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Nucleic Acids Research, 1995, Vol. 23, No. 24 4939-4945
© 1995


Articles

RBP-Jkrepression activity is mediated by a co-repressor and antagonized by the Epstein-Barr virus transcription factor EBNA2

L. Waltzer, P.Y. Bourillot, A. Sergeant and E. Manet*

Unit de Virologie Humaine, ENS-INSERM U412, Ecole Normale Supeèrieure de Lyon 46 Alleèe d'Italie, 69364 Lyon Cedex 07, France

*To whom correspondence should be addressed

Received October 10, 1995. Accepted November 13, 1995.

The Epstein-Barr virus (EBV) protein EBNA2 is a transcriptional activator that can be targeted to its DN A responsive elements by direct interaction with the cellular protein RBP-Jk. RBP-Jk is a ubiquitous factor, highly conserved between man, mouse and Drosophila, whose function In mammalian cells is largely unknown. Here we provide evidence that RBP-Jk IS a transcriptional repressor and, more importantly, that RBP-Jk repression is mediated by a co-repressor. The function of the co-repressor could be counterbalanced by making a fusion protein (RBPVP16) between RBP-Jk and the VP16 activation domain. This RBP-VP16-mediated activation could be strongly increased by an EBNA2 protein deprived of its activation domain, but not by an EBNA2 protein incapable of making physical contact with RBP-Jk. Our results suggest that EBNA2 activates transcription by both interfering with the function of a co-repressor recruited by RBP-Jk and providing an activation domain.


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