Isolation and characterization of plasmid mutations that enable partitioning of pSC101 replicons lacking the partition (par) locus.
Second-site mutations that allow stable inheritance of partition-defective pSC101 plasmids mapped to seven distinct sites in the 5' half of the plasmid repA gene. While the mutations also elevated pSC101 copy number, there was no correlation between copy number increase and plasmid stability. Combinations of mutations enabled pSC101 DNA replication in the absence of integration host factor and also stabilized par-deleted plasmids in cells deficient in DNA gyrase or defective in DnaA binding. Our findings suggest that repA mutations compensate for par deletion by enabling the origin region RepA-DNA-DnaA complex to form under suboptimal conditions. They also provide evidence that this complex has a role in partitioning that is separate from its known ability to promote plasmid DNA replication.
Department of Genetics, Stanford University School of Medicine, California 94305.
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Conley
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Cohen
D001426:Bacterial Proteins / Q000235:genetics*; D002455:Cell Division; D004265:DNA Helicases; D004261:DNA Replication / Q000235:genetics*; D004268:DNA-Binding Proteins; D004926:Escherichia coli / Q000235:genetics* / Q000254:growth & development; D034982:Integration Host Factors; D009154:Mutation; D010957:Plasmids / Q000235:genetics*; D011506:Proteins; D012093:Replicon / Q000235:genetics*; D017384:Sequence Deletion; D013489:Suppression, Genetic; D015534:Trans-Activators
D001426:Bacterial Proteins; D004268:DNA-Binding Proteins; D034982:Integration Host Factors; D011506:Proteins; D015534:Trans-Activators; C045264:replication initiator protein; D004265:DNA Helicases