Author
Listed:
- Takashi Sutani
(Research Center for Epigenetic Disease, Institute of Molecular and Cellular Biosciences, The University of Tokyo)
- Toyonori Sakata
(Research Center for Epigenetic Disease, Institute of Molecular and Cellular Biosciences, The University of Tokyo)
- Ryuichiro Nakato
(Research Center for Epigenetic Disease, Institute of Molecular and Cellular Biosciences, The University of Tokyo)
- Koji Masuda
(Research Center for Epigenetic Disease, Institute of Molecular and Cellular Biosciences, The University of Tokyo)
- Mai Ishibashi
(Research Center for Epigenetic Disease, Institute of Molecular and Cellular Biosciences, The University of Tokyo)
- Daisuke Yamashita
(Chromosome Dynamics Laboratory, RIKEN
Present address: Otsuka Pharmaceutical Co., Ltd, Ako, Hyogo 678-0207, Japan.)
- Yutaka Suzuki
(Graduate School of Frontier Sciences, The University of Tokyo)
- Tatsuya Hirano
(Chromosome Dynamics Laboratory, RIKEN)
- Masashige Bando
(Research Center for Epigenetic Disease, Institute of Molecular and Cellular Biosciences, The University of Tokyo)
- Katsuhiko Shirahige
(Research Center for Epigenetic Disease, Institute of Molecular and Cellular Biosciences, The University of Tokyo
CREST, Japan Science and Technology Agency (JST))
Abstract
Chromosome condensation is a hallmark of mitosis in eukaryotes and is a prerequisite for faithful segregation of genetic material to daughter cells. Here we show that condensin, which is essential for assembling condensed chromosomes, helps to preclude the detrimental effects of gene transcription on mitotic condensation. ChIP-seq profiling reveals that the fission yeast condensin preferentially binds to active protein-coding genes in a transcription-dependent manner during mitosis. Pharmacological and genetic attenuation of transcription largely rescue bulk chromosome segregation defects observed in condensin mutants. We also demonstrate that condensin is associated with and reduces unwound DNA segments generated by transcription, providing a direct link between an in vitro activity of condensin and its in vivo function. The human condensin isoform condensin I also binds to unwound DNA regions at the transcription start sites of active genes, implying that our findings uncover a fundamental feature of condensin complexes.
Suggested Citation
Takashi Sutani & Toyonori Sakata & Ryuichiro Nakato & Koji Masuda & Mai Ishibashi & Daisuke Yamashita & Yutaka Suzuki & Tatsuya Hirano & Masashige Bando & Katsuhiko Shirahige, 2015.
"Condensin targets and reduces unwound DNA structures associated with transcription in mitotic chromosome condensation,"
Nature Communications, Nature, vol. 6(1), pages 1-13, November.
Handle:
RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms8815
DOI: 10.1038/ncomms8815
Download full text from publisher
Citations
Citations are extracted by the
CitEc Project, subscribe to its
RSS feed for this item.
Cited by:
- Rebecca J. Harris & Maninder Heer & Mark D. Levasseur & Tyrell N. Cartwright & Bethany Weston & Jennifer L. Mitchell & Jonathan M. Coxhead & Luke Gaughan & Lisa Prendergast & Daniel Rico & Jonathan M., 2023.
"Release of Histone H3K4-reading transcription factors from chromosomes in mitosis is independent of adjacent H3 phosphorylation,"
Nature Communications, Nature, vol. 14(1), pages 1-17, December.
- Osamu Iwasaki & Sanki Tashiro & Claire Yik-Lok Chung & Tomomi Hayashi & Hideki Tanizawa & Xuebing Wang & Shinya Ohta & Yuko Fujioka & Joseph Han & Gabrielle Tabor & Mikihiro Kawagoe & Ronen Marmorstei, 2026.
"A role for condensin-mediator interaction in mitotic chromosome organization,"
Nature Communications, Nature, vol. 17(1), pages 1-18, December.
Corrections
All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms8815. See general information about how to correct material in RePEc.
If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.
We have no bibliographic references for this item. You can help adding them by using this form .
If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.
For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .
Please note that corrections may take a couple of weeks to filter through
the various RePEc services.