Evidence map›Paper›PMID 21317883›Full record

ArticleNature cell biology2011

53BP1 nuclear bodies form around DNA lesions generated by mitotic transmission of chromosomes under replication stress.

Claudia Lukas, Velibor Savic, Simon Bekker-Jensen, Carsten Doil, Beate Neumann, Ronni Sølvhøj Pedersen, Merete Grøfte, Kok Lung Chan, Ian David Hickson, Jiri Bartek and 1 more

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In one paragraph

Article in Nature cell biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 446 papers.

0numbers the graph read from it
0cells of the map it votes in
446citing papers in PubMed
–field-weighted citation impact
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

446 citing papers in PubMed.

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386 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors.

Claudia LukasCentre for Genotoxic Stress Research, Institute of Cancer Biology, Danish Cancer Society, Strandboulevarden 49, DK-2100 Copenhagen, Denmark.
Velibor Savic
Simon Bekker-Jensen
Carsten Doil
Beate Neumann
Ronni Sølvhøj Pedersen
Merete Grøfte
Kok Lung Chan
Ian David Hickson
Jiri Bartek
Jiri Lukas

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Completion of genome duplication is challenged by structural and topological barriers that impede progression of replication forks. Although this can seriously undermine genome integrity, the fate of DNA with unresolved replication intermediates is not known. Here, we show that mild replication stress increases the frequency of chromosomal lesions that are transmitted to daughter cells. Throughout G1, these lesions are sequestered in nuclear compartments marked by p53-binding protein 1 (53BP1) and other chromatin-associated genome caretakers. We show that the number of such 53BP1 nuclear bodies increases after genetic ablation of BLM, a DNA helicase associated with dissolution of entangled DNA. Conversely, 53BP1 nuclear bodies are partially suppressed by knocking down SMC2, a condensin subunit required for mechanical stability of mitotic chromosomes. Finally, we provide evidence that 53BP1 nuclear bodies shield chromosomal fragile sites sequestered in these compartments against erosion. Together, these data indicate that restoration of DNA or chromatin integrity at loci prone to replication problems requires mitotic transmission to the next cell generations.

Indexed as

DNA ReplicationMitosisCell CycleCell Line, TumorCell NucleusChromatinChromosomesDNADNA DamageDNA HelicasesGene Expression Regulation, NeoplasticHumansIntracellular Signaling Peptides and ProteinsRNA, Small InterferingTime FactorsTumor Suppressor p53-Binding Protein 1ChromatinDNADNA HelicasesIntracellular Signaling Peptides and ProteinsRNA, Small InterferingTP53BP1 protein, humanTumor Suppressor p53-Binding Protein 1

Identifiers

PMID21317883

What OpenQuestion holds

Textmetadata
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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.