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DNA replication in bacteriophage-infected Staphylococcus aureus

M H Ubelaker, E D Rosenblum

    Journal of Virology
    |December 1, 1977
    PubMed

    Insights

    Phage 52HJD infection of Staphylococcus aureus inhibits bacterial chromosome and penicillinase plasmid replication. However, a tetracycline plasmid under relaxed control continues to replicate during phage infection.

    Area of Science:

    • Microbiology
    • Molecular Biology
    • Virology

    Background:

    • Bacteriophage infection impacts host DNA synthesis.
    • Staphylococcus aureus harbors various plasmids with different replication controls.

    Purpose of the Study:

    • To investigate the effects of phage 52HJD infection on DNA synthesis in Staphylococcus aureus.
    • To characterize the intracellular forms of phage DNA during infection.
    • To determine the impact of phage infection on host and plasmid DNA replication.

    Main Methods:

    • Infection of Staphylococcus aureus strains with phage 52HJD.
    • Analysis of intracellular phage DNA forms (covalently closed circular, open circular, linear).
    • Monitoring of bacterial chromosome and plasmid replication post-infection.

    Main Results:

    • Three intracellular forms of phage 52HJD DNA were identified.
    • Phage 52HJD infection inhibited replication of the bacterial chromosome and a penicillinase plasmid.
    • A tetracycline plasmid with relaxed replication control continued to replicate.

    Conclusions:

    • Phage 52HJD differentially affects host DNA replication based on plasmid control mechanisms.
    • Replication of specific plasmids in S. aureus can persist despite phage infection.
    • No evidence of host DNA degradation or its utilization for phage DNA synthesis was found.

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