@article{tomeo_palermo_tove_parks_1997, title={A conditional sterol esterification defect in yeast having either a SEC1 or SEC5 mutation in the secretory pathway}, volume={13}, DOI={10.1002/(sici)1097-0061(199704)13:5<449::aid-yea99>3.0.co;2-a}, abstractNote={Two temperature‐conditional secretory mutations, sec1 and sec5, cause the accumulation of post‐Golgi vesicles when strains containing these mutations are grown at 37°C. In addition to accumulating vesicles, the mutants do not esterify free sterol on rich media at the restrictive temperature. It is the high level of inositol in the media that causes this condition in the yeast Saccharomyces cerevisiae, not a defective steryl ester synthase or lack of substrates. When strains containing the sec1 or sec5 mutation were transformed separately with a plasmid carrying SEC1 and SEC5, the esterification and secretory defects were alleviated. Double mutants containing sec6, sec14 or sec18 with either a sec1 or sec5 mutation have normal esterification levels. Strains with suppressor mutations were isolated that grew at 37°C, esterified sterols and had diminished accumulation of vesicles, when grown at the restrictive temperature on defined media with additional inositol. Electron microscopy was used to examine vesicle accumulation, the number of lipid droplets, and to further characterize the esterification defect. When grown at 37°C on defined medium, the strains with sec5 or sec1 accumulated the usual secretory vesicles, but when grown under similar conditions with elevated levels of inositol, accumulated an additional vesicular‐like body. © 1997 John Wiley & Sons, Ltd.}, number={5}, journal={Yeast}, author={Tomeo, M. E. and Palermo, L. M. and Tove, S. R. and Parks, L. W.}, year={1997}, pages={449–462} }
 @article{palermo_leak_tove_parks_1997, title={Assessment of the essentiality of ERG genes late in ergosterol biosynthesis in Saccharomyces cerevisiae}, volume={32}, ISSN={["1432-0983"]}, DOI={10.1007/s002940050252}, abstractNote={Isogenic strains of yeast were constructed, differing only in insertionally inactivated genes for ergosterol biosynthesis. These and their allelic wild-types were grown in competition to ascertain growth differences and any selective advantage for organisms producing sterols with or without specific features of ergosterol. In every instance tested, the wild-type allele afforded a competitive advantage over the isogenic pair producing modified sterol structures instead of ergosterol. A general trend was seen in which the earlier in the biosynthetic pathway that a mutation occurred, the less able the strain producing the defective sterols could compete with the ergosterol-producing strains.}, number={2}, journal={CURRENT GENETICS}, author={Palermo, LM and Leak, FW and Tove, S and Parks, LW}, year={1997}, month={Aug}, pages={93–99} }