The RepA protein of plasmid pSC101 controls Escherichia coli cell division through the SOS response.
Although plasmid copy number varies widely among different plasmid species, normally copy number is maintained within a narrow range for any given plasmid. Such copy number control has been shown to occur by regulation of the rate of plasmid DNA replication. Here we report a novel mechanism by which the pSC101 plasmid also can detect an imbalance between the cellular level of its replication protein, RepA, and plasmid-borne RepA binding sites to inhibit bacterial DNA replication and delay host cell division when RepA is in relative excess. We show that delayed cell division occurs by RepA-mediated induction of the SOS response and can be reversed by over-expression of the host DNA primase, DnaG. The effects of RepA excess are prevented by introducing a surfeit of RepA binding sites. The mechanism reported here may help to limit variation in plasmid copy number and allow repopulation of cells with plasmids when copy number falls--potentially pre-empting plasmid loss in cultures of dividing cells.
Ingmer
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Department of Genetics, Stanford University School of Medicine, Stanford, CA 94305-5120, USA.
Miller
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Cohen
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D001665:Binding Sites; D002455:Cell Division; D002876:Chromosomes, Bacterial / Q000235:genetics / Q000378:metabolism; D004265:DNA Helicases; D019915:DNA Primase / Q000378:metabolism; D004261:DNA Replication; D004268:DNA-Binding Proteins / Q000235:genetics / Q000378:metabolism; D004926:Escherichia coli / Q000166:cytology* / Q000235:genetics / Q000378:metabolism*; D018628:Gene Dosage; D015964:Gene Expression Regulation, Bacterial; D005838:Genotype; D010957:Plasmids / Q000235:genetics*; D011506:Proteins / Q000235:genetics / Q000378:metabolism*; D013014:SOS Response, Genetics; D015534:Trans-Activators
D004268:DNA-Binding Proteins; D011506:Proteins; D015534:Trans-Activators; C045264:replication initiator protein; D019915:DNA Primase; D004265:DNA Helicases