ArticleMolecular and cellular biology2001
Coupling of mitotic chromosome tethering and replication competence in epstein-barr virus-based plasmids.
Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
57 citing papers in PubMed, 99 citations in OpenAlex.
- Article
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- Genetic elements promote retention of extrachromosomal DNA in cancer cells.bioRxiv : the preprint server for biology · 2025Article
- Modern biology of extrachromosomal DNA: A decade-long voyage of discovery.Cell research · 2025Review
- Epstein-Barr virus induces host shutoff extensively via BGLF5-independent mechanisms.Cell reports · 2024Article
- Article
- Broken chromosomes heading into mitosis: More than one way to patch a flat tire.The Journal of cell biology · 2024Review
- Review
- Adoptive T-cell therapy targeting Epstein-Barr virus as a treatment for multiple sclerosis.Clinical & translational immunology · 2023Review
- Functional diversity: update of the posttranslational modification of Epstein-Barr virus coding proteins.Cellular and molecular life sciences : CMLS · 2022Review
- A synthetic circuit for buffering gene dosage variation between individual mammalian cells.Nature communications · 2021Article
- Mechanisms driving acentric chromosome transmission.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2020Review
- Article
- Cross-species chromatin interactions drive transcriptional rewiring in Epstein-Barr virus-positive gastric adenocarcinoma.Nature genetics · 2020Article
- Review
- Extrachromosomal circular DNA-based amplification and transmission of herbicide resistance in crop weedProceedings of the National Academy of Sciences of the United States of America · 2018Article
- Epstein-Barr Virus (EBV)-Related Lymphoproliferative Disorders in Ataxia Telangiectasia: Does ATM Regulate EBV Life Cycle?Frontiers in immunology · 2018Review
- EBNA1-targeted inhibitors: Novel approaches for the treatment of Epstein-Barr virus-associated cancers.Theranostics · 2018Review
- Rebuilding Chromosomes After Catastrophe: Emerging Mechanisms of Chromothripsis.Trends in cell biology · 2017Review
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Epstein-Barr virus (EBV) replicates once per cell cycle and segregates with high efficiency yet does not encode the enzymes needed for DNA replication or the proteins required to contact mitotic spindles. The virus-encoded EBNA-1 (EBV nuclear antigen 1) and latent replication origin (oriP) are required for both replication and segregation. We developed a sensitive and specific fluorescent labeling strategy to analyze the interactions of both EBNA-1 with viral episomes and viral episomes with host chromosomes. This enabled investigation of the hypothesis that replication and chromosome tethering are linked through the EBNA-1 protein. We show that deleting EBNA-1 or oriP disrupts mitotic chromosome tethering but removing the dyad symmetry element of oriP does not. Microscopic and biochemical approaches demonstrated that an EBNA-1 mutant lacking residues 16 to 372 bound to oriP plasmids but did not support their mitotic chromosome association and that the mutant lost the ability of wild-type EBNA-1 to associate with interphase chromatin. Importantly, the transient-replication abilities of various mutant forms of EBV plasmids, including the mutant form with the EBNA-1 internal deletion, correlated directly with their chromosome-tethering abilities. These data lead us to propose that EBNA-1 recruits oriP-containing plasmids into chromatin subdomains in interphase nuclei to both engage the host replication machinery and enable the plasmids to adhere to host chromosomes to increase their segregation efficiency.
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Registered trials
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.