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Determinant for multiple drug resistance possessing features of a mitochondrial episome in Saccharomyces cerevisiae

O V Nevzglyadova, V L Larionov, S A Neifakh

    Molecular and Cellular Biochemistry
    |February 4, 1977
    PubMed

    Insights

    Multiple drug resistance mutations in mitochondria can lead to genome reconstruction, forming new nucleotide sequences. A nuclear gene suppressor can delete these resistance determinants, even after mitochondrial DNA loss.

    Area of Science:

    • Mitochondrial genetics
    • Molecular biology
    • Genomics

    Background:

    • Mitochondrial genomes are susceptible to mutations conferring resistance to various drugs.
    • Understanding the mechanisms of drug resistance and genome plasticity is crucial in molecular biology.

    Purpose of the Study:

    • To investigate the impact of a mutation conferring multiple drug resistance on mitochondrial genome structure.
    • To explore the role of nuclear genes in regulating mitochondrial drug resistance determinants.
    • To examine the stability and state of resistance determinants following mitochondrial DNA loss.

    Main Methods:

    • Analysis of mitochondrial genome reconstruction following drug resistance mutations.
    • Genetic crosses to study the inheritance and interaction of resistance factors.
    • Investigation of nuclear gene suppressor effects on mitochondrial determinants.
    • Assessment of resistance determinant stability after ethidium bromide treatment.

    Main Results:

    • A mutation for multiple resistance (tetracycline, cycloheximide, oligomycin) leads to mitochondrial genome reconstruction and independent nucleotide sequences.
    • Heterozygotes for this resistance factor lack the specific tetracycline resistance locus (locus T).
    • A nuclear recessive gene suppressor (gene i) induces deletion of the multiple resistance determinant.
    • The resistance determinant persists even after mitochondrial DNA loss induced by ethidium bromide, remaining in either an active or passive state.

    Conclusions:

    • Mitochondrial genome plasticity allows for the formation of novel resistant phenotypes through sequence reconstruction.
    • Nuclear genes play a significant role in controlling or eliminating mitochondrial drug resistance elements.
    • Mitochondrial drug resistance determinants can exhibit remarkable stability, persisting independently of the mitochondrial DNA molecule.

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