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BIM promoter directly targeted by EBNA3C in polycomb-mediated repression by EBV.
Nucleic Acids Res. 2012 Aug; 40(15):7233-46.NA

Abstract

Detailed analyses of the chromatin around the BIM promoter has revealed that latent Epstein-Barr virus (EBV) triggers the recruitment of polycomb repressive complex 2 (PRC2) core subunits and the trimethylation of histone H3 lysine 27 (H3K27me3) at this locus. The recruitment is absolutely dependent on nuclear proteins EBNA3A and EBNA3C; what is more, epitope-tagged EBNA3C could be shown bound near the transcription start site (TSS). EBV induces no consistent changes in the steady-state expression of PRC2 components, but lentivirus delivery of shRNAs against PRC2 and PRC1 subunits disrupted EBV repression of BIM. The activation mark H3K4me3 is largely unaltered at this locus irrespective of H3K27me3 status, suggesting the establishment of a 'bivalent' chromatin domain. Consistent with the 'poised' nature of these domains, RNA polymerase II (Pol II) occupancy was not altered by EBV at the BIM TSS, but analysis of phospho-serine 5 on Pol II indicated that EBNA3A and EBNA3C together inhibit initiation of BIM transcripts. B cell lines carrying EBV encoding a conditional EBNA3C-oestrogen receptor-fusion revealed that this epigenetic repression of BIM was reversible, but took more than 3 weeks from when EBNA3C was inactivated.

Authors+Show Affiliations

Section of Virology, Faculty of Medicine, Imperial College London, Norfolk Place, London W2 1PG, UK.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22584624

Citation

Paschos, Kostas, et al. "BIM Promoter Directly Targeted By EBNA3C in Polycomb-mediated Repression By EBV." Nucleic Acids Research, vol. 40, no. 15, 2012, pp. 7233-46.
Paschos K, Parker GA, Watanatanasup E, et al. BIM promoter directly targeted by EBNA3C in polycomb-mediated repression by EBV. Nucleic Acids Res. 2012;40(15):7233-46.
Paschos, K., Parker, G. A., Watanatanasup, E., White, R. E., & Allday, M. J. (2012). BIM promoter directly targeted by EBNA3C in polycomb-mediated repression by EBV. Nucleic Acids Research, 40(15), 7233-46. https://doi.org/10.1093/nar/gks391
Paschos K, et al. BIM Promoter Directly Targeted By EBNA3C in Polycomb-mediated Repression By EBV. Nucleic Acids Res. 2012;40(15):7233-46. PubMed PMID: 22584624.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - BIM promoter directly targeted by EBNA3C in polycomb-mediated repression by EBV. AU - Paschos,Kostas, AU - Parker,Gillian A, AU - Watanatanasup,Ekularn, AU - White,Robert E, AU - Allday,Martin J, Y1 - 2012/05/14/ PY - 2012/5/16/entrez PY - 2012/5/16/pubmed PY - 2012/11/9/medline SP - 7233 EP - 46 JF - Nucleic acids research JO - Nucleic Acids Res. VL - 40 IS - 15 N2 - Detailed analyses of the chromatin around the BIM promoter has revealed that latent Epstein-Barr virus (EBV) triggers the recruitment of polycomb repressive complex 2 (PRC2) core subunits and the trimethylation of histone H3 lysine 27 (H3K27me3) at this locus. The recruitment is absolutely dependent on nuclear proteins EBNA3A and EBNA3C; what is more, epitope-tagged EBNA3C could be shown bound near the transcription start site (TSS). EBV induces no consistent changes in the steady-state expression of PRC2 components, but lentivirus delivery of shRNAs against PRC2 and PRC1 subunits disrupted EBV repression of BIM. The activation mark H3K4me3 is largely unaltered at this locus irrespective of H3K27me3 status, suggesting the establishment of a 'bivalent' chromatin domain. Consistent with the 'poised' nature of these domains, RNA polymerase II (Pol II) occupancy was not altered by EBV at the BIM TSS, but analysis of phospho-serine 5 on Pol II indicated that EBNA3A and EBNA3C together inhibit initiation of BIM transcripts. B cell lines carrying EBV encoding a conditional EBNA3C-oestrogen receptor-fusion revealed that this epigenetic repression of BIM was reversible, but took more than 3 weeks from when EBNA3C was inactivated. SN - 1362-4962 UR - https://www.unboundmedicine.com/medline/citation/22584624/BIM_promoter_directly_targeted_by_EBNA3C_in_polycomb_mediated_repression_by_EBV_ L2 - https://academic.oup.com/nar/article-lookup/doi/10.1093/nar/gks391 DB - PRIME DP - Unbound Medicine ER -