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Nucleic Acids Research Advance Access originally published online on August 21, 2009
Nucleic Acids Research 2009 37(18):6054-6063; doi:10.1093/nar/gkp684
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Nucleic Acids Research, 2009, Vol. 37, No. 18 6054-6063
© The Author 2009. Published by Oxford University Press.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses?by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Genome Integrity, Repair and Replication

Increased sister chromatid cohesion and DNA damage response factor localization at an enzyme-induced DNA double-strand break in vertebrate cells

Helen Dodson and Ciaran G. Morrison*

Centre for Chromosome Biology, School of Natural Sciences, National University of Ireland Galway, University road, Galway, Ireland

*To whom correspondence should be addressed. Tel: +353 91 49 20 56; Fax: +353 91 49 55 04; Email: ciaran.morrison{at}nuigalway.ie

Received March 26, 2009. Revised July 29, 2009. Accepted August 3, 2009.

The response to DNA damage in vertebrate cells involves successive recruitment of DNA signalling and repair factors. We used light microscopy to monitor the genetic dependencies of such localization to a single, induced DNA double strand break (DSB) in vertebrate cells. We used an inducible version of the rare-cutting I-SceI endonuclease to cut a chromosomally integrated I-SceI site beside a Tet operator array that was visualized by binding a Tet repressor-GFP fusion. Formation of {gamma}-H2AX foci at a single DSB was independent of ATM or Ku70. ATM-deficient cells showed normal kinetics of 53Bp1 recruitment to DSBs, but Rad51 localization was retarded. 53Bp1 and Rad51 foci formation at a single DSB was greatly reduced in H2AX-null DT40 cells. We also observed decreased inter-sister chromatid distances after DSB induction, suggesting that cohesin loading at DSBs causes elevated sister chromatid cohesion. Loss of ATM reduced DSB-induced cohesion, consistent with cohesin being an ATM target in the DSB response. These data show that the same genetic pathways control how cells respond to single DSBs and to multiple lesions induced by whole-cell DNA damage.


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