期刊
MOLECULAR CELL
卷 52, 期 2, 页码 206-220出版社
CELL PRESS
DOI: 10.1016/j.molcel.2013.08.025
关键词
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资金
- NNF
- Danish Cancer Society
- Danish National Research Foundation
- Lundbeck Foundation
- European Commission
- European Molecular Biology Organization
- Lundbeck Foundation [R52-2010-4895] Funding Source: researchfish
- Novo Nordisk Fonden [NNF12OC0001893] Funding Source: researchfish
- Novo Nordisk Foundation Center for Protein Research [PI Jiri Lukas] Funding Source: researchfish
Although the general relevance of chromatin modifications for genotoxic stress signaling, cell-cycle checkpoint activation, and DNA repair is well established, how these modifications reach initial thresholds in order to trigger robust responses remains largely unexplored. Here, we identify the chromatin-associated scaffold attachment factor SAFB1 as a component of the DNA damage response and show that SAFB1 cooperates with histone acetylation to allow for efficient gamma H2AX spreading and genotoxic stress signaling. SAFB1 undergoes a highly dynamic exchange at damaged chromatin in a poly(ADP-ribose)-polymerase 1- and poly(ADP-ribose)-dependent manner and is required for unperturbed cell-cycle checkpoint activation and guarding cells against replicative stress. Altogether, our data reveal that transient recruitment of an architectural chromatin component is required in order to overcome physiological barriers by making chromatin permissive for DNA damage signaling, whereas the ensuing exclusion of SAFB1 may help prevent excessive signaling.
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