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J. Bacteriol. doi:10.1128/JB.00975-06
Copyright (c) 2006, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

The Escherichia coli K-12 NarL and NarP proteins insulate the nrf promoter from the effects of IHF

Douglas F. Browning*, David J. Lee, Alan J. Wolfe, Jeffrey A. Cole, and Stephen J. W. Busby

School of Biosciences, University of Birmingham, Birmingham, B15 2TT, UK.; Department of Microbiology and Immunology, Stritch School of Medicine, Loyola University Chicago, Maywood, IL 60153, USA

* To whom correspondence should be addressed. Email: D.F.Browning{at}bham.ac.uk,


   Abstract

The Escherichia coli K-12 nrf operon promoter can be fully activated by FNR protein binding to a site centred at position -41.5. FNR-dependent transcription is suppressed by IHF binding at position -54, and this suppression is counteracted by the binding of the NarL or NarP response-regulators at position -74.5. The E. coli acs gene is transcribed from a divergent promoter upstream from the nrf operon promoter. Transcription from the major acsP2 promoter is dependent on CRP and is modulated by IHF and Fis binding at multiple sites. We show that IHF binding to one of these sites, located at position -127 with respect to the nrf promoter, has a positive effect on nrf promoter activity. This activation is ‘face of the DNA helix’-dependent, independent of IHF binding at other locations, and found only when NarL/NarP are not bound at position -74.5. Binding of NarL/NarP appears to insulate the nrf promoter from the effects of IHF. The acs-nrf regulatory region is conserved in other pathogenic E. coli strains and related enteric bacteria but differs in Salmonella enterica serovar Typhimurium.




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