QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

First published online 3 April 2007
doi: 10.1242/jcs.03434

This Article Figures Only Full Text Full Text (PDF) Supplementary Material All Versions of this Article: jcs.03434v1 120/9/1529    most recent Alert me when this article is cited Alert me if a correction is posted 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 Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kanda, T. Articles by Takada, K. Search for Related Content PubMed PubMed Citation Articles by Kanda, T. Articles by Takada, K. Social Bookmarking                         What's this?

Symmetrical localization of extrachromosomally replicating viral genomes on sister chromatids

¹ Center for Virus Vector Development, Institute for Genetic Medicine, Hokkaido University, Sapporo 060-0815, Japan
² Department of Tumor Virology, Institute for Genetic Medicine, Hokkaido University, Sapporo 060-0815, Japan

^* Author for correspondence (e-mail: tkanda{at}igm.hokudai.ac.jp)

Accepted 27 February 2007

In eukaryotes, many latent viruses replicate as extrachromosomal molecules, called episomes, and efficiently segregate to daughter cells by noncovalently attaching to mitotic chromosomes. To understand the mechanism governing the processes, we analyzed the detailed subcellular localization of Epstein-Barr virus (EBV) genomes and a viral protein EBNA1, a bridging molecule between viral genomes and cellular chromatin. In the cells that were infected with a recombinant EBV expressing epitope-tagged EBNA1, EBNA1 localized to intranuclear punctate dots, which coincided with the localization of EBV genomes as revealed by fluorescence in situ hybridization (FISH). A significant number of EBNA1 dots were found to localize symmetrically on sister chromatids of mitotic chromosomes. Such symmetrical localization of EBNA1 dots was observed in prematurely condensed G2 chromosomes as well, correlating with the presence of closely spaced double dots of EBNA1 in G2-phase-enriched cells. The EBNA1 double dots were occasionally interconnected by the FISH signals of EBV episomes, exhibiting a dumbbell-like appearance. Thus, we propose that the partitioning of EBNA1 molecules onto sister chromatids during cellular DNA replication underlies the non-stochastic segregation of extrachromosomally replicating viral genomes.

Key words: Epstein-Barr virus, Episome, EBNA1, Segregation, Sister chromatid

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

This article has been cited by other articles:

				K. M Feeney and J. L Parish Targeting mitotic chromosomes: a conserved mechanism to ensure viral genome persistence Proc R Soc B, May 7, 2009; 276(1662): 1535 - 1544. [Abstract] [Full Text] [PDF]

				H. Cui, S. K. Ghosh, and M. Jayaram The selfish yeast plasmid uses the nuclear motor Kip1p but not Cin8p for its localization and equal segregation J. Cell Biol., April 20, 2009; 185(2): 251 - 264. [Abstract] [Full Text] [PDF]