ArticleJournal of virology2000
Initiation of DNA replication within oriP is dispensable for stable replication of the latent Epstein-Barr virus chromosome after infection of established cell lines.
Article in Journal of virology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed.
- Episomes and Transposases-Utilities to Maintain Transgene Expression from Nonviral Vectors.Genes · 2022Review
- Control of Viral Latency by Episome Maintenance Proteins.Trends in microbiology · 2020Review
- Hitchhiking of Viral Genomes on Cellular Chromosomes.Annual review of virology · 2019Review
- Review
- Bacterial artificial chromosomes establish replication timing and sub-nuclear compartment de novo as extra-chromosomal vectors.Nucleic acids research · 2018Article
- Efficient replication of Epstein-Barr virus-derived plasmids requires tethering by EBNA1 to host chromosomes.Journal of virology · 2013Article
- Keeping it quiet: chromatin control of gammaherpesvirus latency.Nature reviews. Microbiology · 2013Review
- Timeless-dependent DNA replication-coupled recombination promotes Kaposi's Sarcoma-associated herpesvirus episome maintenance and terminal repeat stability.Journal of virology · 2013Article
- Replication of Epstein-Barr viral DNA.Cold Spring Harbor perspectives in biology · 2013Review
- The latency-associated nuclear antigen, a multifunctional protein central to Kaposi's sarcoma-associated herpesvirus latency.Future microbiology · 2011Review
- The replisome pausing factor Timeless is required for episomal maintenance of latent Epstein-Barr virus.Journal of virology · 2011Article
- The dyad symmetry element of Epstein-Barr virus is a dominant but dispensable replication origin.PloS one · 2011Article
- The latent origin of replication of Epstein-Barr virus directs viral genomes to active regions of the nucleus.Journal of virology · 2010Article
- The microRNAs of Epstein-Barr Virus are expressed at dramatically differing levels among cell lines.Virology · 2009Article
- Identifying a property of origins of DNA synthesis required to support plasmids stably in human cells.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Review
- The minimal replicator element of the Kaposi's sarcoma-associated herpesvirus terminal repeat supports replication in a semiconservative and cell-cycle-dependent manner.Journal of virology · 2007Article
- Cell cycle regulation of chromatin at an origin of DNA replication.The EMBO journal · 2005Article
- In search of the holy replicator.Nature reviews. Molecular cell biology · 2004Review
- Plasticity of DNA replication initiation in Epstein-Barr virus episomes.PLoS biology · 2004Article
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3 authors.
Funding
Abstract
The 165-kb circularized chromosome of Epstein-Barr virus (EBV) is replicated in latently infected cells once per cell cycle by host proteins during S phase. Replication initiates at multiple sites on latent EBV chromosomes, including within a 1.8-kb region called oriP, which can provide both replication and stabilization for recombinant plasmids in the presence of the EBV-encoded protein, EBNA-1. Replication initiates at or near the dyad symmetry component (DS) of oriP, which depends on multiple EBNA-1 binding sites for activity. To test the importance of the replication function of oriP, the DS was deleted from the viral genome. EBV mutants lacking the DS and carrying a selectable gene could establish latent infections in BL30 cells, in which circular, mutant viral chromosomes were stably maintained. Analysis of replication fork movement using two-dimensional gel electrophoresis showed that the deletion of the DS reduced the initiation events to an undetectable level within the oriP region so that this segment was replicated exclusively by forks entering the region from either direction. A significant slowing or stalling of replication forks that occurs normally at the approximate position of the DS was also eliminated by deletion of the DS. The results confirm the DS as both a replication origin and a place where replication forks pause. Since the replication function of oriP is dispensable at least in certain cell lines, the essential role of EBNA-1 for infection of these cell lines is likely to be that of stabilizing the EBV chromosome by associating with the 30-bp repeats of oriP. The results also imply that in established cell lines, the EBV chromosome can be efficiently replicated entirely from origins that are activated by cellular factors. Presumably, initiation of replication at the DS, mediated by EBNA-1, is important for the natural life cycle of EBV, perhaps in establishing latent infections of normal B cells.
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