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Curr Opin Genet Dev. 2013 Apr;23(2):156-65. doi: 10.1016/j.gde.2012.11.001. Epub 2013 Jan 9.

To spread or not to spread--chromatin modifications in response to DNA damage.

Author information

1
Chromosome Stability and Dynamics Unit, Department of Disease Biology, Novo Nordisk Foundation Center for Protein Research, University of Copenhagen, Blegdamsvej 3B, DK-2200 Copenhagen, Denmark. matthias.altmeyer@cpr.ku.dk

Abstract

Chromatin modifications in response to DNA damage are vital for genome integrity. Multiple proteins and pathways required to generate specialized chromatin domains around DNA lesions have been identified and the increasing amount of information calls for unifying concepts that would allow us to grasp the ever-increasing complexity. This review aims at contributing to this trend by focusing on feed-forward and feedback mechanisms, which in mammalian cells determine the extent of chromatin modifications after DNA damage. We highlight the emerging notion that the nodal points of these highly dynamic pathways operate in a rate-limiting mode, whose deregulation can disrupt physiological boundaries between damaged and undamaged chromatin, dictate repair pathway choice, and determine the fate of cells exposed to genotoxic stress.

PMID:
23312207
DOI:
10.1016/j.gde.2012.11.001
[Indexed for MEDLINE]

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