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Nucleic Acids Research Advance Access originally published online on May 30, 2008
Nucleic Acids Research 2008 36(12):3950-3955; doi:10.1093/nar/gkn339
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Nucleic Acids Research, 2008, Vol. 36, No. 12 3950-3955
© 2008 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Molecular Biology

The Escherichia coli RutR transcription factor binds at targets within genes as well as intergenic regions

Tomohiro Shimada1, Akira Ishihama1,2, Stephen J. W. Busby3 and David C. Grainger3,*

1Department of Frontier Bioscience and Micro-Nano Technology Research Centre, Hosei University, Koganei, Tokyo 184-8584, 2Nippon Institute for Biological Science, Ome, Tokyo 198-0024, Japan and 3School of Biosciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

*To whom correspondence should be addressed. Tel: 0121 414 5435; Fax: 0121 414 7366; Email: d.grainger{at}bham.ac.uk

Received April 1, 2008. Revised May 6, 2008. Accepted May 11, 2008.

The Escherichia coli RutR protein is the master regulator of genes involved in pyrimidine catabolism. Here we have used chromatin immunoprecipitation in combination with DNA microarrays to measure the binding of RutR across the chromosome of exponentially growing E. coli cells. Twenty RutR-binding targets were identified and analysis of these targets generated a DNA consensus logo for RutR binding. Complementary in vitro binding assays showed high-affinity RutR binding to 16 of the 20 targets, with the four low-affinity RutR targets lacking predicted key binding determinants. Surprisingly, most of the DNA targets for RutR are located within coding segments of the genome and appear to have little or no effect on transcript levels in the conditions tested. This contrasts sharply with other E. coli transcription factors whose binding sites are primarily located in intergenic regions. We suggest that either RutR has yet undiscovered function or that evolution has been slow to eliminate non-functional DNA sites for RutR because they do not have an adverse effect on cell fitness.


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