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The Epstein-Barr virus nuclear antigen-1 reprograms transcription by mimicry of high mobility group A proteins
Department of Cell and Molecular Biology, Karolinska Institutet, 17177 Stockholm, Sweden.
Department of Cell and Molecular Biology, Karolinska Institutet, 17177 Stockholm, Sweden.
Department of Cell and Molecular Biology, Karolinska Institutet, 17177 Stockholm, Sweden.
Department of Biostatistics, Harvard School of Public Health, Boston, MA 02115, USA.
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2013 (English)In: Nucleic Acids Research, ISSN 0305-1048, E-ISSN 1362-4962, Vol. 41, no 5, 2950-2962 p.Article in journal (Refereed) Published
Abstract [en]

Viral proteins reprogram their host cells by hijacking regulatory components of protein networks. Here we describe a novel property of the Epstein-Barr virus (EBV) nuclear antigen-1 (EBNA1) that may underlie the capacity of the virus to promote a global remodeling of chromatin architecture and cellular transcription. We found that the expression of EBNA1 in transfected human and mouse cells is associated with decreased prevalence of heterochromatin foci, enhanced accessibility of cellular DNA to micrococcal nuclease digestion and decreased average length of nucleosome repeats, suggesting de-protection of the nucleosome linker regions. This is a direct effect of EBNA1 because targeting the viral protein to heterochromatin promotes large-scale chromatin decondensation with slow kinetics and independent of the recruitment of adenosine triphosphate-dependent chromatin remodelers. The remodeling function is mediated by a bipartite Gly-Arg rich domain of EBNA1 that resembles the AT-hook of High Mobility Group A (HMGA) architectural transcription factors. Similar to HMGAs, EBNA1 is highly mobile in interphase nuclei and promotes the mobility of linker histone H1, which counteracts chromatin condensation and alters the transcription of numerous cellular genes. Thus, by regulating chromatin compaction, EBNA1 may reset cellular transcription during infection and prime the infected cells for malignant transformation.

Place, publisher, year, edition, pages
2013. Vol. 41, no 5, 2950-2962 p.
National Category
Medical and Health Sciences
URN: urn:nbn:se:uu:diva-197881DOI: 10.1093/nar/gkt032ISI: 000318062600021PubMedID: 23358825OAI: oai:DiVA.org:uu-197881DiVA: diva2:614652
Available from: 2013-04-05 Created: 2013-04-05 Last updated: 2014-02-19Bibliographically approved

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Caja Puigsubira, LaiaMoustakas, Aristidis
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