Impact of mitochondrial function on yeast susceptibility to antifungal compounds
Jazyk angličtina Země Spojené státy americké Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
17702459
DOI
10.1007/bf02931302
Knihovny.cz E-zdroje
- MeSH
- antifungální látky farmakologie MeSH
- buněčná stěna fyziologie MeSH
- fosfatidylglyceroly genetika metabolismus MeSH
- fungální léková rezistence genetika MeSH
- kardiolipiny genetika metabolismus MeSH
- Kluyveromyces účinky léků genetika MeSH
- mikrobiální testy citlivosti MeSH
- mitochondriální DNA genetika MeSH
- mitochondrie genetika fyziologie MeSH
- mutace MeSH
- Saccharomyces cerevisiae účinky léků genetika MeSH
- transport elektronů * účinky léků genetika MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- antifungální látky MeSH
- fosfatidylglyceroly MeSH
- kardiolipiny MeSH
- mitochondriální DNA MeSH
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.
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