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Involvement of condensin in cellular senescence through gene regulation and compartmental reorganization

Author

Listed:
  • Osamu Iwasaki

    (University of Oregon)

  • Hideki Tanizawa

    (University of Oregon)

  • Kyoung-Dong Kim

    (Chung-Ang University)

  • Andrew Kossenkov

    (The Wistar Institute)

  • Timothy Nacarelli

    (The Wistar Institute)

  • Sanki Tashiro

    (University of Oregon)

  • Sonali Majumdar

    (The Wistar Institute)

  • Louise C. Showe

    (The Wistar Institute)

  • Rugang Zhang

    (The Wistar Institute)

  • Ken-ichi Noma

    (University of Oregon)

Abstract

Senescence is induced by various stimuli such as oncogene expression and telomere shortening, referred to as oncogene-induced senescence (OIS) and replicative senescence (RS), respectively, and accompanied by global transcriptional alterations and 3D genome reorganization. Here, we demonstrate that the human condensin II complex participates in senescence via gene regulation and reorganization of euchromatic A and heterochromatic B compartments. Both OIS and RS are accompanied by A-to-B and B-to-A compartmental transitions, the latter of which occur more frequently and are undergone by 14% (430 Mb) of the human genome. Mechanistically, condensin is enriched in A compartments and implicated in B-to-A transitions. The full activation of senescence genes (SASP genes and p53 targets) requires condensin; its depletion impairs senescence markers. This study describes that condensin reinforces euchromatic A compartments and promotes B-to-A transitions, both of which are coupled to optimal expression of senescence genes, thereby allowing condensin to contribute to senescent processes.

Suggested Citation

  • Osamu Iwasaki & Hideki Tanizawa & Kyoung-Dong Kim & Andrew Kossenkov & Timothy Nacarelli & Sanki Tashiro & Sonali Majumdar & Louise C. Showe & Rugang Zhang & Ken-ichi Noma, 2019. "Involvement of condensin in cellular senescence through gene regulation and compartmental reorganization," Nature Communications, Nature, vol. 10(1), pages 1-20, December.
    • Handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-13604-5
    DOI: 10.1038/s41467-019-13604-5
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    Cited by:

    1. Chen Wang & Hideki Tanizawa & Connor Hill & Aaron Havas & Qiang Zhang & Liping Liao & Xue Hao & Xue Lei & Lu Wang & Hao Nie & Yuan Qi & Bin Tian & Alessandro Gardini & Andrew V. Kossenkov & Aaron Gold, 2024. "METTL3-mediated chromatin contacts promote stress granule phase separation through metabolic reprogramming during senescence," Nature Communications, Nature, vol. 15(1), pages 1-16, December.

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