Evidence map›Paper›PMID 24806966›Full record

ArticleJournal of cell science2014

The extent of error-prone replication restart by homologous recombination is controlled by Exo1 and checkpoint proteins.

Ellen Tsang, Izumi Miyabe, Ismail Iraqui, Jiping Zheng, Sarah A E Lambert, Antony M Carr

Open access · hybridAbstract read
In one paragraph

Article in Journal of cell science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.3field-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

32 citing papers in PubMed, 46 citations in OpenAlex.

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  14. Exonuclease 1 (Exo1) Participates in Mammalian Non-Homologous End Joining and Contributes to Drug Resistance in Ovarian Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2020
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  15. Genes · 2020
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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

6 authors at 2 institutions in 2 countries.

Ellen TsangGenome Damage and Stability Centre, University of Sussex, Brighton, Sussex BN1 9RQ, UK.
Izumi MiyabeGenome Damage and Stability Centre, University of Sussex, Brighton, Sussex BN1 9RQ, UK.
Ismail IraquiInstitut Curie-Centre National de la Recherche Scientifique, UMR3348, Réponse Cellulaire aux Perturbations de la Réplication, Centre Universitaire, Bat 110, 91405 Orsay, France.
Jiping ZhengDepartment of Biotechnology, College of Agriculture, No.58 Renmin Avenue, Haikou, Hainan Province 570228, P.R. China.
Sarah A E LambertInstitut Curie-Centre National de la Recherche Scientifique, UMR3348, Réponse Cellulaire aux Perturbations de la Réplication, Centre Universitaire, Bat 110, 91405 Orsay, France Sarah.Lambert@curie.fr a.m.carr@sussex.ac.uk.
Antony M CarrGenome Damage and Stability Centre, University of Sussex, Brighton, Sussex BN1 9RQ, UK Sarah.Lambert@curie.fr a.m.carr@sussex.ac.uk.
University of Sussex · GBInstitut Curie · FR

Funding

Medical Research Council G1100074
6 · The paper itself

Abstract

Genetic instability, a hallmark of cancer, can occur when the replication machinery encounters a barrier. The intra-S-phase checkpoint maintains stalled replication forks in a replication-competent configuration by phosphorylating replisome components and DNA repair proteins to prevent forks from catastrophically collapsing. Here, we report a novel function of the core Schizosaccharomyces pombe checkpoint sensor kinase, Rad3 (an ATR orthologue), that is independent of Chk1 and Cds1 (a CHK2 orthologue); Rad3(ATR) regulates the association of recombination factors with collapsed forks, thus limiting their genetic instability. We further reveal antagonistic roles for Rad3(ATR) and the 9-1-1 clamp - Rad3(ATR) restrains MRN- and Exo1-dependent resection, whereas the 9-1-1 complex promotes Exo1 activity. Interestingly, the MRN complex, but not its nuclease activity, promotes resection and the subsequent association of recombination factors at collapsed forks. The biological significance of this regulation is revealed by the observation that Rad3(ATR) prevents Exo1-dependent genome instability upstream of a collapsed fork without affecting the efficiency of recombination-mediated replication restart. We propose that the interplay between Rad3(ATR) and the 9-1-1 clamp functions to fine-tune the balance between the need for the recovery of replication through recombination and the risk of increased genome instability.

Indexed as

Cell Cycle ProteinsCheckpoint Kinase 1DNA ReplicationExodeoxyribonucleasesGenomic InstabilityHomologous RecombinationProtein KinasesSchizosaccharomycesSchizosaccharomyces pombe ProteinsCell Cycle ProteinsCheckpoint Kinase 1Chk1 protein, S pombeexodeoxyribonuclease IExodeoxyribonucleasesProtein KinasesSchizosaccharomyces pombe ProteinsCheckpointGenome instabilityHomologous recombination

Identifiers

PMID24806966
PMCPMC4075360
OpenAlexW2163600757

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.