing cells. We identified the signaling pathways affected by some of these inhibitors, and importantly, we showed that three inhibitors, ETYA, buhytrinA, and CGP37157, blocked biofilm formation. The most potent inhibitor, ETYA, has several mechanisms of action in mammalian cells, but how it functions in C. albicans is unknown. <P>Therefore, we will test two hypotheses: 1. ETYA blocks biofilm formation by inhibiting reactive oxygen species and/or oxygenase activity; and 2. ETYA, buhytrinA, and CGP37157 can be incorporated into maple sap plastic tubing and inhibit biofilm formation. These investigations may lead to the development of applied methods to block fungal biofilms on maple sap plastic tubing.
Non-Technical Summary:<br/>
Biofilms caused by Candida albicans and other fungi lead to significant losses in the maple syrup industry by blocking/clogging maple sap plastic tubing. The studies described herein will allow us to examine the ability of biofilm inhibitors to block biofilms on this type of tubing and other abiotic surfaces. These studies will also give us insight into the mechanism by which one of the inhibitors, ETYA, is able to block these biofilms.
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Approach:<br/>
We will use established in vitro assays to examine the ability of the inhibitors ETYA, buhytrinA and CGP37157 to block biofilm formation on abiotic surfaces such as maple sap tubing. We will also use established biochemical and pharmacological techniques to examine the mechanism of action of ETYA, the most potent of the inhibitors. These studies will be performed by the PI, graduate student Todd Cramer, and several undergraduate researchers.