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Cohesin and the nucleolus constrain the mobility of spontaneous repair foci

Vincent Dion, Véronique Kalck, Andrew Seeber, Thomas Schleker, Susan M Gasser

Author Affiliations

  1. Vincent Dion1,
  2. Véronique Kalck1,
  3. Andrew Seeber1,2,
  4. Thomas Schleker1, and
  5. Susan M Gasser*,1,2
  1. 1 Friedrich Miescher Institute for Biomedical Research, Maulbeerstrasse 66, Basel, Switzerland
  2. 2 Faculty of Natural Sciences, University of Basel, CH‐4056, Basel, Switzerland
  1. *Corresponding author. Tel:+41 61 697 5025; Fax:+41 61 697 3976; E-mail: susan.gasser{at}
  • Present address: BioCampus Straubing GmbH, Europaring 4, 94315 Straubing, Germany

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The regulation of chromatin mobility in response to DNA damage is important for homologous recombination in yeast. Anchorage reduces rates of recombination, whereas increased chromatin mobility correlates with more efficient homology search. Here we tracked the mobility and localization of spontaneous S‐phase lesions bound by Rad52, and find that these foci have reduced movement, unlike enzymatically induced double‐strand breaks. Moreover, spontaneous repair foci are positioned in the nuclear core, abutting the nucleolus. We show that cohesin and nucleolar integrity constrain the mobility of these foci, consistent with the notion that spontaneous, S‐phase damage is preferentially repaired from the sister chromatid.

  • Received May 17, 2013.
  • Revision received August 13, 2013.
  • Accepted August 13, 2013.
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