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.

• MeSH
• antifungální látky farmakologie   MeSH
• CDPdiacylglycerolserin-O-fosfatidyltransferasa genetika   metabolismus   MeSH
• flukonazol farmakologie   MeSH
• fungální léková rezistence MeSH
• glukosa metabolismus   MeSH
• křížení genetické MeSH
• kultivační média MeSH
• membránové potenciály fyziologie   MeSH
• mitochondrie MeSH
• mutace * MeSH
• Saccharomyces cerevisiae - proteiny genetika   metabolismus   MeSH
• Saccharomyces cerevisiae genetika   růst a vývoj   MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• antifungální látky MeSH
• CDPdiacylglycerolserin-O-fosfatidyltransferasa MeSH
• flukonazol MeSH
• glukosa MeSH
• kultivační média MeSH
• PGS1 protein, S cerevisiae MeSH Prohlížeč
• Saccharomyces cerevisiae - proteiny MeSH

The effect of ethidium bromide on the growth of a yeast mutant with an impaired mitochrondrial translocation system of adenine nucleotides (op-1 mutant) was investigated. It was found that the op-1 mutant stops growing both under growing and non-growing conditions after treatment with ethidium bromide and that the growth cannot be restored by adding low-molecular compounds to the growth medium. It was the aim of the experiments to clarify whether the cessation of growth of the op-1 mutant after induction of the rho- mutation can be simulated by inhibitors phenotypically changing the mitochondrial function. It appears likely that the op-1 mutant stops growing only after the rho- mutation has been induced, because the phenotypic simulation of the rho- mutation does not lead the cessation of growth of the op-1 mutant.

• MeSH
• adeninnukleotidy metabolismus   MeSH
• antibakteriální látky farmakologie   MeSH
• buněčné dělení MeSH
• ethidium farmakologie   MeSH
• kultivační média MeSH
• kvasinky účinky léků   růst a vývoj   metabolismus   MeSH
• mitochondrie metabolismus   MeSH
• mutace * MeSH
• mutageny MeSH
• spotřeba kyslíku MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• adeninnukleotidy MeSH
• antibakteriální látky MeSH
• ethidium MeSH
• kultivační média MeSH
• mutageny MeSH

A yeast mutant with an impaired system of translocation of adenine nucleotides across the mitochondrial membrane, which stops dividing after superposition of the q- mutation, was investigated. The results of this work indicate that combination of the op1 mutation with the q- mutation in a single cell results in interruption of synthesis of polysaccharides and DNA leading to cessation of division of the op1q- mutant. The mechanism of this effect remains unclear.

• MeSH
• adeninnukleotidy metabolismus   MeSH
• buněčné dělení MeSH
• DNA biosyntéza   MeSH
• ethidium MeSH
• fungální proteiny biosyntéza   MeSH
• kinetika MeSH
• kvasinky růst a vývoj   metabolismus   MeSH
• lipidy biosyntéza   MeSH
• mitochondrie metabolismus   MeSH
• mutace MeSH
• mutageny MeSH
• nukleové kyseliny biosyntéza   MeSH
• polysacharidy biosyntéza   MeSH
• RNA biosyntéza   MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• adeninnukleotidy MeSH
• DNA MeSH
• ethidium MeSH
• fungální proteiny MeSH
• lipidy MeSH
• mutageny MeSH
• nukleové kyseliny MeSH
• polysacharidy MeSH
• RNA MeSH