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Molecular and Cellular Biology, May 2004, p. 3804-3814, Vol. 24, No. 9
0270-7306/04/$08.00+0     DOI: 10.1128/MCB.24.9.3804-3814.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

CREB Binds to Multiple Loci on Human Chromosome 22

Ghia Euskirchen,1 Thomas E. Royce,2 Paul Bertone,1 Rebecca Martone,1 John L. Rinn,2 F. Kenneth Nelson,1 Fred Sayward,3 Nicholas M. Luscombe,2 Perry Miller,3 Mark Gerstein,2 Sherman Weissman,4 and Michael Snyder1,2*

Department of Molecular, Cellular and Developmental Biology,1 Department of Molecular Biophysics and Biochemistry,2 Department of Medical Anesthesiology,3 Department of Genetics, Yale University, New Haven, Connecticut 06520-80054

Received 3 November 2003/ Returned for modification 15 December 2003/ Accepted 29 January 2004

The cyclic AMP-responsive element-binding protein (CREB) is an important transcription factor that can be activated by hormonal stimulation and regulates neuronal function and development. An unbiased, global analysis of where CREB binds has not been performed. We have mapped for the first time the binding distribution of CREB along an entire human chromosome. Chromatin immunoprecipitation of CREB-associated DNA and subsequent hybridization of the associated DNA to a genomic DNA microarray containing all of the nonrepetitive DNA of human chromosome 22 revealed 215 binding sites corresponding to 192 different loci and 100 annotated potential gene targets. We found binding near or within many genes involved in signal transduction and neuronal function. We also found that only a small fraction of CREB binding sites lay near well-defined 5' ends of genes; the majority of sites were found elsewhere, including introns and unannotated regions. Several of the latter lay near novel unannotated transcriptionally active regions. Few CREB targets were found near full-length cyclic AMP response element sites; the majority contained shorter versions or close matches to this sequence. Several of the CREB targets were altered in their expression by treatment with forskolin; interestingly, both induced and repressed genes were found. Our results provide novel molecular insights into how CREB mediates its functions in humans.

* Corresponding author. Mailing address: Department of Molecular, Cellular and Developmental Biology, Yale University, P.O. Box 208103, New Haven, CT 06520-8103. Phone: (203) 432-6139. Fax: (203) 432-6161. E-mail: michael.snyder{at}yale.edu.

Molecular and Cellular Biology, May 2004, p. 3804-3814, Vol. 24, No. 9
0022-538X/04/$08.00+0     DOI: 10.1128/MCB.24.9.3804-3814.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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