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Cycloheximide resistance can be mediated through either ribosomal subunit.

C A Sutton, M Ares, R L Hallberg

    Proceedings of the National Academy of Sciences of the United States of America
    |July 1, 1978
    PubMed
    Summary

    Two Tetrahymena thermophila mutants exhibit cycloheximide resistance. Resistance is localized to distinct ribosomal subunits (40S and 60S), indicating different resistance mechanisms.

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    Area of Science:

    • Molecular Biology
    • Genetics
    • Cell Biology

    Background:

    • Cycloheximide is a potent inhibitor of protein synthesis.
    • Understanding drug resistance mechanisms is crucial for biological research.
    • Tetrahymena thermophila serves as a model organism for studying eukaryotic cellular processes.

    Purpose of the Study:

    • To determine the molecular basis of cycloheximide resistance in two Tetrahymena thermophila mutant strains.
    • To investigate the genetic loci and cellular components responsible for conferring resistance.

    Main Methods:

    • Analysis of cycloheximide-resistant Tetrahymena thermophila mutants (Chx-A and Chx-B).
    • Assay of cell-free extracts for protein synthetic activity.
    • Fractionation of cell-free systems to localize resistance to ribosomes.

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  • Ribosome dissociation and subunit mixing experiments.

    • Main Results:

    • Both Chx-A and Chx-B mutations confer cycloheximide resistance.
    • Resistance is localized to the ribosome in both mutant strains.
    • The 60S ribosomal subunit confers resistance in one strain, while the 40S subunit confers resistance in the other.
    • Reconstruction experiments confirmed the subunit-specific resistance phenotypes.

    Conclusions:

    • The two cycloheximide resistance mutations in Tetrahymena thermophila are associated with different ribosomal subunits.
    • The mechanisms conferring resistance are distinct for the Chx-A and Chx-B mutations.
    • This study provides insights into the structure-function relationship of ribosomes and drug resistance.