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Nucleic Acids Research 2005 33(20):6528-6539; doi:10.1093/nar/gki956
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Published online 28 November 2005

© The Author 2005. Published by Oxford University Press. All rights reserved
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions{at}oxfordjournals.org

Article

Activation of Sp1-mediated transcription by Rta of Epstein–Barr virus via an interaction with MCAF1

Li-Kwan Chang, Jian-Ying Chung1, Yi-Ren Hong, Takaya Ichimura2, Mitsuyoshi Nakao2 and Shih-Tung Liu1,*

Faculty of Biological Medicine and Environmental Biology and Graduate Institute of Biochemistry, Kaohsiung Medical University Kaohsiung, Taiwan 1Department of Microbiology and Immunology, Chang Gung University Taoyuan, Taiwan 2Department of Regeneration Medicine, Kumamoto University Kumamoto, Japan

*To whom correspondence should be addressed. Tel/Fax: +886 3211 8292; Email: cgliu{at}mail.cgu.edu.tw

Received September 28, 2005. Revised October 26, 2005. Accepted October 26, 2005.

Rta is a transcription factor encoded by BRLF1 of the Epstein–Barr virus (EBV). This factor is expressed during the immediate-early stage of the lytic cycle to activate the genes required for EBV lytic development. Although transcription activation by Rta is frequently associated with the binding of Rta to the Rta-response element (RRE) in promoters, Rta sometimes activates promoters without an RRE. Here we show that Rta interacts with an Sp1-interacting protein, MBD1-containing chromatin-associated factor 1 (MCAF1). This interaction is critical to the formation of an Sp1–MCAF1–Rta complex at Sp1 sites. Therefore, following lytic induction and the expression of Rta, Rta increases Sp1-mediated transcription. The genes that are thus activated include p16, p21, SNRPN and BRLF1. However, the binding of Rta to RRE prevents the interaction between Rta and MCAF1; therefore, transcription activation by RRE depends only on Rta, and not on MCAF1 or Sp1. Furthermore, this study finds that MCAF1 promotes the expression of Rta and Zta from EBV, indicating that MCAF1 participates EBV lytic activation. Our study documents the critical role of Rta in regulating the transcription of the genes that are mediated by Sp1.


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