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Widespread disruption of host transcription termination in HSV-1 infection

Author

Listed:
  • Andrzej J. Rutkowski

    (University of Cambridge)

  • Florian Erhard

    (Institut für Informatik, Ludwig-Maximilians-Universität München)

  • Anne L’Hernault

    (University of Cambridge)

  • Thomas Bonfert

    (Institut für Informatik, Ludwig-Maximilians-Universität München)

  • Markus Schilhabel

    (Institut für Klinische Molekularbiologie, Christian-Albrechts-Universität Kiel)

  • Colin Crump

    (University of Cambridge)

  • Philip Rosenstiel

    (Institut für Klinische Molekularbiologie, Christian-Albrechts-Universität Kiel)

  • Stacey Efstathiou

    (University of Cambridge)

  • Ralf Zimmer

    (Institut für Informatik, Ludwig-Maximilians-Universität München)

  • Caroline C. Friedel

    (Institut für Informatik, Ludwig-Maximilians-Universität München)

  • Lars Dölken

    (University of Cambridge
    Institut für Virologie, Julius-Maximilians-Universität Würzburg)

Abstract

Herpes simplex virus 1 (HSV-1) is an important human pathogen and a paradigm for virus-induced host shut-off. Here we show that global changes in transcription and RNA processing and their impact on translation can be analysed in a single experimental setting by applying 4sU-tagging of newly transcribed RNA and ribosome profiling to lytic HSV-1 infection. Unexpectedly, we find that HSV-1 triggers the disruption of transcription termination of cellular, but not viral, genes. This results in extensive transcription for tens of thousands of nucleotides beyond poly(A) sites and into downstream genes, leading to novel intergenic splicing between exons of neighbouring cellular genes. As a consequence, hundreds of cellular genes seem to be transcriptionally induced but are not translated. In contrast to previous reports, we show that HSV-1 does not inhibit co-transcriptional splicing. Our approach thus substantially advances our understanding of HSV-1 biology and establishes HSV-1 as a model system for studying transcription termination.

Suggested Citation

  • Andrzej J. Rutkowski & Florian Erhard & Anne L’Hernault & Thomas Bonfert & Markus Schilhabel & Colin Crump & Philip Rosenstiel & Stacey Efstathiou & Ralf Zimmer & Caroline C. Friedel & Lars Dölken, 2015. "Widespread disruption of host transcription termination in HSV-1 infection," Nature Communications, Nature, vol. 6(1), pages 1-15, November.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms8126
    DOI: 10.1038/ncomms8126
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    Cited by:

    1. Lara Djakovic & Thomas Hennig & Katharina Reinisch & Andrea Milić & Adam W. Whisnant & Katharina Wolf & Elena Weiß & Tobias Haas & Arnhild Grothey & Christopher S. Jürges & Michael Kluge & Elmar Wolf , 2023. "The HSV-1 ICP22 protein selectively impairs histone repositioning upon Pol II transcription downstream of genes," Nature Communications, Nature, vol. 14(1), pages 1-17, December.
    2. Yange Cui & Luyang Wang & Qingbao Ding & Jihae Shin & Joel Cassel & Qin Liu & Joseph M. Salvino & Bin Tian, 2023. "Elevated pre-mRNA 3′ end processing activity in cancer cells renders vulnerability to inhibition of cleavage and polyadenylation," Nature Communications, Nature, vol. 14(1), pages 1-20, December.
    3. Buki Kwon & Mervin M. Fansler & Neil D. Patel & Jihye Lee & Weirui Ma & Christine Mayr, 2022. "Enhancers regulate 3′ end processing activity to control expression of alternative 3′UTR isoforms," Nature Communications, Nature, vol. 13(1), pages 1-14, December.
    4. Valter Bergant & Daniel Schnepf & Niklas Andrade Krätzig & Philipp Hubel & Christian Urban & Thomas Engleitner & Ronald Dijkman & Bernhard Ryffel & Katja Steiger & Percy A. Knolle & Georg Kochs & Rola, 2023. "mRNA 3’UTR lengthening by alternative polyadenylation attenuates inflammatory responses and correlates with virulence of Influenza A virus," Nature Communications, Nature, vol. 14(1), pages 1-17, December.

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