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J. Biol. Chem., Vol. 279, Issue 52, 54817-54825, December 24, 2004

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In Vivo Dynamics of EBNA1-oriP Interaction during Latent and Lytic Replication of Epstein-Barr Virus^*

Tohru Daikoku, Ayumi Kudoh, Masatoshi Fujita¶, Yutaka Sugaya, Hiroki Isomura, and Tatsuya Tsurumi||

From the Division of Virology, Aichi Cancer Center Research Institute, 1-1 Kanokoden, Chikusa-ku, Nagoya 464-8681, Japan and the ^¶Virology Division, National Cancer Center, Chuo-ku, Tokyo 104-0045, Japan

The Epstein-Barr virus (EBV) nuclear antigen 1 (EBNA1) is required for maintenance of the viral genome DNA during the latent phase of EBV replication but continues to be synthesized after the induction of viral productive replication. An EBV genome-wide chromatin immunoprecipitation assay revealed that EBNA1 constantly binds to oriP of the EBV genome during not only latent but also lytic infection. Although the total levels of EBNA1 proved constant throughout the latter, the levels of the oriP-bound form were increased as lytic infection proceeded. EBV productive DNA replication occurs at discrete sites in nuclei, called replication compartments, where viral replication proteins are clustered. Confocal laser microscopic analyses revealed that whereas EBNA1 was distributed broadly in nuclei as fine punctate dots during the latent phase of infection, the protein became redistributed to the viral replication compartments and localized as distinct spots within and/or nearby the compartments after the induction of lytic replication. Taking these findings into consideration, oriP regions of the EBV genome might be organized by EBNA1 into replication domains that may set up scaffolding for lytic replication and transcription.

Received for publication, May 27, 2004 , and in revised form, September 7, 2004.

^* This work was supported by Grants-in-aid for Scientific Research on Priority Areas from the Ministry of Education, Science, Sports, Culture, and Technology of Japan 16017322 and 15390153 (to T. T.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Both of these authors contributed equally to this work.

^|| To whom correspondence should be addressed. Tel.: 81-52-764-2979; Fax: 81-52-764-2979; E-mail: ttsurumi{at}aichi-cc.jp.

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