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Molecular and Cellular Biology, October 2003, p. 6901-6908, Vol. 23, No. 19
0270-7306/03/$08.00+0     DOI: 10.1128/MCB.23.19.6901-6908.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

EBNA-1, a Bifunctional Transcriptional Activator

Gregory Kennedy1,2 and Bill Sugden1*

McArdle Laboratory for Cancer Research,1 Department of Surgery, University of Wisconsin—Madison, Madison, Wisconsin 537062

Received 27 April 2003/ Returned for modification 13 June 2003/ Accepted 22 June 2003

Transient-transfection assays have been used to identify transcription factors, and genetic analyses of these factors can allow a dissection of their mechanism of activation. Epstein-Barr nuclear antigen 1 (EBNA-1) has been shown to activate transcription from transfected templates, but its ability to activate transcription from nuclear templates has been controversial. We have established cells with integrated EBNA-1-responsive templates and have shown that EBNA-1 activates transcription from these chromatin-embedded templates dose dependently. A mutational analysis of EBNA-1 has identified a domain required for transcriptional activation of integrated templates, but not of transfected templates. The ability of EBNA-1 to activate transcription from both integrated and transfected templates can be inhibited by a derivative of EBNA-1 lacking the amino acids required for activation from integrated templates. EBNA-1's mode of activating transfected templates is therefore genetically distinct from that acting on integrated templates.

* Corresponding author. Mailing address: McArdle Laboratory for Cancer Research, University of Wisconsin—Madison Medical School, 1400 University Ave., Madison, WI 53706. Phone: (608) 262-6697. Fax: (608) 262-2824. E-mail: sugden{at}oncology.wisc.edu.

Molecular and Cellular Biology, October 2003, p. 6901-6908, Vol. 23, No. 19
0022-538X/03/$08.00+0     DOI: 10.1128/MCB.23.19.6901-6908.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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