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DNA replication in bacteriophage-infected Staphylococcus aureus
Journal of Virology
|December 1, 1977
Summary
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.