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Molecular and Cellular Biology, March 2000, p. 2004-2013, Vol. 20, No. 6
Karolinska Institute, Department of
Biosciences, NOVUM, S-14157 Huddinge,1 and
Södertörns högskola, S-14104
Huddinge,3 Sweden, and Howard Hughes
Medical Institute, Department of Biochemistry and Molecular
Biology, The Pennsylvania State University, University Park,
Pennsylvania 16802-45002
Received 9 August 1999/Returned for modification 14 September
1999/Accepted 20 December 1999
The SWI-SNF complex has been shown to alter nucleosome conformation
in an ATP-dependent manner, leading to increased accessibility of
nucleosomal DNA to transcription factors. In this study, we show that
the SWI-SNF complex can potentiate the activity of the glucocorticoid
receptor (GR) through the N-terminal transactivation domain,
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Recruitment of the SWI-SNF Chromatin Remodeling
Complex as a Mechanism of Gene Activation by the Glucocorticoid
Receptor
1 Activation Domain
1, in
both yeast and mammalian cells. GR-
1 can directly interact with
purified SWI-SNF complex, and mutations in
1 that affect the
transactivation activity in vivo also directly affect
1 interaction
with SWI-SNF. Furthermore, the SWI-SNF complex can stimulate
1-driven transcription from chromatin templates in vitro. Taken
together, these results support a model in which the GR can directly
recruit the SWI-SNF complex to target promoters during
glucocorticoid-dependent gene activation. We also provide evidence that
the SWI-SNF and SAGA complexes represent independent pathways of
1-mediated activation but play overlapping roles that are able to
compensate for one another under some conditions.
*
Corresponding author. Mailing address: The Rockefeller
University, Box 166, c/o Roeder Lab, 1230 York Ave., New York, NY
10021. Phone: (212) 327-7604. Fax: (212) 327-7949. E-mail:
wallbea{at}rockvax.rockefeller.edu.
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