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Mitochondrial mutagenesis in Saccharomyces cerevisiae. II. Methyl methanesulphonate and diepoxybutane

R Polakowska, A Putrament

    Mutation Research
    |July 1, 1979
    PubMed

    Insights

    Methyl methanesulphonate and diepoxybutane caused significant damage to nuclear DNA in Saccharomyces cerevisiae. However, these agents showed minimal impact on mitochondrial DNA, suggesting distinct cellular responses to genotoxicity.

    Area of Science:

    • Molecular Biology
    • Genetics
    • Yeast Biology

    Background:

    • Saccharomyces cerevisiae is a model organism for studying DNA damage and repair mechanisms.
    • Nuclear and mitochondrial DNA can exhibit differential sensitivity to genotoxic agents.
    • Understanding these differences is crucial for comprehending cellular responses to mutagens.

    Purpose of the Study:

    • To investigate the differential effects of methyl methanesulphonate (MMS) and diepoxybutane (DEB) on nuclear and mitochondrial DNA in Saccharomyces cerevisiae.
    • To compare the mutagenic and lethal potential of these agents in different cellular compartments.

    Main Methods:

    • Exposure of Saccharomyces cerevisiae to methyl methanesulphonate and diepoxybutane under controlled conditions.
    • Assessing lethal effects on cell viability.
    • Quantifying point mutations in mitochondrial DNA by measuring resistance to erythromycin and chloramphenicol.
    • Evaluating induction of cytoplasmic petite mutations.

    Main Results:

    • MMS and DEB induced significant lethal and mutagenic damage in nuclear DNA.
    • These agents failed to induce cytoplasmic petite mutations in mitochondria.
    • MMS and DEB poorly induced point mutations in mitochondrial DNA under the tested conditions.

    Conclusions:

    • Nuclear DNA in Saccharomyces cerevisiae is highly susceptible to damage by MMS and DEB.
    • Mitochondrial DNA exhibits a lower susceptibility to these specific genotoxic agents.
    • Differential accessibility, repair mechanisms, or protective factors may explain the observed variations in DNA damage response between nuclear and mitochondrial compartments.

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