@article{lorenz_parks_1991, title={PHYSIOLOGICAL-EFFECTS OF FENPROPIMORPH ON WILD-TYPE SACCHAROMYCES-CEREVISIAE AND FENPROPIMORPH-RESISTANT MUTANTS}, volume={35}, ISSN={["0066-4804"]}, DOI={10.1128/AAC.35.8.1532}, abstractNote={Fenpropimorph-resistant mutants of Saccharomyces cerevisiae were isolated by a gradient selection procedure. The mutants were cross-resistant to other morpholines (fenpropidin, dodemorph, tridemorph) and 15-azasterol, but were susceptible to azoles (miconazole, clotrimazole, ketoconazole) and nystatin. In the absence of fenpropimorph, the major sterol produced by the mutants and the parental strain was ergosterol. In the presence of fenpropimorph, ignosterol (ergosta-8,14-dien-3 beta-ol) was the major sterol produced by the mutants and the parental strain. The resistance to fenpropimorph involves two recessive genes, each of which allows a semiresistance, when they are isolated apart from one another. Strain JR4 (erg3 erg11), which produces 14-methylfecosterol [14 alpha-methyl-ergosta-8,24(28)-dien- 3-beta-ol) as the major sterol in the presence or absence of fenpropimorph, was also found to be resistant to the drug. The growth inhibitory effect of fenpropimorph on wild-type cells appears to be linked to the production of ignosterol. The uptake of exogenous sterol by wild-type cells was greatly enhanced in the presence of fenpropimorph. The growth inhibition caused by fenpropimorph could only be overcome with bulk levels of exogenous C-5,6-unsaturated sterols.}, number={8}, journal={ANTIMICROBIAL AGENTS AND CHEMOTHERAPY}, author={LORENZ, RT and PARKS, LW}, year={1991}, month={Aug}, pages={1532–1537} }
 @article{lorenz_parks_1990, title={EFFECTS OF LOVASTATIN (MEVINOLIN) ON STEROL LEVELS AND ON ACTIVITY OF AZOLES IN SACCHAROMYCES-CEREVISIAE}, volume={34}, ISSN={["0066-4804"]}, DOI={10.1128/AAC.34.9.1660}, abstractNote={The hypocholesterolemic drug lovastatin (mevinolin) was found to be very effective in lowering the sterol levels of the wild-type yeast Saccharomyces cerevisiae. Lovastatin dramatically decreased the steryl ester content from 2.62 to 0.8 micrograms/mg (dry weight), whereas the free sterol content decreased only from 2.79 to 2.24 micrograms/mg (dry weight) when lovastatin was present in the medium at 10 micrograms/ml. At higher concentrations (100 micrograms/ml), lovastatin nearly abolished the accumulation of steryl esters and decreased the free sterol concentration to less than 1.3 micrograms/mg (dry weight). As a result of the lowered sterol levels, proportional amounts of exogenous sterol were taken up from the medium during aerobic, respiratory conditions. Nearly all of the exogenous sterol taken up was partitioned into the free sterol fraction. The inhibition of sterol esterification in the presence of lovastatin was dependent on heme synthesis. The result of these combined effects caused the MICs of three azole antifungal drugs (ketoconazole, clotrimazole, and miconazole) to be lowered from 6- to 32-fold when lovastatin was present in the medium at 10 micrograms/ml.}, number={9}, journal={ANTIMICROBIAL AGENTS AND CHEMOTHERAPY}, author={LORENZ, RT and PARKS, LW}, year={1990}, month={Sep}, pages={1660–1665} }