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Targeting mitotic chromosomes : a conserved mechanism to ensure viral genome persistence
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dc.contributor.author | Feeney, Katherine Martha | |
dc.contributor.author | Parish, Joanna Louise | |
dc.date.accessioned | 2012-03-27T23:28:52Z | |
dc.date.available | 2012-03-27T23:28:52Z | |
dc.date.issued | 2009-05-07 | |
dc.identifier | 427169 | |
dc.identifier | 7918890c-11d9-4bb4-bcb5-9f15562b8151 | |
dc.identifier | 000264445000001 | |
dc.identifier | 66349129914 | |
dc.identifier.citation | Feeney , K M & Parish , J L 2009 , ' Targeting mitotic chromosomes : a conserved mechanism to ensure viral genome persistence ' , Proceedings of the Royal Society B: Biological Sciences , vol. 276 , no. 1662 , pp. 1535-1544 . https://doi.org/10.1098/rspb.2008.1642 | en |
dc.identifier.issn | 0962-8452 | |
dc.identifier.uri | https://hdl.handle.net/10023/2472 | |
dc.description.abstract | Viruses that maintain their genomes as extrachromosomal circular DNA molecules and establish infection in actively dividing cells must ensure retention of their genomes within the nuclear envelope in order to prevent genome loss. The loss of nuclear membrane integrity during mitosis dictates that paired host cell chromosomes are captured and organized by the mitotic spindle apparatus before segregation to daughter cells. This prevents inaccurate chromosomal segregation and loss of genetic material. A similar mechanism may also exist for the nuclear retention of extrachromosomal viral genomes or episomes during mitosis, particularly for genomes maintained at a low copy number in latent infections. It has been heavily debated whether such a mechanism exists and to what extent this mechanism is conserved among diverse viruses. Research over the last two decades has provided a wealth of information regarding the mechanisms by which specific tumour viruses evade mitotic and DNA damage checkpoints. Here, we discuss the similarities and differences in how specific viruses tether episomal genomes to host cell chromosomes during mitosis to ensure long-term persistence. | |
dc.format.extent | 10 | |
dc.format.extent | 350331 | |
dc.language.iso | eng | |
dc.relation.ispartof | Proceedings of the Royal Society B: Biological Sciences | en |
dc.subject | Viral persistence | en |
dc.subject | Segregation | en |
dc.subject | DNA tumour virus | en |
dc.subject | Genome | en |
dc.subject | Mitosis | en |
dc.subject | Sarcoma-associated herpesvirus | en |
dc.subject | Epstein-Barr-virus | en |
dc.subject | Papillomavirus E2 protein | en |
dc.subject | Nuclear antigen lana | en |
dc.subject | Latent DNA-replication | en |
dc.subject | Kaposis-sarcoma | en |
dc.subject | Transcriptional activation | en |
dc.subject | Terminal repeats | en |
dc.subject | Mammalian-cells | en |
dc.subject | Murine gammaherpesvirus-68 | en |
dc.subject | QH426 Genetics | en |
dc.subject.lcc | QH426 | en |
dc.title | Targeting mitotic chromosomes : a conserved mechanism to ensure viral genome persistence | en |
dc.type | Journal article | en |
dc.contributor.sponsor | The Royal Society | en |
dc.contributor.institution | University of St Andrews. School of Medicine | en |
dc.contributor.institution | University of St Andrews. Biomedical Sciences Research Complex | en |
dc.identifier.doi | https://doi.org/10.1098/rspb.2008.1642 | |
dc.description.status | Peer reviewed | en |
dc.identifier.url | http://www.scopus.com/inward/record.url?scp=66349129914&partnerID=8YFLogxK | en |
dc.identifier.grantnumber | 516002.K | en |
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