ArticleProceedings of the National Academy of Sciences of the United States of America2008
Identifying a property of origins of DNA synthesis required to support plasmids stably in human cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Control of Viral Latency by Episome Maintenance Proteins.Trends in microbiology · 2020Review
- Plasmid Partitioning by Human Tumor Viruses.Journal of virology · 2018Review
- Kaposi's sarcoma-associated herpesvirus stably clusters its genomes across generations to maintain itself extrachromosomally.The Journal of cell biology · 2017Article
- Identification of properties of the Kaposi's sarcoma-associated herpesvirus latent origin of replication that are essential for the efficient establishment and maintenance of intact plasmids.Journal of virology · 2014Article
- Efficient replication of Epstein-Barr virus-derived plasmids requires tethering by EBNA1 to host chromosomes.Journal of virology · 2013Article
- Replication of Epstein-Barr viral DNA.Cold Spring Harbor perspectives in biology · 2013Review
- The dyad symmetry element of Epstein-Barr virus is a dominant but dispensable replication origin.PloS one · 2011Article
- Telomeric repeat mutagenicity in human somatic cells is modulated by repeat orientation and G-quadruplex stability.DNA repair · 2010Article
- Phosphorylation sites of Epstein-Barr virus EBNA1 regulate its function.The Journal of general virology · 2009Article
- The microRNAs of Epstein-Barr Virus are expressed at dramatically differing levels among cell lines.Virology · 2009Article
- Identifying sites bound by Epstein-Barr virus nuclear antigen 1 (EBNA1) in the human genome: defining a position-weighted matrix to predict sites bound by EBNA1 in viral genomes.Journal of virology · 2009Article
- Epstein-Barr Nuclear Antigen 1 modulates replication of oriP-plasmids by impeding replication and transcription fork migration through the family of repeats.Virology journal · 2009Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The plasmid origin of replication, oriP, of Epstein-Barr Virus (EBV) was identified in an assay to detect autonomously replicating sequences (ARSs) in human cells. Raji ori, a second origin in EBV, functions in vivo but fails in long-term ARS assays. We examined the initiating element, DS, within oriP and Raji ori to resolve this paradox. DS, but not Raji ori, binds EBNA1; whereas both act as ARSs in short-term assays, with DS being more efficient, only DS can act as an ARS in long-term assays. Surprisingly, we found that DS supported the establishment of a plasmid with Raji ori in cis and that after deletion of DS, Raji ori could now act as an ARS in the long term. This finding explains the frequent failure of ARS assays in mammalian cells. More origins can initially act as ARSs than can be established. We identified one requirement for ARSs to be established: They must function efficiently enough initially to generate a wide distribution of numbers of plasmids per cell. Only the cells that have more than a threshold number of plasmids can survive selections imposed on the cells to retain these replicons.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.