Evidence map›Paper›PMID 20861312›Full record

ArticleMolecular biology of the cell2010

A centrosome-autonomous signal that involves centriole disengagement permits centrosome duplication in G2 phase after DNA damage.

Burcu Inanç, Helen Dodson, Ciaran G Morrison

Abstract read
In one paragraph

Article in Molecular biology of the cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

34 citing papers in PubMed, 56 citations in OpenAlex.

  1. Review
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  11. Building the right centriole for each cell type.The Journal of cell biology · 2018
    Review
  12. Article
  13. Article
  14. Article
  15. Centrosomes are multifunctional regulators of genome stability.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2016
    Review
  16. Centrosomes in the DNA damage response--the hub outside the centre.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2016
    Review
  17. Article
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  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

3 authors at 1 institution in 1 country.

Burcu InançCentre for Chromosome Biology, School of Natural Sciences, National University of Ireland Galway, Galway, Ireland.
Helen Dodson
Ciaran G Morrison
Ollscoil na Gaillimhe – University of Galway · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA damage can induce centrosome overduplication in a manner that requires G2-to-M checkpoint function, suggesting that genotoxic stress can decouple the centrosome and chromosome cycles. How this happens is unclear. Using live-cell imaging of cells that express fluorescently tagged NEDD1/GCP-WD and proliferating cell nuclear antigen, we found that ionizing radiation (IR)-induced centrosome amplification can occur outside S phase. Analysis of synchronized populations showed that significantly more centrosome amplification occurred after irradiation of G2-enriched populations compared with G1-enriched or asynchronous cells, consistent with G2 phase centrosome amplification. Irradiated and control populations of G2 cells were then fused to test whether centrosome overduplication is allowed through a diffusible stimulatory signal, or the loss of a duplication-inhibiting signal. Irradiated G2/irradiated G2 cell fusions showed significantly higher centrosome amplification levels than irradiated G2/unirradiated G2 fusions. Chicken-human cell fusions demonstrated that centrosome amplification was limited to the irradiated partner. Our finding that only the irradiated centrosome can duplicate supports a model where a centrosome-autonomous inhibitory signal is lost upon irradiation of G2 cells. We observed centriole disengagement after irradiation. Although overexpression of dominant-negative securin did not affect IR-induced centrosome amplification, Plk1 inhibition reduced radiation-induced amplification. Together, our data support centriole disengagement as a licensing signal for DNA damage-induced centrosome amplification.

Indexed as

DNA DamageAnimalsCalcium-Binding ProteinsCell CycleCell Cycle ProteinsCell Line, TumorCentriolesCentrosomeG2 PhaseHumansImmunoblottingLuminescent ProteinsMicroscopy, FluorescenceMicrotubule-Associated ProteinsProliferating Cell Nuclear AntigenSignal TransductionCalcium-Binding ProteinsCell Cycle ProteinsCETN2 protein, humanLuminescent ProteinsMicrotubule-Associated ProteinsNEDD1 protein, humanProliferating Cell Nuclear Antigen

Identifiers

PMID20861312
PMCPMC2982117
OpenAlexW2038747158

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.