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Originally published In Press as doi:10.1074/jbc.M205159200 on July 8, 2002

J. Biol. Chem., Vol. 277, Issue 37, 33818-33824, September 13, 2002
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The Myogenic Basic Helix-Loop-Helix Family of Transcription Factors Shows Similar Requirements for SWI/SNF Chromatin Remodeling Enzymes during Muscle Differentiation in Culture*

Kanaklata Roy, Ivana L. de la Serna, and Anthony N. ImbalzanoDagger

From the Department of Cell Biology, University of Massachusetts Medical School, Worcester, Massachusetts 01655

The myogenic basic helix-loop-helix family of transcription factors, MyoD, Myf5, myogenin, and MRF4, can each activate the muscle differentiation program when ectopically expressed in non-muscle cells. SWI/SNF complexes are ATP-dependent chromatin remodeling enzymes. We demonstrated previously that SWI/SNF enzymes promote MyoD-mediated muscle differentiation. To ascertain the requirement for SWI/SNF enzymes in muscle differentiation mediated by different MyoD family members, we examined MyoD, Myf5, MRF4, and myogenin-mediated induction of muscle differentiation in cells expressing dominant negative versions of BRG1 or BRM-based SWI/SNF enzymes. We demonstrated that expression of dominant negative BRG1 or BRM inhibited the induction of muscle-specific gene expression by Myf5 and MRF4; however, myogenin failed to induce measurable quantities of muscle-specific mRNAs, even in cells not expressing dominant negative SWI/SNF. In contrast, all four myogenic regulators induced expression of the cell cycle regulators p21, Rb, and cyclin D3 and promoted cell cycle arrest independently of the SWI/SNF enzymes. We proposed that SWI/SNF enzymes are required for the induction of all muscle-specific gene expression by MyoD, Myf5, and MRF4, whereas induction of the cell cycle regulators, p21, Rb, and cyclin D3 occurred independently of SWI/SNF function.

* This work was supported by National Institutes of Health Grant GM56244, by a Scholar Award from the Leukemia and Lymphoma Society (to A. N. I.), and by National Institutes of Health Fellowship GM20371 (to I. d. l. S.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Dagger To whom correspondence should be addressed: Dept. of Cell Biology, University of Massachusetts Medical School, 55 Lake Ave. N., Worcester, MA 01655. Tel.: 508-856-1029; Fax: 508-856-5612; E-mail: anthony.imbalzano@umassmed.edu.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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