ArticleProceedings of the National Academy of Sciences of the United States of America1998
Segregation of viral plasmids depends on tethering to chromosomes and is regulated by phosphorylation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.
What it found
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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
90 citing papers in PubMed, 184 citations in OpenAlex.
- Article
- Genetic elements promote retention of extrachromosomal DNA in cancer cells.bioRxiv : the preprint server for biology · 2025Article
- E2 Tyrosine 102 Regulates MmuPV1 Pathogenesis In Vivo.Pathogens (Basel, Switzerland) · 2025Article
- Enhancer-promoter activation by the Kaposi sarcoma-associated herpesvirus episome maintenance protein LANA.Cell reports · 2024Article
- BRD4 as a potential target for human papillomaviruses associated cancer.Journal of medical virology · 2023Review
- HPV and the Risk of HIV Acquisition in Women.Frontiers in cellular and infection microbiology · 2022Review
- Mechanisms of persistence by small DNA tumor viruses.Current opinion in virology · 2018Review
- Article
- Metabolism and function of hepatitis B virus cccDNA: Implications for the development of cccDNA-targeting antiviral therapeutics.Antiviral research · 2015Review
- Kaposi's sarcoma-associated herpesvirus LANA recruits the DNA polymerase clamp loader to mediate efficient replication and virus persistence.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Manipulation of cellular DNA damage repair machinery facilitates propagation of human papillomaviruses.Seminars in cancer biology · 2014Review
- Papillomavirus genomes associate with BRD4 to replicate at fragile sites in the host genome.PLoS pathogens · 2014Article
- Phosphorylation of HPV-16 E2 at serine 243 enables binding to Brd4 and mitotic chromosomes.PloS one · 2014Article
- The papillomavirus E2 proteins.Virology · 2013Review
- Current understanding of the role of the Brd4 protein in the papillomavirus lifecycle.Viruses · 2013Review
- Co-segregation of yeast plasmid sisters under monopolin-directed mitosis suggests association of plasmid sisters with sister chromatids.Nucleic acids research · 2013Article
- Analysis of the papillomavirus E2 and bromodomain protein Brd4 interaction using bimolecular fluorescence complementation.PloS one · 2013Article
- Crystal structure of the gamma-2 herpesvirus LANA DNA binding domain identifies charged surface residues which impact viral latency.PLoS pathogens · 2013Article
- Characterization of nucleosome positioning in hepadnaviral covalently closed circular DNA minichromosomes.Journal of virology · 2012Article
- Small molecule inhibitors of human papillomavirus protein - protein interactions.The open virology journal · 2011Article
30 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Eukaryotic viruses can maintain latency in dividing cells as extrachromosomal nuclear plasmids. Segregation and nuclear retention of DNA is, therefore, a key issue in retaining copy number. The E2 enhancer protein of the papillomaviruses is required for viral DNA replication and transcription. Viral mutants that prevent phosphorylation of the bovine papillomavirus type 1 (BPV) E2 protein are transformation-defective, despite normal viral gene expression and replication function. Cell colonies harboring such mutants show sectoring of viral DNA and are unable to maintain the episome. We find that transforming viral DNA attaches to mitotic chromosomes, in contrast to the mutant genome encoding the E2 phosphorylation mutant. Second-site suppressor mutations were uncovered in both E1 and E2 genes that allow for transformation, maintenance, and chromosomal attachment. E2 protein was also found to colocalize to mitotic chromosomes, whereas the mutant did not, suggesting a direct role for E2 in viral attachment to chromosomes. Such viral hitch-hiking onto cellular chromosomes is likely to provide a general mechanism for maintaining nuclear plasmids.
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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.