Sterol uptake in Candida glabrata: rescue of sterol auxotrophic strains.

Candida glabrata is emerging as a more common and important human pathogen. It is less susceptible to azole antifungals than Candida albicans, thus, posing some unique treatment challenges. Previously undetected C.

Dap1p, a heme-binding protein that regulates the cytochrome P450 protein Erg11p/Cyp51p in Saccharomyces cerevisiae.

Alkylating agents chemically modify DNA and cause mutations that lead to cancer. In the budding yeast Saccharomyces cerevisiae, resistance to the alkylating agent methyl methanesulfonate (MMS) is mediated in part by Dap1p (damage resistance protein 1). Dap1p is related to cytochrome b5, which activates cytochrome P450 proteins, elevating the metabolism of lipids and xenobiotic compounds.

Candida glabrata erg1 mutant with increased sensitivity to azoles and to low oxygen tension.

A Candida glabrata erg1 (Cgerg1) mutant, CgTn201S, was identified by transposon mutagenesis and by increased fluconazole susceptibility. CgERG1 encodes a 489-amino-acid protein which, on the basis of its homology with Saccharomyces cerevisiae ERG1, is a squalene epoxidase essential for ergosterol synthesis. Interruption following codon 475 of CgErg1p decreased the ergosterol content by 50%; caused accumulation of the squalene precursor; increased the levels of susceptibility to fluconazole, itraconazole, and terbinafine; increased the level of resistance to amphotericin B; increased the levels of rhodamine 6G and [(3)H]-fluconazole uptake; reduced the level of growth; and blocked growth under conditions of low oxygen tension.

Identification of an allele of CLA1 associated with variegation in Arabidopsis thaliana.

We have identified a mutant of Arabidopsis thaliana (lvr111) that exhibits a variegated phenotype, reduced isoprenoid pigmentation, and dwarfism in comparison with wild-type plants. Segregation analysis indicated that this phenotype was caused by a single, semi-dominant mutation and PCR-based marker mapping placed the mutation near position 56 on the RI map of chromosome IV. The lvr111 lesion was identified by genomic PCR and sequence analysis as a missense mutation (D306N) in the CLA1 gene (AT4g15560) and complementation analysis confirmed the allelic relationship between lvr111 and CLA1.