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J. Biol. Chem., Vol. 282, Issue 20, 14992-14999, May 18, 2007

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Extracellular Matrix-regulated Gene Expression Requires Cooperation of SWI/SNF and Transcription Factors^*

From the Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720

Extracellular cues play crucial roles in the transcriptional regulation of tissue-specific genes, but whether and how these signals lead to chromatin remodeling is not understood and subject to debate. Using chromatin immunoprecipitation assays and mammary-specific genes as models, we show here that extracellular matrix molecules and prolactin cooperate to induce histone acetylation and binding of transcription factors and the SWI/SNF complex to the - and -casein promoters. Introduction of a dominant negative Brg1, an ATPase subunit of SWI/SNF complex, significantly reduced both - and -casein expression, suggesting that SWI/SNF-dependent chromatin remodeling is required for transcription of mammary-specific genes. Chromatin immunoprecipitation analyses demonstrated that the ATPase activity of SWI/SNF is necessary for recruitment of RNA transcriptional machinery, but not for binding of transcription factors or for histone acetylation. Co-immunoprecipitation analyses showed that the SWI/SNF complex is associated with STAT5, CCAAT/enhancer-binding protein , and glucocorticoid receptor. Thus, extracellular matrix- and prolactin-regulated transcription of the mammary-specific casein genes requires the concerted action of chromatin remodeling enzymes and transcription factors.

Received for publication, November 6, 2006 , and in revised form, January 30, 2007.

^* This work was supported by U. S. Department of Energy, Office of Biological and Environmental Research Grant DE-AC03-76SF00098, a distinguished fellow award by the same Office, U. S. Department of Defense Breast Cancer Research Program Innovator Award DAMD17-02-1-0438 (to M. J. B.), as well as NCI, National Institutes of Health Grant CA057621-13 (to Z. W. and M. J. B.), and in part by Department of Defense Breast Cancer Research Program Postdoctoral Fellowships DAMD17-02-1-0441 (to R. X.) and W81XWH0410581 (to V. A. S.) and a postdoctoral fellowship from the Canadian Institute for Health Research (to V. A. S.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The on-line version of this article (available at http://www.jbc.org) contains supplemental Fig. S1.

¹ To whom correspondence should be addressed: Life Sciences Division, Lawrence Berkeley National Laboratory, 1 Cyclotron Rd., MS 977R225A, Berkeley, CA 94720. Tel.: 510-486-4365; Fax: 510-486-5586; E-mail: MJBissell{at}lbl.gov.

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