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Nucleic Acids Research 2006 34(8):2238-2246; doi:10.1093/nar/gkl248
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Published online 2 May 2006

© The Author 2006. Published by Oxford University Press. All rights reserved
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org

Article

A clustering property of highly-degenerate transcription factor binding sites in the mammalian genome

Chaolin Zhang1,2, Zhenyu Xuan1, Stefanie Otto3, John R. Hover3, Sean R. McCorkle4, Gail Mandel3 and Michael Q. Zhang1,*

1 Cold Spring Harbor Laboratory 1 Bungtown Road, Cold Spring Harbor, NY 11724, USA 2 Department of Biomedical Engineering, State University of New York at Stony Brook NY 11794, USA 3 Howard Hughes Medical Institute, Department of Neurobiology and Behavior, State University of New York at Stony Brook NY 11794, USA 4 Biology Department, Brookhaven National Laboratory Upton, NY 11973, USA

*To whom correspondence should be addressed. Tel: +1 516 367 8393; Fax: +1 516 367 8461; Email: mzhang{at}cshl.edu

Received January 7, 2006. Revised February 15, 2006. Accepted March 29, 2006.

Transcription factor binding sites (TFBSs) are short DNA sequences interacting with transcription factors (TFs), which regulate gene expression. Due to the relatively short length of such binding sites, it is largely unclear how the specificity of protein–DNA interaction is achieved. Here, we have performed a genome-wide analysis of TFBS-like sequences for the transcriptional repressor, RE1 Silencing Transcription Factor (REST), as well as for several other representative mammalian TFs (c-myc, p53, HNF-1 and CREB). We find a nonrandom distribution of inexact sites for these TFs, referred to as highly-degenerate TFBSs, that are enriched around the cognate binding sites. Comparisons among human, mouse and rat orthologous promoters reveal that these highly-degenerate sites are conserved significantly more than expected by random chance, suggesting their positive selection during evolution. We propose that this arrangement provides a favorable genomic landscape for functional target site selection.


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