Evidence map›Paper›PMID 26873106›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

Transcription-associated processes cause DNA double-strand breaks and translocations in neural stem/progenitor cells.

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

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
9.1field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

71 citing papers in PubMed, 100 citations in OpenAlex.

  1. Article
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  4. Manipulating alternative end-joining alters carbon-ion beam-induced genome mutation profiles in Arabidopsis thaliana.DNA research : an international journal for rapid publication of reports on genes and genomes · 2025
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  9. Building the brain mosaic: an expanded view.Trends in genetics : TIG · 2024
    Review
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11 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Bjoern SchwerHoward Hughes Medical Institute, Program in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA 02115; Department of Genetics, Harvard Medical School, Boston, MA 02115; Department of Pediatrics, Harvard Medical School, Boston, MA 02115 Bjoern.Schwer@childrens.harvard.edu alt@enders.tch.harvard.edu.
Pei-Chi WeiHoward Hughes Medical Institute, Program in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA 02115; Department of Genetics, Harvard Medical School, Boston, MA 02115; Department of Pediatrics, Harvard Medical School, Boston, MA 02115.
Amelia N ChangHoward Hughes Medical Institute, Program in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA 02115; Department of Genetics, Harvard Medical School, Boston, MA 02115; Department of Pediatrics, Harvard Medical School, Boston, MA 02115.
Jennifer KaoHoward Hughes Medical Institute, Program in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA 02115; Department of Genetics, Harvard Medical School, Boston, MA 02115; Department of Pediatrics, Harvard Medical School, Boston, MA 02115.
Zhou DuHoward Hughes Medical Institute, Program in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA 02115; Department of Genetics, Harvard Medical School, Boston, MA 02115; Department of Pediatrics, Harvard Medical School, Boston, MA 02115.
Robin M MeyersHoward Hughes Medical Institute, Program in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA 02115; Department of Genetics, Harvard Medical School, Boston, MA 02115; Department of Pediatrics, Harvard Medical School, Boston, MA 02115.
Frederick W AltHoward Hughes Medical Institute, Program in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA 02115; Department of Genetics, Harvard Medical School, Boston, MA 02115; Department of Pediatrics, Harvard Medical School, Boston, MA 02115 Bjoern.Schwer@childrens.harvard.edu alt@enders.tch.harvard.edu.
Boston Children's Hospital · USHoward Hughes Medical Institute · USHarvard University · US

Funding

Elucidation of The Role Of SIRT6 In Neural Function, Aging, And NeurodegenerationK01AG043630 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SCHWER, BJOERN · 2012 to 2016
$647k
Howard Hughes Medical InstituteNIA NIH HHS K01 AG043630NIA NIH HHS K01AG043630
6 · The paper itself

Abstract

High-throughput, genome-wide translocation sequencing (HTGTS) studies of activated B cells have revealed that DNA double-strand breaks (DSBs) capable of translocating to defined bait DSBs are enriched around the transcription start sites (TSSs) of active genes. We used the HTGTS approach to investigate whether a similar phenomenon occurs in primary neural stem/progenitor cells (NSPCs). We report that breakpoint junctions indeed are enriched around TSSs that were determined to be active by global run-on sequencing analyses of NSPCs. Comparative analyses of transcription profiles in NSPCs and B cells revealed that the great majority of TSS-proximal junctions occurred in genes commonly expressed in both cell types, possibly because this common set has higher transcription levels on average than genes transcribed in only one or the other cell type. In the latter context, among all actively transcribed genes containing translocation junctions in NSPCs, those with junctions located within 2 kb of the TSS show a significantly higher transcription rate on average than genes with junctions in the gene body located at distances greater than 2 kb from the TSS. Finally, analysis of repair junction signatures of TSS-associated translocations in wild-type versus classical nonhomologous end-joining (C-NHEJ)-deficient NSPCs reveals that both C-NHEJ and alternative end-joining pathways can generate translocations by joining TSS-proximal DSBs to DSBs on other chromosomes. Our studies show that the generation of transcription-associated DSBs is conserved across divergent cell types.

Indexed as

DNA Breaks, Double-StrandedTranscription, GeneticTranslocation, GeneticAnimalsAtaxia Telangiectasia Mutated ProteinsB-LymphocytesCells, CulturedDNA-Binding ProteinsDNA End-Joining RepairGenes, mycGenes, p53MiceMice, KnockoutNeural Stem CellsProto-Oncogene Proteins c-mycTranscription Initiation SiteAtaxia Telangiectasia Mutated ProteinsAtm protein, mouseDNA-Binding ProteinsMyc protein, mouseProto-Oncogene Proteins c-mycTumor Suppressor Protein p53XRCC4 protein, mousealternative end-joiningneural stem cellsnonhomologous end-joiningtranscriptiontranslocation

Identifiers

PMID26873106
PMCPMC4776469
OpenAlexW2256829667

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.