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Monomer–dimer control of the ColE1 P_cer promoter

Department of Genetics, University of Cambridge, Downing Site, Cambridge CB2 3EH, UK¹

Author for correspondence: David K. Summers. Tel: +44 1223 333991. Fax: +44 1223 333992. e-mail: dks11{at}cam.ac.uk

XerCD-mediated recombination at cer converts multimers of plasmid ColE1 to monomers, maximizing the number of independently segregating molecules and minimizing the frequency of plasmid loss. In addition to XerCD, recombination requires the accessory factors ArgR and PepA. The promoter P_cer, located centrally within cer, is also required for stable plasmid maintenance. P_cer is active in plasmid multimers and directs transcription of a short RNA, Rcd, which appears to inhibit cell division. It has been proposed that Rcd is part of a checkpoint which ensures that multimer resolution is complete before the cell divides. This study has shown that ArgR does not act as a transcriptional repressor of P_cer in plasmid monomers. P_cer is unusual in that the -35 and -10 hexamers are separated by only 15 bp and this study has demonstrated that increasing this to a more conventional spacing results in elevated activity. An increase to 17 bp resulted in a 10- to 20-fold increase in activity, while smaller effects were seen when the spacer was increased to 16 bp or 18 bp. These observations are consistent with the hypothesis that P_cer activation involves realignment of the -35 and -10 sequences within a recombinational synaptic complex. This predicts that a 17 bp spacer promoter derivative should be down-regulated by plasmid multimerization, and this is confirmed experimentally.

Keywords: dimer resolution, cer–Xer recombination system, cell-cycle checkpoint, Rcd, plasmid stability

Abbreviations: GalK, galactokinase

^a Present address: Laboratory of Receptor Signalling, The Babraham Institute, Babraham Hall, Cambridge CB2 4AT, UK.

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