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

Osamu Iwasaki, Hideki Tanizawa, Kyoung-Dong Kim, Andrew Kossenkov, Timothy Nacarelli, Sanki Tashiro, Sonali Majumdar, Louise C. Showe, Rugang Zhang and Ken-ichi Noma ()
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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

Nature Communications, 2019, vol. 10, issue 1, 1-20

Abstract: 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.

Date: 2019
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DOI: 10.1038/s41467-019-13604-5

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