Cited by 741DNA Repair MechanismsGenomics and Chromatin DynamicsChromatin Remodeling and Cancer

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ATM-Dependent Chromatin Changes Silence Transcription In cis to DNA Double-Strand Breaks

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Shanbhag, Niraj M., Rafalska-Metcalf, Ilona U., Balane-Bolivar, Carlo, Janicki, Susan M., Greenberg, Roger A.·2010·Cell

DOI 10.1016/j.cell.2010.04.038PMC PMC2920610

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Abstract

DNA double-strand breaks (DSBs) initiate extensive local and global alterations in chromatin structure, many of which depend on the ATM kinase. Histone H2A ubiquitylation (uH2A) on chromatin surrounding DSBs is one example, thought to be important for recruitment of repair proteins. uH2A is also implicated in transcriptional repression; an intriguing yet untested hypothesis is that this function is conserved in the context of DSBs. Using a novel reporter that allows for visualization of repair protein recruitment and local transcription in single cells, we describe an ATM-dependent transcriptional silencing program in cis to DSBs. ATM prevents RNA polymerase II elongation-dependent chromatin decondensation at regions distal to DSBs. Silencing is partially dependent on E3 ubiquitin ligases RNF8 and RNF168, whereas reversal of silencing relies on the uH2A deubiquitylating enzyme USP16. These findings give insight into the role of posttranslational modifications in mediating crosstalk between diverse processes occurring on chromatin.

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Authors: Shanbhag, N. M., Rafalska-Metcalf, I. U., Balane-Bolivar, C., Janicki, S. M., & Greenberg, R. A.
Affiliations: Abramson Cancer Center (US)
The Wistar Institute (US)
Corresponding author: Greenberg, Roger A.
ORCID: Janicki, Susan M.
Greenberg, Roger A.
Venue: Cell
Publisher: Elsevier BV
Published: 2010-06
Volume: 141
Issue: 6
Pages: 970-981
ISSN: 0092-8674 (ISSN-L)
DOI: 10.1016/j.cell.2010.04.038
PMC: PMC2920610
OpenAlex: W2135144687
Cited by: 737
References: 53
Citations by year: 2026: 30 · 2025: 28 · 2024: 45 · 2023: 45 · 2022: 49 · 2021: 71 · 2020: 51 · 2019: 45 · 2018: 38 · 2017: 49 · 2016: 45 · 2015: 44 · 2014: 46 · 2013: 54 · 2012: 42
FWCI: 19.66
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 1142 d)
doi.org/10.15223/policy-017 (stm-asf)
doi.org/10.15223/policy-037 (stm-asf)
doi.org/10.15223/policy-012 (stm-asf)
doi.org/10.15223/policy-029 (stm-asf)
doi.org/10.15223/policy-004 (stm-asf)
Locations: Cell (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: Genentech
National Cancer Institute (K08CA106597, T32CA115299, R01CA138835, 1-T32-CA-115299-01A2)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
Keywords: ATM kinase, DNA double-strand breaks, transcriptional silencing, chromatin decondensation, RNA polymerase II elongation, RNF8, RNF168, USP16, E3 ubiquitin ligase, post-translational modification
MeSH terms: Chromatin, DNA Damage, DNA-Binding Proteins, Histones, Humans, Transcription, Genetic, Protein Serine-Threonine Kinases, Cell Cycle Proteins, Gene Silencing, Tumor Suppressor Proteins, Ubiquitin Thiolesterase, Cell Line, Tumor, DNA Breaks, Double-Stranded, Ubiquitination, Ataxia Telangiectasia Mutated Proteins

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ATM-Dependent Chromatin Changes Silence Transcription In cis to DNA Double-Strand Breaks

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