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The human leukemia virus HTLV-1 alters the structure and transcription of host chromatin in cis

View ORCID ProfileAnat Melamed, Hiroko Yaguchi, Michi Miura, Aviva Witkover, Tomas W Fitzgerald, Ewan Birney, View ORCID ProfileCharles R M Bangham
doi: https://doi.org/10.1101/277335
Anat Melamed
1Division of Infectious Diseases, Imperial College London, Norfolk Place, London W2 1PG, UK
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Hiroko Yaguchi
1Division of Infectious Diseases, Imperial College London, Norfolk Place, London W2 1PG, UK
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  • For correspondence: c.bangham@imperial.ac.uk
Michi Miura
1Division of Infectious Diseases, Imperial College London, Norfolk Place, London W2 1PG, UK
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Aviva Witkover
1Division of Infectious Diseases, Imperial College London, Norfolk Place, London W2 1PG, UK
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Tomas W Fitzgerald
2European Molecular Biology Laboratory, European Bioinformatics Institute, Wellcome Genome Campus, Cambridge CB10 1SD, UK
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Ewan Birney
2European Molecular Biology Laboratory, European Bioinformatics Institute, Wellcome Genome Campus, Cambridge CB10 1SD, UK
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Charles R M Bangham
1Division of Infectious Diseases, Imperial College London, Norfolk Place, London W2 1PG, UK
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  • ORCID record for Charles R M Bangham
  • For correspondence: c.bangham@imperial.ac.uk
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Abstract

Chromatin looping controls gene expression by regulating promoter-enhancer contacts, the spread of epigenetic modifications, and the segregation of the genome into transcriptionally active and inactive compartments. We studied the impact on the structure and expression of host chromatin by the human retrovirus HTLV-1. We show that HTLV-1 disrupts host chromatin structure by forming loops between the provirus and the host genome; certain loops depend on the critical chromatin architectural protein CTCF, which we recently showed binds to the HTLV-1 provirus. Finally, we show that the provirus causes two distinct patterns of abnormal transcription of the host genome in cis: bidirectional transcription in the host genome immediately flanking the provirus, and clone-specific transcription in cis at non-contiguous loci up to >300 kb from the integration site. We conclude that HTLV-1 causes insertional mutagenesis up to the megabase range in the host genome in >104 persistently-maintained HTLV-1+ T-cell clones in vivo.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY 4.0 International license.
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Posted March 07, 2018.
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The human leukemia virus HTLV-1 alters the structure and transcription of host chromatin in cis
Anat Melamed, Hiroko Yaguchi, Michi Miura, Aviva Witkover, Tomas W Fitzgerald, Ewan Birney, Charles R M Bangham
bioRxiv 277335; doi: https://doi.org/10.1101/277335
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The human leukemia virus HTLV-1 alters the structure and transcription of host chromatin in cis
Anat Melamed, Hiroko Yaguchi, Michi Miura, Aviva Witkover, Tomas W Fitzgerald, Ewan Birney, Charles R M Bangham
bioRxiv 277335; doi: https://doi.org/10.1101/277335

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