Evidence map›Paper›PMID 24651490›Full record

ArticlePloS one2014

ATM alters the otherwise robust chromatin mobility at sites of DNA double-strand breaks (DSBs) in human cells.

Annabelle Becker, Marco Durante, Gisela Taucher-Scholz, Burkhard Jakob

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

26 citing papers in PubMed, 43 citations in OpenAlex.

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  11. Complex Chromatin Motions for DNA Repair.Frontiers in genetics · 2020
    Review
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  14. Article
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  17. And yet, it moves: nuclear and chromatin dynamics of a heterochromatic double-strand break.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017
    Review
  18. Review
  19. Article
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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

4 authors at 2 institutions in 1 country.

Annabelle BeckerGSI, Helmholtzzentrum für Schwerionenforschung GmbH, Darmstadt, Germany.
Marco DuranteGSI, Helmholtzzentrum für Schwerionenforschung GmbH, Darmstadt, Germany; Technical University of Darmstadt, Darmstadt, Germany.
Gisela Taucher-ScholzGSI, Helmholtzzentrum für Schwerionenforschung GmbH, Darmstadt, Germany; Technical University of Darmstadt, Darmstadt, Germany.
Burkhard JakobGSI, Helmholtzzentrum für Schwerionenforschung GmbH, Darmstadt, Germany.
GSI Helmholtz Centre for Heavy Ion Research · DETechnical University of Darmstadt · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ionizing radiation induces DNA double strand breaks (DSBs) which can lead to the formation of chromosome rearrangements through error prone repair. In mammalian cells the positional stability of chromatin contributes to the maintenance of genome integrity. DSBs exhibit only a small, submicron scale diffusive mobility, but a slight increase in the mobility of chromatin domains by the induction of DSBs might influence repair fidelity and the formation of translocations. The radiation-induced local DNA decondensation in the vicinity of DSBs is one factor potentially enhancing the mobility of DSB-containing chromatin domains. Therefore in this study we focus on the influence of different chromatin modifying proteins, known to be activated by the DNA damage response, on the mobility of DSBs. IRIF (ionizing radiation induced foci) in U2OS cells stably expressing 53BP1-GFP were used as a surrogate marker of DSBs. Low angle charged particle irradiation, known to trigger a pronounced DNA decondensation, was used for the defined induction of linear tracks of IRIF. Our results show that movement of IRIF is independent of the investigated chromatin modifying proteins like ACF1 or PARP1 and PARG. Also depletion of proteins that tether DNA strands like MRE11 and cohesin did not alter IRIF dynamics significantly. Inhibition of ATM, a key component of DNA damage response signaling, resulted in a pronounced confinement of DSB mobility, which might be attributed to a diminished radiation induced decondensation. This confinement following ATM inhibition was confirmed using X-rays, proving that this effect is not restricted to densely ionizing radiation. In conclusion, repair sites of DSBs exhibit a limited mobility on a small spatial scale that is mainly unaffected by depletion of single remodeling or DNA tethering proteins. However, it relies on functional ATM kinase which is considered to influence the chromatin structure after irradiation.

Indexed as

DNA Breaks, Double-StrandedAtaxia Telangiectasia Mutated ProteinsBromodomain Containing ProteinsCell Cycle ProteinsCell LineChromatinChromatin Assembly and DisassemblyChromosomal Proteins, Non-HistoneCohesinsDNA RepairGene ExpressionGene Knockdown TechniquesGenes, ReporterHumansMultiprotein ComplexesPoly(ADP-ribose) PolymerasesAtaxia Telangiectasia Mutated ProteinsBAZ1A protein, humanBromodomain Containing ProteinsCell Cycle ProteinsChromatinChromosomal Proteins, Non-HistoneCohesinsMultiprotein ComplexesPoly(ADP-ribose) PolymerasesTranscription Factors

Identifiers

PMID24651490
PMCPMC3961414
OpenAlexW2028307133

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.