C. Koegel

TL;DR: The sterol profile of an ERG25 disruptant was consistent with the erg25 allele obtained by mutagenesis, and the amino acid sequence shows a C-terminal endoplasmic reticulum retrieval signal KKXX and three histidine-rich clusters found in eukaryotic membrane desaturases and in a bacterial alkane hydroxylase and xylene monooxygenase.

TL;DR: Inhibitors of the ERG6gene product would make the cell increasingly susceptible to antifungal agents as well as to new agents which normally would be excluded and would allow for clinical treatment at lower dosages.

TL;DR: Results show that these double disruption strains are viable and that spontaneously arising suppressors of theERG11 disruption areerg3 mutants, compared to similar mutants ofCandida albicans that are viable in the absence of theerg3 lesion.

TL;DR: Gene disruption demonstrates that ERG5 is not essential for cell viability and the putative gene encoding the C-22 sterol desaturase required in ergosterol biosynthesis is identified.

TL;DR: It is demonstrated that treatment of the sterol auxotrophs erg25 slu1 or erg11 slu2 with azole antibiotics paradoxically restores viability to these strains in the absence of sterol supplementation via the suppression system described.