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J. Virol., Aug 1997, 5972-5981, Vol 71, No. 8
Copyright © 1997, American Society for Microbiology

VBP and RelA regulate avian leukosis virus long terminal repeat- enhanced transcription in B cells

SM Curristin, KJ Bird, RJ Tubbs and A Ruddell
Department of Microbiology and Immunology and Cancer Center, University of Rochester, School of Medicine and Dentistry, New York 14642, USA.

The avian leukosis virus (ALV) long terminal repeat (LTR) contains a compact transcription enhancer that is active in many cell types. A major feature of the enhancer is multiple CCAAT/enhancer element motifs that could be important for the strong transcriptional activity of this unit. The contributions of the three CCAAT/enhancer elements to LTR function were examined in B cells, as this cell type is targeted for ALV tumor induction following integration of LTR sequences next to the c-myc proto-oncogene. One CCAAT/enhancer element, termed a3, was found to be the most critical for LTR enhancement in transiently transfected B lymphoma cells, while in chicken embryo fibroblasts all three elements contributed equally to enhancement. Gel shift assays demonstrated that vitellogenin gene-binding protein (VBP), a member of the PAR subfamily of C/EBP factors, is a major component of the nuclear proteins binding to the a3 CCAAT/enhancer element. VBP activated transcription through the a3 CCAAT/enhancer element, supporting the idea that VBP is important for LTR enhancement in B cells. A member of the Rel family of proteins was also identified as a component of the a3 protein binding complex in B cells. Gel shift and immunoprecipitation assays indicated that this factor is RelA. Gel shift assays demonstrated that while RelA does not bind directly to the LTR CCAAT/enhancer elements, it does interact with VBP to potentiate VBP DNA binding activity. The synergistic interaction of VBP and RelA increased CCAAT/enhancer element-mediated transcription, indicating that both factors may be important for viral LTR regulation and also for expression of many cellular genes.

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