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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, Vol. 41, No. 5, 5, 2011, p. 529-542.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Moyal, L, Lerenthal, Y, Gana-Weisz, M, Mass, G, So, S, Wang, S-Y, Eppink, B, Chung, YM, Shalev, G, Shema, E, Shkedy, D, Smorodinsky, NI, van Vliet, N, Kuster, B, Mann, M, Ciechanover, A, Dahm-Daphi, J, Kanaar, R, Hu, MC-T, Chen, DJ, Oren, M & Shiloh, Y 2011, 'Requirement of ATM-dependent monoubiquitylation of histone H2B for timely repair of DNA double-strand breaks.', MOL CELL, vol. 41, no. 5, 5, pp. 529-542. <http://www.ncbi.nlm.nih.gov/pubmed/21362549?dopt=Citation>

APA

Moyal, L., Lerenthal, Y., Gana-Weisz, M., Mass, G., So, S., Wang, S-Y., Eppink, B., Chung, Y. M., Shalev, G., Shema, E., Shkedy, D., Smorodinsky, N. I., van Vliet, N., Kuster, B., Mann, M., Ciechanover, A., Dahm-Daphi, J., Kanaar, R., Hu, M. C-T., ... Shiloh, Y. (2011). Requirement of ATM-dependent monoubiquitylation of histone H2B for timely repair of DNA double-strand breaks. MOL CELL, 41(5), 529-542. [5]. http://www.ncbi.nlm.nih.gov/pubmed/21362549?dopt=Citation

Vancouver

Moyal L, Lerenthal Y, Gana-Weisz M, Mass G, So S, Wang S-Y et al. Requirement of ATM-dependent monoubiquitylation of histone H2B for timely repair of DNA double-strand breaks. MOL CELL. 2011;41(5):529-542. 5.

Bibtex

@article{2055af5a6bda400d8f2f4b37aba07005,
title = "Requirement of ATM-dependent monoubiquitylation of histone H2B for timely repair of DNA double-strand breaks.",
abstract = "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.",
keywords = "Humans, Protein Processing, Post-Translational, Kinetics, Hela Cells, Phosphorylation, RNA Interference, Cell Cycle Proteins/*metabolism, *DNA Damage, Recombination, Genetic, *DNA Repair, Chromatin/chemistry/metabolism, Comet Assay/methods, DNA-Binding Proteins/*metabolism, Histones/chemistry/*metabolism, Protein-Serine-Threonine Kinases/*metabolism, Tumor Suppressor Proteins/*metabolism, Ubiquitin/*chemistry, Ubiquitin-Protein Ligases/metabolism, Humans, Protein Processing, Post-Translational, Kinetics, Hela Cells, Phosphorylation, RNA Interference, Cell Cycle Proteins/*metabolism, *DNA Damage, Recombination, Genetic, *DNA Repair, Chromatin/chemistry/metabolism, Comet Assay/methods, DNA-Binding Proteins/*metabolism, Histones/chemistry/*metabolism, Protein-Serine-Threonine Kinases/*metabolism, Tumor Suppressor Proteins/*metabolism, Ubiquitin/*chemistry, Ubiquitin-Protein Ligases/metabolism",
author = "Lilach Moyal and Yaniv Lerenthal and Mali Gana-Weisz and Gilad Mass and Sairei So and Shih-Ya Wang and Berina Eppink and Chung, {Young Min} and Gil Shalev and Efrat Shema and Dganit Shkedy and Smorodinsky, {Nechama I} and {van Vliet}, Nicole and Bernhard Kuster and Matthias Mann and Aaron Ciechanover and Jochen Dahm-Daphi and Roland Kanaar and Hu, {Mickey C-T} and Chen, {David J} and Moshe Oren and Yosef Shiloh",
year = "2011",
language = "English",
volume = "41",
pages = "529--542",
journal = "MOL CELL",
issn = "1097-2765",
publisher = "Cell Press",
number = "5",

}

RIS

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 -