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- W2026687517 abstract "Two azole resistant isolates of Saccharomyces cerevisiae carried mutations allelic to erg 3 and were blocked to differing degrees at the C5-6 desaturation step of ergosterol biosynthesis. When treated with the sterol 14α-demethylation inhibitor fluconazole the wild-type sensitive strain accumulated lanosterol and 14α-methyl-ergosta-8,24(28)-dien-3β,6α-diol (14-methyl-3,6 diol). The stringent desaturase mutant, A2, accumulated 14α-methyl-8,24(28)-dien-3β-ol (14-methyl fecosterol) and lanosterol as the major sterol components when treated with fluconazole. Resistant isolate A3 accumulated 14-methyl-3,6-diol, 14-methyl fecosterol, and lanosterol and was only partially blocked at sterol C5-6 desaturation. We conclude that functional sterol C5-6 desaturase is required for the synthesis of 14-methyl-3,6-diol under conditions of azole inhibition. We present a new hypothesis for the mode of action of azole antifungals based on the inability of 14-methyl-3,6-diol to support growth, and suggest that growth can occur through utilisation of 14-methyl fecosterol, produced by a combination of azole inhibition and defective sterol C5-6 desaturation." @default.
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- W2026687517 date "1989-11-01" @default.
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- W2026687517 title "Defective sterol C5-6 desaturation and azole resistance: A new hypothesis for the mode of action of azole antifungals" @default.
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- W2026687517 doi "https://doi.org/10.1016/0006-291x(89)91792-0" @default.
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