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Originally published In Press as doi:10.1074/jbc.M100836200 on April 6, 2001
J. Biol. Chem., Vol. 276, Issue 24, 21325-21330, June 15, 2001
Transcriptional Activation by a Matrix Associating
Region-binding Protein
CONTEXTUAL REQUIREMENTS FOR THE FUNCTION OF BRIGHT*
Mark H.
Kaplan §,
Rui-Ting
Zong ,
Richard F.
Herrscher ,
Richard H.
Scheuermann¶, and
Philip W.
Tucker
From the Institute for Molecular and Cellular
Biology, University of Texas at Austin, Austin, Texas 78712-1075 and the ¶ Department of Pathology, University of Texas
Southwestern Medical Center, Dallas, Texas 75235
Bright (B cell regulator
of IgH transcription) is a B cell-specific,
matrix associating region-binding protein that transactivates gene expression from the IgH intronic enhancer (Eµ). We show here that Bright has multiple contextual requirements to function as a
transcriptional activator. Bright cannot transactivate via out of
context, concatenated binding sites. Transactivation is maximal on
integrated substrates. Two of the three previously identified binding
sites in Eµ are required for full Bright transactivation. The Bright
DNA binding domain defined a new family, which includes SWI1, a
component of the SWI·SNF complex shown to have high mobility group-like DNA binding characteristics. Similar to one group of high mobility group box proteins, Bright distorts Eµ binding
site-containing DNA on binding, supporting the concept that it mediates
Eµ remodeling. Transfection studies further implicate Bright in
facilitating spatially separated promoter-enhancer interactions in both
transient and stable assays. Finally, we show that overexpression of
Bright leads to enhanced DNase I sensitivity of the endogenous Eµ
matrix associating regions. These data further suggest that Bright may contribute to increased gene expression by remodeling the
immunoglobulin locus during B cell development.
*
This work was supported by National Institutes of Health
Grants AI18016 and CA31534 (to P. W. T.) and GM50329 (to R. H. 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.
§
Present address: Dept. of Immunology and Microbiology and the
Walther Oncology Center, Indiana University School of Medicine, Indianapolis, IN 46202.
To whom correspondence should be addressed: Inst. for
Molecular and Cellular Biology, University of Texas at Austin, 100 W 24th St., ESB-534, Austin, TX 78712-1095. Tel.: 512-475-7705; Fax:
512-475-7707; E-mail: philtucker@mail.utexas.edu.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.

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Copyright © 2001 by the American Society for Biochemistry and Molecular Biology.
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