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Molecular and Cellular Biology, June 2006, p. 4758-4768, Vol. 26, No. 12
0270-7306/06/$08.00+0     doi:10.1128/MCB.02009-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Induction of Immunoglobulin Heavy-Chain Transcription through the Transcription Factor Bright Requires TFII-I

Jaya Rajaiya,1 Jamee C. Nixon,1 Neil Ayers,1 Zana P. Desgranges,2 Ananda L. Roy,2 and Carol F. Webb1,3*

Oklahoma Medical Research Foundation, Immunobiology and Cancer Research Program,1 University of Oklahoma Health Sciences Center, Departments of Microbiology and Immunology and Cell Biology, Oklahoma City, Oklahoma 73104,3 Tufts University School of Medicine, Departments of Pathology and Biochemistry, Programs in Immunology and Genetics, Boston, Massachusetts 021112

Received 14 October 2005/ Returned for modification 30 November 2005/ Accepted 1 April 2006

Bright/ARID3a/Dril1, a member of the ARID family of transcription factors, is expressed in a highly regulated fashion in B lymphocytes, where it enhances immunoglobulin transcription three- to sixfold. Recent publications from our lab indicated that functional, but not kinase-inactive, Bruton's tyrosine kinase (Btk) is critical for Bright activity in an in vitro model system, yet Bright itself is not appreciably tyrosine phosphorylated. These data suggested that a third protein, and Btk substrate, must contribute to Bright-enhanced immunoglobulin transcription. The ubiquitously expressed transcription factor TFII-I was identified as a substrate for Btk several years ago. In this work, we show that TFII-I directly interacts with human Bright through amino acids in Bright's protein interaction domain and that specific tyrosine residues of TFII-I are essential for Bright-induced activity of an immunoglobulin reporter gene. Moreover, inhibition of TFII-I function in a B-cell line resulted in decreased heavy-chain transcript levels. These data suggest that Bright functions as a three-component protein complex in the immunoglobulin locus and tie together previous data indicating important roles for Btk and TFII-I in B lymphocytes.

* Corresponding author. Mailing address: Oklahoma Medical Research Foundation, Immunobiology and Cancer Research Program, 825 N. E. 13th Street, Oklahoma City, OK 73104. Phone: (405) 271-7564. Fax: (405) 271-7128. E-mail: carol-webb{at}omrf.ouhsc.edu.

Molecular and Cellular Biology, June 2006, p. 4758-4768, Vol. 26, No. 12
0270-7306/06/$08.00+0     doi:10.1128/MCB.02009-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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