Requirement of ATM-dependent monoubiquitylation of histone H2B for timely repair of DNA double-strand breaks.
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Requirement of ATM-dependent monoubiquitylation of histone H2B for timely repair of DNA double-strand breaks. / Moyal, Lilach; Lerenthal, Yaniv; Gana-Weisz, Mali; Mass, Gilad; So, Sairei; Wang, Shih-Ya; Eppink, Berina; Chung, Young Min; Shalev, Gil; Shema, Efrat; Shkedy, Dganit; Smorodinsky, Nechama I; van Vliet, Nicole; Kuster, Bernhard; Mann, Matthias; Ciechanover, Aaron; Dahm-Daphi, Jochen; Kanaar, Roland; Hu, Mickey C-T; Chen, David J; Oren, Moshe; Shiloh, Yosef.
in: MOL CELL, Jahrgang 41, Nr. 5, 5, 2011, S. 529-542.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Requirement of ATM-dependent monoubiquitylation of histone H2B for timely repair of DNA double-strand breaks.
AU - Moyal, Lilach
AU - Lerenthal, Yaniv
AU - Gana-Weisz, Mali
AU - Mass, Gilad
AU - So, Sairei
AU - Wang, Shih-Ya
AU - Eppink, Berina
AU - Chung, Young Min
AU - Shalev, Gil
AU - Shema, Efrat
AU - Shkedy, Dganit
AU - Smorodinsky, Nechama I
AU - van Vliet, Nicole
AU - Kuster, Bernhard
AU - Mann, Matthias
AU - Ciechanover, Aaron
AU - Dahm-Daphi, Jochen
AU - Kanaar, Roland
AU - Hu, Mickey C-T
AU - Chen, David J
AU - Oren, Moshe
AU - Shiloh, Yosef
PY - 2011
Y1 - 2011
N2 - The cellular response to DNA double-strand breaks (DSBs) is mobilized by the protein kinase ATM, which phosphorylates key players in the DNA damage response (DDR) network. A major question is how ATM controls DSB repair. Optimal repair requires chromatin relaxation at damaged sites. Chromatin reorganization is coupled to dynamic alterations in histone posttranslational modifications. Here, we show that in human cells, DSBs induce monoubiquitylation of histone H2B, a modification that is associated in undamaged cells with transcription elongation. We find that this process relies on recruitment to DSB sites and ATM-dependent phosphorylation of the responsible E3 ubiquitin ligase: the RNF20-RNF40 heterodimer. H2B monoubiquitylation is required for timely recruitment of players in the two major DSB repair pathways-nonhomologous end-joining and homologous recombination repair-and optimal repair via both pathways. Our data and previous data suggest a two-stage model for chromatin decondensation that facilitates DSB repair.
AB - The cellular response to DNA double-strand breaks (DSBs) is mobilized by the protein kinase ATM, which phosphorylates key players in the DNA damage response (DDR) network. A major question is how ATM controls DSB repair. Optimal repair requires chromatin relaxation at damaged sites. Chromatin reorganization is coupled to dynamic alterations in histone posttranslational modifications. Here, we show that in human cells, DSBs induce monoubiquitylation of histone H2B, a modification that is associated in undamaged cells with transcription elongation. We find that this process relies on recruitment to DSB sites and ATM-dependent phosphorylation of the responsible E3 ubiquitin ligase: the RNF20-RNF40 heterodimer. H2B monoubiquitylation is required for timely recruitment of players in the two major DSB repair pathways-nonhomologous end-joining and homologous recombination repair-and optimal repair via both pathways. Our data and previous data suggest a two-stage model for chromatin decondensation that facilitates DSB repair.
KW - Humans
KW - Protein Processing, Post-Translational
KW - Kinetics
KW - Hela Cells
KW - Phosphorylation
KW - RNA Interference
KW - Cell Cycle Proteins/metabolism
KW - DNA Damage
KW - Recombination, Genetic
KW - DNA Repair
KW - Chromatin/chemistry/metabolism
KW - Comet Assay/methods
KW - DNA-Binding Proteins/metabolism
KW - Histones/chemistry/metabolism
KW - Protein-Serine-Threonine Kinases/metabolism
KW - Tumor Suppressor Proteins/metabolism
KW - Ubiquitin/chemistry
KW - Ubiquitin-Protein Ligases/metabolism
KW - Humans
KW - Protein Processing, Post-Translational
KW - Kinetics
KW - Hela Cells
KW - Phosphorylation
KW - RNA Interference
KW - Cell Cycle Proteins/metabolism
KW - DNA Damage
KW - Recombination, Genetic
KW - DNA Repair
KW - Chromatin/chemistry/metabolism
KW - Comet Assay/methods
KW - DNA-Binding Proteins/metabolism
KW - Histones/chemistry/metabolism
KW - Protein-Serine-Threonine Kinases/metabolism
KW - Tumor Suppressor Proteins/metabolism
KW - Ubiquitin/chemistry
KW - Ubiquitin-Protein Ligases/metabolism
M3 - SCORING: Journal article
VL - 41
SP - 529
EP - 542
JO - MOL CELL
JF - MOL CELL
SN - 1097-2765
IS - 5
M1 - 5
ER -