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Epigenetic specifications of host chromosome docking sites for latent Epstein-Barr virus

Author

Listed:
  • Kyoung-Dong Kim

    (Chung-Ang University)

  • Hideki Tanizawa

    (University of Oregon)

  • Alessandra De Leo

    (The Wistar Institute)

  • Olga Vladimirova

    (The Wistar Institute)

  • Andrew Kossenkov

    (The Wistar Institute)

  • Fang Lu

    (The Wistar Institute)

  • Louise C. Showe

    (The Wistar Institute)

  • Ken-ichi Noma

    (University of Oregon)

  • Paul M. Lieberman

    (The Wistar Institute)

Abstract

Epstein-Barr virus (EBV) genomes persist in latently infected cells as extrachromosomal episomes that attach to host chromosomes through the tethering functions of EBNA1, a viral encoded sequence-specific DNA binding protein. Here we employ circular chromosome conformation capture (4C) analysis to identify genome-wide associations between EBV episomes and host chromosomes. We find that EBV episomes in Burkitt’s lymphoma cells preferentially associate with cellular genomic sites containing EBNA1 binding sites enriched with B-cell factors EBF1 and RBP-jK, the repressive histone mark H3K9me3, and AT-rich flanking sequence. These attachment sites correspond to transcriptionally silenced genes with GO enrichment for neuronal function and protein kinase A pathways. Depletion of EBNA1 leads to a transcriptional de-repression of silenced genes and reduction in H3K9me3. EBV attachment sites in lymphoblastoid cells with different latency type show different correlations, suggesting that host chromosome attachment sites are functionally linked to latency type gene expression programs.

Suggested Citation

  • Kyoung-Dong Kim & Hideki Tanizawa & Alessandra De Leo & Olga Vladimirova & Andrew Kossenkov & Fang Lu & Louise C. Showe & Ken-ichi Noma & Paul M. Lieberman, 2020. "Epigenetic specifications of host chromosome docking sites for latent Epstein-Barr virus," Nature Communications, Nature, vol. 11(1), pages 1-13, December.
  • Handle: RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-019-14152-8
    DOI: 10.1038/s41467-019-14152-8
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