Saccharomyces cerevisiae pell and crd1 mutants deficient in the biosynthesis of mitochondrial phosphatidylglycerol (PG) and cardiolipin (CL) as well as Kluyveromyces lactis mutants impaired in the respiratory chain function (RCF) containing dysfunctional mitochondria show altered sensitivity to metabolic inhibitors. The S. cerevisiae pell mutant displayed increased sensitivity to cycloheximide, chloramphenicol, oligomycin and the cell-wall perturbing agents caffeine, caspofungin and hygromycin. On the other hand, the pel1 mutant was less sensitive to fluconazole, similarly as the K. lactis mutants impaired in the function of mitochondrial cytochromes. Mitochondrial dysfunction resulting either from the absence of PG and CL or impairment of the RCF presumably renders the cells more resistant to fluconazole. The increased tolerance of K. lactis respiratory chain mutants to amphotericin B, caffeine and hygromycin is probably related to a modification of the cell wall.
The KlPGS1 gene encoding phosphatidylglycerolphosphate synthase (PGPS) is essential for the viability and multiplication of Kluyveromyces lactis. Regulation of PGPS expression by factors affecting mitochondrial development (C source, growth phase) and general phospholipid biosynthesis was followed. PGS1 mRNA levels were not altered as cells progressed from the exponential to the stationary phase of growth in glucose. PGS1 mRNA abundance was nearly identical in cells growing in a medium with glucose or glycerol as the sole C source during the different growth phases. Regulation of PGS1 expression by exogenous myo-inositol and choline was not mediated at the transcriptional level, the PGPS activity dropped to 70 % after myo-inositol addition.
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