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. 2016 Mar 10;3(3):e1134411. doi: 10.1080/23723556.2015.1134411

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© 2016 The Author(s). Published with license by Taylor & Francis Group, LLC

This is an Open Access article distributed under the terms of the Creative Commons Attribution-Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.

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Figure 1. — ATM-mediated H2 AX phosphorylation and DSB clustering. Upon damage detection, ataxia telangiectasia mutated (ATM) is recruited to a restricted region surrounding the double-strand break (DSB). H2AX-containing nucleosomes present within the damaged topologically associated domain (TAD, in red) are then phosphorylated, possibly as a result of local chromatin mobility that brings nucleosomes into the spatial vicinity of ATM. This leads to spreading of γH2AX through the entire damaged TAD. ATM may also phosphorylate other chromatin substrate(s) (in yellow) to locally enhance the mobility. This enhanced mobility could lead to increased H2AX phosphorylation within the TAD and favor DSB clustering.