The Saccharomyces cerevisiae mutant strain containing the op1 mutation affecting the function of a mitochondrial ATP/ADP translocator has been crossed to the pel1 and crd1 mutants deficient in the biosynthesis of mitochondrial phosphatidylglycerol (PG) and cardiolipin (CL). Using tetrad analysis of diploids issued from corresponding crosses a synthetic lethal interaction has been observed between the op1 and pel1 mutations resulting in the lack of growth of a corresponding double mutant on minimal medium containing glucose. The op1 pel1 double mutant also displayed a decreased susceptibility to fluconazole and a compromised growth even in complex medium containing glucose. The viability of mutant cells was strongly reduced, corresponding to <30 % and 10 % of colony-forming units observed after growth in complex and minimal medium, respectively. A lower viability of the double mutant in minimal medium was accompanied by an increased formation of mitochondrial petite mutants (as determined by mtDNA rescue into diploid cells). The results indicate that in the simultaneous absence of mitochondrial anionic phospholipids (PG plus CL) and ATP/ADP exchange across the inner mitochondrial membrane the yeast mitochondrial functions are severely limited, leading to a strongly compromised cell multiplication. Since under similar conditions the op1 crd1 double mutant was able to grow on minimal medium this deleterious effect of anionic phospholipid deficiency could be at least partially substituted by PG accumulated in the cardiolipin deficient delta crd1 mutant cells.

Department of Microbiology and Virology Faculty of Science Comenius University 842 15 Bratislava Slovakia

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Biochim Biophys Acta. 1974 Sep 20;357(3):453-6 PubMed

J Biol Chem. 1988 Oct 15;263(29):14812-8 PubMed

Biochim Biophys Acta. 1968 Aug 20;162(2):157-63 PubMed

Prog Lipid Res. 2000 May;39(3):257-88 PubMed

Mol Microbiol. 1997 Nov;26(3):481-91 PubMed

Yeast. 1998 Dec;14(16):1471-510 PubMed

Curr Genet. 1993 Oct;24(4):307-12 PubMed

J Biol Chem. 1998 Apr 17;273(16):9829-36 PubMed

FEBS Lett. 1974 Sep 1;45(1):263-6 PubMed

Microbiol Rev. 1996 Mar;60(1):1-20 PubMed

J Biol Chem. 1990 Jul 25;265(21):12711-6 PubMed

Biochem J. 2002 May 15;364(Pt 1):317-22 PubMed

J Biol Chem. 2001 Dec 21;276(51):47844-52 PubMed

Yeast. 1995 Oct;11(13):1223-31 PubMed

Antimicrob Agents Chemother. 2004 May;48(5):1600-13 PubMed

FEMS Yeast Res. 2004 Oct;5(1):19-27 PubMed

FEMS Microbiol Lett. 1996 Jun 15;140(1):43-7 PubMed

Biochem Biophys Res Commun. 1972 Oct 6;49(1):192-8 PubMed

J Biol Chem. 1994 Jan 21;269(3):1940-4 PubMed

Biochem Biophys Res Commun. 1968 Feb 15;30(3):232-9 PubMed

Biochim Biophys Acta. 1968 Jan 15;153(1):43-54 PubMed

J Biol Chem. 1990 Nov 15;265(32):19434-40 PubMed

FEBS Lett. 1974 Jun 15;42(3):309-13 PubMed

Mol Gen Genet. 1980;179(1):141-6 PubMed

FEBS Lett. 1998 Jan 2;421(1):15-8 PubMed

Curr Genet. 1998 Oct;34(4):297-302 PubMed

FEBS Lett. 2002 Mar 27;515(1-3):25-8 PubMed

Yeast. 2000 Apr;16(6):547-52 PubMed

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