Cited by 280DNA Repair MechanismsGenomic variations and chromosomal abnormalitiesGenomics and Chromatin Dynamics

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Long Neural Genes Harbor Recurrent DNA Break Clusters in Neural Stem/Progenitor Cells

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Wei, Pei-Chi, Chang, Amelia N., Kao, Jennifer, Du, Zhou, Meyers, Robin M., Alt, Frederick W., Schwer, Bjoern·2016·Cell

DOI 10.1016/j.cell.2015.12.039PMC PMC4752721

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Abstract

Repair of DNA double-strand breaks (DSBs) by non-homologous end joining is critical for neural development, and brain cells frequently contain somatic genomic variations that might involve DSB intermediates. We now use an unbiased, high-throughput approach to identify genomic regions harboring recurrent DSBs in primary neural stem/progenitor cells (NSPCs). We identify 27 recurrent DSB clusters (RDCs), and remarkably, all occur within gene bodies. Most of these NSPC RDCs were detected only upon mild, aphidicolin-induced replication stress, providing a nucleotide-resolution view of replication-associated genomic fragile sites. The vast majority of RDCs occur in long, transcribed, and late-replicating genes. Moreover, almost 90% of identified RDC-containing genes are involved in synapse function and/or neural cell adhesion, with a substantial fraction also implicated in tumor suppression and/or mental disorders. Our characterization of NSPC RDCs reveals a basis of gene fragility and suggests potential impacts of DNA breaks on neurodevelopment and neural functions.

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Authors: Wei, P.-C., Chang, A. N., Kao, J., Du, Z., Meyers, R. M., Alt, F. W., & Schwer, B.
Affiliations: Boston Children's Hospital (US)
Corresponding author: Alt, Frederick W.
Schwer, Bjoern
ORCID: Wei, Pei-Chi
Du, Zhou
Meyers, Robin M.
Alt, Frederick W.
Schwer, Bjoern
Venue: Cell
Publisher: Elsevier BV
Published: 2016-02
Volume: 164
Issue: 4
Pages: 644-655
ISSN: 0092-8674 (ISSN-L)
DOI: 10.1016/j.cell.2015.12.039
PMC: PMC4752721
OpenAlex: W2268858163
Cited by: 280
References: 55
Citations by year: 2026: 20 · 2025: 13 · 2024: 15 · 2023: 23 · 2022: 24 · 2021: 32 · 2020: 31 · 2019: 20 · 2018: 37 · 2017: 40 · 2016: 25
FWCI: 21.13
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, 376 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)
PubMed Central (acceptedVersion)
Funders: Howard Hughes Medical Institute
National Institute on Aging (K01AG043630)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genomic variations and chromosomal abnormalities
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
Keywords: neural stem/progenitor cells, DNA double-strand breaks, non-homologous end joining, replication stress, synaptic function, neuronal adhesion, tumor suppression genes, mental illness, brain development
MeSH terms: Animals, Brain, Cell Adhesion, DNA Repair, Humans, Nerve Tissue Proteins, Synapses, Transcription Factors, Translocation, Genetic, Cell Adhesion Molecules, Neuronal, Aphidicolin, Genome, Mice, Basic Helix-Loop-Helix Proteins, DNA Breaks, GPI-Linked Proteins, Neural Stem Cells, DNA End-Joining Repair

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Long Neural Genes Harbor Recurrent DNA Break Clusters in Neural Stem/Progenitor Cells

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