Regulation of avian leukosis virus long terminal repeat-enhanced transcription by C/EBP-Rel interactions

The avian leukosis and sarcoma virus long terminal repeat (LTR) enhancers feature directly repeated CCAAT/enhancer element sequences which are also found in many viral and cellular gene enhancers. While most members of the CCAAT/enhancer element-binding protein (C/EBP) transcription factor family ex...

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Published inJournal of Virology Vol. 70; no. 5; pp. 3051 - 3059
Main Authors Bowers, W.J. (University of Rochester, Rochester, NY.), Baglia, L.A, Ruddell, A
Format Journal Article
LanguageEnglish
Published United States American Society for Microbiology 01.05.1996
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Summary:The avian leukosis and sarcoma virus long terminal repeat (LTR) enhancers feature directly repeated CCAAT/enhancer element sequences which are also found in many viral and cellular gene enhancers. While most members of the CCAAT/enhancer element-binding protein (C/EBP) transcription factor family exhibit tissue-restricted expression, there may be ubiquitously expressed C/EBP-like factors that regulate widespread CCAAT/enhancer element-driven transcription. An avian C/EBP-related factor designated A1/EBP was previously shown to bind CCAAT/enhancer elements within the avian leukosis virus (ALV) and Rous sarcoma virus (RSV) LTR enhancers in a pattern identical to that of a B-cell LTR-binding factor (W. J. Bowers and A. Ruddell, J. Virol. 66:6578-6586, 1992). An A1/EBP-specific antiserum recognizes a 40-kDa LTR CCAAT/enhancer element-binding protein purified from avian B lymphoma cells. A1/EBP is widely expressed at the mRNA and protein levels, suggesting that this protein could be important not only in regulating widespread expression of the ALV and RSV retroviruses but also in controlling the expression of other viral and cellular gene enhancers that possess CCAAT/enhancer motifs. We also found that an NF-kappaB/Rel-related protein is a component of the LTR CCAAT/enhancer element binding complex through its interaction with A1/EBP. At least one of the NF-kappaB family members, p65 (RelA), is capable of activating LTR CCAAT/enhancer element-driven transcription. These findings suggest a role for Rel-related factors in the regulation of ALV or RSV LTR-driven transcription via an interaction with A1/EBP
Bibliography:9612999
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ISSN:0022-538X
1098-5514
DOI:10.1128/jvi.70.5.3051-3059.1996