HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

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

This Article Full Text Full Text (PDF) All Versions of this Article: 279/52/54817    most recent M405911200v1 Submit a Letter to Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Daikoku, T. Articles by Tsurumi, T. Search for Related Content PubMed PubMed Citation Articles by Daikoku, T. Articles by Tsurumi, T. Social Bookmarking                      What's this?

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.

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				A. Kudoh, S. Iwahori, Y. Sato, S. Nakayama, H. Isomura, T. Murata, and T. Tsurumi Homologous Recombinational Repair Factors Are Recruited and Loaded onto the Viral DNA Genome in Epstein-Barr Virus Replication Compartments J. Virol., July 1, 2009; 83(13): 6641 - 6651. [Abstract] [Full Text] [PDF]

				J. Zhu, G. Liao, L. Shan, J. Zhang, M.-R. Chen, G. S. Hayward, S. D. Hayward, P. Desai, and H. Zhu Protein Array Identification of Substrates of the Epstein-Barr Virus Protein Kinase BGLF4 J. Virol., May 15, 2009; 83(10): 5219 - 5231. [Abstract] [Full Text] [PDF]

				T. Murata, Y. Sato, S. Nakayama, A. Kudoh, S. Iwahori, H. Isomura, M. Tajima, T. Hishiki, T. Ohshima, M. Hijikata, et al. TORC2, a Coactivator of cAMP-response Element-binding Protein, Promotes Epstein-Barr Virus Reactivation from Latency through Interaction with Viral BZLF1 Protein J. Biol. Chem., March 20, 2009; 284(12): 8033 - 8041. [Abstract] [Full Text] [PDF]

				Z. Qian, B. Xuan, T. T. Hong, and D. Yu The Full-Length Protein Encoded by Human Cytomegalovirus Gene UL117 Is Required for the Proper Maturation of Viral Replication Compartments J. Virol., April 1, 2008; 82(7): 3452 - 3465. [Abstract] [Full Text] [PDF]

				T. Kanda, M. Kamiya, S. Maruo, D. Iwakiri, and K. Takada Symmetrical localization of extrachromosomally replicating viral genomes on sister chromatids J. Cell Sci., May 1, 2007; 120(9): 1529 - 1539. [Abstract] [Full Text] [PDF]

				A. Kudoh, T. Daikoku, Y. Ishimi, Y. Kawaguchi, N. Shirata, S. Iwahori, H. Isomura, and T. Tsurumi Phosphorylation of MCM4 at Sites Inactivating DNA Helicase Activity of the MCM4-MCM6-MCM7 Complex during Epstein-Barr Virus Productive Replication. J. Virol., October 1, 2006; 80(20): 10064 - 10072. [Abstract] [Full Text] [PDF]

				T. Daikoku, A. Kudoh, Y. Sugaya, S. Iwahori, N. Shirata, H. Isomura, and T. Tsurumi Postreplicative Mismatch Repair Factors Are Recruited to Epstein-Barr Virus Replication Compartments J. Biol. Chem., April 21, 2006; 281(16): 11422 - 11430. [Abstract] [Full Text] [PDF]

				N. Shirata, A. Kudoh, T. Daikoku, Y. Tatsumi, M. Fujita, T. Kiyono, Y. Sugaya, H. Isomura, K. Ishizaki, and T. Tsurumi Activation of Ataxia Telangiectasia-mutated DNA Damage Checkpoint Signal Transduction Elicited by Herpes Simplex Virus Infection J. Biol. Chem., August 26, 2005; 280(34): 30336 - 30341. [Abstract] [Full Text] [PDF]

				P. Kapoor, B. D. Lavoie, and L. Frappier EBP2 Plays a Key Role in Epstein-Barr Virus Mitotic Segregation and Is Regulated by Aurora Family Kinases Mol. Cell. Biol., June 15, 2005; 25(12): 4934 - 4945. [Abstract] [Full Text] [PDF]