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Journal of Bacteriology, September 2003, p. 5563-5572, Vol. 185, No. 18
0021-9193/03/$08.00+0 DOI: 10.1128/JB.185.18.5563-5572.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.
Ann Karen C. Brassinga,
and Gregory T. Marczynski*
Department of Microbiology and Immunology, McGill University, Montreal, Quebec, Canada H3A 2B4
Received 27 February 2003/ Accepted 2 July 2003
The response regulator CtrA controls chromosome replication by binding to five sites, a, b, c, d, and e, inside the Caulobacter crescentus replication origin (Cori). In this study, we demonstrate that integration host factor (IHF) binds Cori over the central CtrA binding site c. Surprisingly, IHF and CtrA share DNA recognition sequences. Rather than promoting cooperative binding, IHF binding hinders CtrA binding to site c and nearby site d. Unlike other CtrA binding sites, DNA mutations in the CtrA c/IHF site uniquely impair autonomous Cori plasmid replication. These mutations also alter transcription from distant promoters more than 100 bp away. When the CtrA c/IHF site was deleted from the chromosome, these cells grew slowly and became selectively intolerant to a CtrA phosphor-mimic allele (D51E). Since CtrA protein concentration decreases during the cell cycle as IHF protein concentration increases, we propose a model in which IHF displaces CtrA in order to bend Cori and promote efficient chromosome replication.
Present address: Mol. and Cell Biology Laboratory, Salk Institute for Biological Studies, San Diego, CA 92186-5800.
Present address: Dept. of Microbiol. and Immunology, Dalhousie University, Halifax, Nova Scotia, Canada B3H 4H7.
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