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Two complementation groups mediate tetracycline resistance determined by Tn10.

M S Curiale, S B Levy

    Journal of Bacteriology
    |July 1, 1982
    PubMed
    Summary
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    Two complementation groups, tetA and tetB, within the tetracycline resistance structural region of transposon Tn10 are essential for resistance. Mutations in these groups, particularly tetB encoding the inner-membrane protein, reveal complex interactions for tetracycline resistance.

    Area of Science:

    • Molecular biology
    • Genetics
    • Microbiology

    Background:

    • Transposon Tn10 confers tetracycline resistance through specific genes.
    • Understanding the genetic basis of antibiotic resistance is crucial for combating infections.

    Purpose of the Study:

    • To identify and characterize the complementation groups responsible for tetracycline resistance in transposon Tn10.
    • To determine the location and function of these groups within the resistance gene cluster.

    Main Methods:

    • Cloning of tetracycline-sensitive mutations from Tn10 into compatible plasmids.
    • Genetic complementation analysis using plasmids with known regulatory or structural regions.
    • Mapping of mutations to specific genes (tetA and tetB) within the structural region.

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    Main Results:

    • Two complementation groups, tetA and tetB, are required for tetracycline resistance.
    • Both tetA and tetB are located within the structural region of the tetracycline resistance genes.
    • Mutations in tetB affect the 36,000-molecular-weight inner-membrane TET protein.
    • Complementation levels suggest complex interactions between tetA and tetB gene products.

    Conclusions:

    • The tetA and tetB genes are essential components of the tetracycline resistance mechanism in Tn10.
    • These genes function within the structural region, with tetB directly involved in encoding the membrane protein.
    • The interaction between tetA and tetB products is complex and crucial for conferring resistance.