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Epstein-Barr virus exploits intrinsic B-lymphocyte transcription programs to achieve immortal cell growth.

Epstein-Barr virus nuclear antigen 2 (EBNA2) regulation of transcription through the cell transcription factor RBPJ is essential for resting B-lymphocyte (RBL) conversion to immortal lymphoblast cell lines (LCLs). ChIP-seq of EBNA2 and RBPJ sites in LCL DNA found EBNA2 at 5,151 and RBPJ at 10,529 si... Full description

Journal Title: Proceedings of the National Academy of Sciences of the United States of America September 6, 2011, Vol.108(36), pp.14902-14907
Main Author: Zhao, Bo
Other Authors: Zou, James , Wang, Hongfang , Johannsen, Eric , Peng, Chih-Wen , Quackenbush, John , Mar, Jessica C , Morton, Cynthia Casson , Freedman, Matthew L , Blacklow, Stephen C , Aster, Jon C , Bernstein, Bradley E , Kieff, Elliott
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1091-6490 ; DOI: 10.1073/pnas.1108892108
Link: http://search.proquest.com/docview/888091725/?pq-origsite=primo
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title: Epstein-Barr virus exploits intrinsic B-lymphocyte transcription programs to achieve immortal cell growth.
format: Article
creator:
  • Zhao, Bo
  • Zou, James
  • Wang, Hongfang
  • Johannsen, Eric
  • Peng, Chih-Wen
  • Quackenbush, John
  • Mar, Jessica C
  • Morton, Cynthia Casson
  • Freedman, Matthew L
  • Blacklow, Stephen C
  • Aster, Jon C
  • Bernstein, Bradley E
  • Kieff, Elliott
subjects:
  • B-Lymphocytes–Metabolism
  • Cell Line, Tumor–Virology
  • Cell Proliferation–Genetics
  • Core Binding Factor Alpha Subunits–Metabolism
  • Epstein-Barr Virus Infections–Genetics
  • Epstein-Barr Virus Nuclear Antigens–Metabolism
  • Genome, Viral–Genetics
  • Herpesvirus 4, Human–Metabolism
  • Humans–Genetics
  • Immunoglobulin J Recombination Signal Sequence-Binding Protein–Genetics
  • Nucleosomes–Metabolism
  • Proto-Oncogene Proteins–Genetics
  • Proto-Oncogene Proteins C-Ets–Metabolism
  • Proto-Oncogene Proteins C-Myc–Genetics
  • Response Elements–Metabolism
  • Trans-Activators–Genetics
  • Transcription Factor Rela–Metabolism
  • Transcription, Genetic–Genetics
  • Viral Proteins–Metabolism
  • Viral Proteins
ispartof: Proceedings of the National Academy of Sciences of the United States of America, September 6, 2011, Vol.108(36), pp.14902-14907
description: Epstein-Barr virus nuclear antigen 2 (EBNA2) regulation of transcription through the cell transcription factor RBPJ is essential for resting B-lymphocyte (RBL) conversion to immortal lymphoblast cell lines (LCLs). ChIP-seq of EBNA2 and RBPJ sites in LCL DNA found EBNA2 at 5,151 and RBPJ at 10,529 sites. EBNA2 sites were enriched for RBPJ (78%), early B-cell factor (EBF, 39%), RUNX (43%), ETS (39%), NF[kappa]B (22%), and PU.1 (22%) motifs. These motif associations were confirmed by LCL RBPJ ChIP-seq finding 72% RBPJ occupancy and Encyclopedia Of DNA Elements LCL ChIP-seq finding EBF, NF[kappa]B RELA, and PU.1 at 54%, 31%, and 17% of EBNA2 sites. EBNA2 and RBPJ were predominantly at intergene and intron sites and only 14% at promoter sites. K-means clustering of EBNA2 site transcription factors identified RELA-ETS, EBF-RUNX, EBF, ETS, RBPJ, and repressive RUNX clusters, which ranked from highest to lowest in H3K4mel signals and nucleosome depletion, indicative of active chromatin. Surprisingly, although quantitatively less, the same genome sites in RBLs exhibited similar high-level H3K4mel signals and nucleosome depletion. The EBV genome also had an LMP1 promoter EBF site, which proved critical for EBNA2 activation. LCL HiC data mapped intergenic EBNA2 sites to EBNA2 upregulated genes. FISH and chromatin conformation capture linked EBNA2/RBPJ enhancers 428 kb 5' of MYC to MYC. These data indicate that EBNA2 evolved to target RBL H3K4me1 modified, nucleosome-depleted, nonpromoter sites to drive B-lymphocyte proliferation in primary human infection. The primed RBL program likely supports antigen-induced proliferation. leukemia | lymphoma | Notch | development doi/ 10.1073/pnas.1108892108
language: eng
source:
identifier: E-ISSN: 1091-6490 ; DOI: 10.1073/pnas.1108892108
fulltext: fulltext
issn:
  • 10916490
  • 1091-6490
url: Link


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titleEpstein-Barr virus exploits intrinsic B-lymphocyte transcription programs to achieve immortal cell growth.
creatorZhao, Bo ; Zou, James ; Wang, Hongfang ; Johannsen, Eric ; Peng, Chih-Wen ; Quackenbush, John ; Mar, Jessica C ; Morton, Cynthia Casson ; Freedman, Matthew L ; Blacklow, Stephen C ; Aster, Jon C ; Bernstein, Bradley E ; Kieff, Elliott
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identifierE-ISSN: 1091-6490 ; DOI: 10.1073/pnas.1108892108
subjectB-Lymphocytes–Metabolism ; Cell Line, Tumor–Virology ; Cell Proliferation–Genetics ; Core Binding Factor Alpha Subunits–Metabolism ; Epstein-Barr Virus Infections–Genetics ; Epstein-Barr Virus Nuclear Antigens–Metabolism ; Genome, Viral–Genetics ; Herpesvirus 4, Human–Metabolism ; Humans–Genetics ; Immunoglobulin J Recombination Signal Sequence-Binding Protein–Genetics ; Nucleosomes–Metabolism ; Proto-Oncogene Proteins–Genetics ; Proto-Oncogene Proteins C-Ets–Metabolism ; Proto-Oncogene Proteins C-Myc–Genetics ; Response Elements–Metabolism ; Trans-Activators–Genetics ; Transcription Factor Rela–Metabolism ; Transcription, Genetic–Genetics ; Viral Proteins–Metabolism ; Viral Proteins
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descriptionEpstein-Barr virus nuclear antigen 2 (EBNA2) regulation of transcription through the cell transcription factor RBPJ is essential for resting B-lymphocyte (RBL) conversion to immortal lymphoblast cell lines (LCLs). ChIP-seq of EBNA2 and RBPJ sites in LCL DNA found EBNA2 at 5,151 and RBPJ at 10,529 sites. EBNA2 sites were enriched for RBPJ (78%), early B-cell factor (EBF, 39%), RUNX (43%), ETS (39%), NF[kappa]B (22%), and PU.1 (22%) motifs. These motif associations were confirmed by LCL RBPJ ChIP-seq finding 72% RBPJ occupancy and Encyclopedia Of DNA Elements LCL ChIP-seq finding EBF, NF[kappa]B RELA, and PU.1 at 54%, 31%, and 17% of EBNA2 sites. EBNA2 and RBPJ were predominantly at intergene and intron sites and only 14% at promoter sites. K-means clustering of EBNA2 site transcription factors identified RELA-ETS, EBF-RUNX, EBF, ETS, RBPJ, and repressive RUNX clusters, which ranked from highest to lowest in H3K4mel signals and nucleosome depletion, indicative of active chromatin. Surprisingly, although quantitatively less, the same genome sites in RBLs exhibited similar high-level H3K4mel signals and nucleosome depletion. The EBV genome also had an LMP1 promoter EBF site, which proved critical for EBNA2 activation. LCL HiC data mapped intergenic EBNA2 sites to EBNA2 upregulated genes. FISH and chromatin conformation capture linked EBNA2/RBPJ enhancers 428 kb 5' of MYC to MYC. These data indicate that EBNA2 evolved to target RBL H3K4me1 modified, nucleosome-depleted, nonpromoter sites to drive B-lymphocyte proliferation in primary human infection. The primed RBL program likely supports antigen-induced proliferation. leukemia | lymphoma | Notch | development doi/ 10.1073/pnas.1108892108
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titleEpstein-Barr virus exploits intrinsic B-lymphocyte transcription programs to achieve immortal cell growth.
authorZhao, Bo ; Zou, James ; Wang, Hongfang ; Johannsen, Eric ; Peng, Chih-Wen ; Quackenbush, John ; Mar, Jessica C ; Morton, Cynthia Casson ; Freedman, Matthew L ; Blacklow, Stephen C ; Aster, Jon C ; Bernstein, Bradley E ; Kieff, Elliott
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