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Eukaryotic Cell, December 2002, p. 1041-1044, Vol. 1, No. 6
1535-9778/02/$04.00+0 DOI: 10.1128/EC.1.6.1041-1044.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
Joseph T. Nickels,2 and Thomas D. Edlind1*
Department of Microbiology and Immunology,1 Department of Biochemistry, Drexel University College of Medicine, Philadelphia, Pennsylvania 191292
Received 5 August 2002/ Accepted 19 September 2002
Yeasts respond to treatment with azoles and other sterol biosynthesis inhibitors by upregulating the expression of the ERG genes responsible for ergosterol production. Previous studies on Saccharomyces cerevisiae implicated the ROX1 repressor in ERG regulation. We report that ROX1 deletion resulted in 2.5- to 16-fold-lower susceptibilities to azoles and terbinafine. In untreated cultures, ERG11 was maximally expressed in mid-log phase and expression decreased in late log phase, while the inverse was observed for ROX1. In azole-treated cultures, ERG11 upregulation was preceded by a decrease in ROX1 RNA. These inverse correlations suggest that transcriptional regulation of ROX1 is an important determinant of ERG expression and hence of azole and terbinafine susceptibilities.
Present address: The Wistar Institute, Philadelphia, PA 19104.
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