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Molecular and Cellular Biology, April 2000, p. 2839-2851, Vol. 20, No. 8
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Mammalian SWI-SNF Complexes Contribute to
Activation of the hsp70 Gene
Ivana L.
de la
Serna,1
Kerri A.
Carlson,1
David A.
Hill,1
Cynthia J.
Guidi,1
Ryan O.
Stephenson,1
Saïd
Sif,2
Robert E.
Kingston,2 and
Anthony
N.
Imbalzano1,*
Department of Cell Biology, University of
Massachusetts Medical School, Worcester, Massachusetts
01655,1 and Department of Genetics,
Harvard Medical School, and Department of Molecular Biology,
Massachusetts General Hospital, Boston, Massachusetts
021142
Received 14 December 1999/Accepted 21 January 2000
ATP-dependent chromatin-remodeling complexes are conserved among
all eukaryotes and function by altering nucleosome structure to allow
cellular regulatory factors access to the DNA. Mammalian SWI-SNF
complexes contain either of two highly conserved ATPase subunits: BRG1
or BRM. To identify cellular genes that require mammalian SWI-SNF
complexes for the activation of gene expression, we have generated cell
lines that inducibly express mutant forms of the BRG1 or BRM ATPases
that are unable to bind and hydrolyze ATP. The mutant subunits
physically associate with at least two endogenous members of mammalian
SWI-SNF complexes, suggesting that nonfunctional, dominant negative
complexes may be formed. We determined that expression of the mutant
BRG1 or BRM proteins impaired the ability of cells to activate the
endogenous stress response gene hsp70 in response to
arsenite, a metabolic inhibitor, or cadmium, a heavy metal. Activation
of hsp70 by heat stress, however, was unaffected.
Activation of the heme oxygenase 1 promoter by arsenite or cadmium and
activation of the cadmium-inducible metallothionein promoter also were
unaffected by the expression of mutant SWI-SNF components. Analysis of
a subset of constitutively expressed genes revealed no or minimal
effects on transcript levels. We propose that the requirement for
mammalian SWI-SNF complexes in gene activation events will be specific
to individual genes and signaling pathways.
*
Corresponding author. Mailing address: Department of
Cell Biology, University of Massachusetts Medical School, 55 Lake Ave. North, Worcester, MA 01655. Phone: (508) 856-1029. Fax: (508) 856-5612. E-mail: anthony.imbalzano{at}umassmed.edu.
Molecular and Cellular Biology, April 2000, p. 2839-2851, Vol. 20, No. 8
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
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