The Chromatin Scaffold Protein SAFB1 Renders Chromatin Permissive for DNA Damage Signaling
| Autor: | Jiri Bartek, Vyacheslav Akimov, Luis I. Toledo, Claudia Lukas, Maj-Britt Rask, Matthias Altmeyer, Thorkell Gudjonsson, Jiri Lukas, Blagoy Blagoev, Merete Grøfte |
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| Rok vydání: | 2013 |
| Předmět: |
Scaffold protein
Poly Adenosine Diphosphate Ribose DNA Repair DNA repair DNA damage Blotting Western Green Fluorescent Proteins Genotoxic Stress Chromatin remodeling Histones Nuclear Matrix-Associated Proteins Cell Line Tumor Humans Histone code DNA Breaks Double-Stranded Phosphorylation Molecular Biology Models Genetic biology Mutagenicity Tests Reverse Transcriptase Polymerase Chain Reaction Acetylation Cell Cycle Checkpoints Matrix Attachment Region Binding Proteins Cell Biology Chromatin Cell biology Histone Microscopy Fluorescence Receptors Estrogen biology.protein RNA Interference Poly(ADP-ribose) Polymerases DNA Damage Signal Transduction |
| Zdroj: | Altmeyer, M F, Toledo, L, Gudjonsson, T, Grøfte, M, Rask, M-B, Lukas, C, Akimov, V, Blagoev, B, Bartek, J & Lukas, J 2013, ' The Chromatin Scaffold Protein SAFB1 Renders Chromatin Permissive for DNA Damage Signaling ', Molecular Cell, vol. 52, no. 2, pp. 206-220 . https://doi.org/10.1016/j.molcel.2013.08.025 |
| ISSN: | 1097-2765 |
| DOI: | 10.1016/j.molcel.2013.08.025 |
| Popis: | 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 γH2AX 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. |
| Databáze: | OpenAIRE |
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