Evidence map›Paper›PMID 27932447›Full record

ArticleThe EMBO journal2017

Unloading of homologous recombination factors is required for restoring double-stranded DNA at damage repair loci.

Yulia Vasianovich, Veronika Altmannova, Oleksii Kotenko, Matthew D Newton, Lumir Krejci, Svetlana Makovets

Open access · hybridAbstract read
In one paragraph

Article in The EMBO journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

20 citing papers in PubMed, 28 citations in OpenAlex.

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  12. Meiosis-specific recombinase Dmc1 is a potent inhibitor of the Srs2 antirecombinase.Proceedings of the National Academy of Sciences of the United States of America · 2018
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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.

Yulia VasianovichInstitute of Cell Biology, School of Biological Sciences, University of Edinburgh, Edinburgh, UK.
Veronika AltmannovaDepartment of Biology, Masaryk University, Brno, Czech Republic.
Oleksii KotenkoInstitute of Cell Biology, School of Biological Sciences, University of Edinburgh, Edinburgh, UK.
Matthew D NewtonInstitute of Cell Biology, School of Biological Sciences, University of Edinburgh, Edinburgh, UK.
Lumir KrejciDepartment of Biology, Masaryk University, Brno, Czech Republic.
Svetlana MakovetsInstitute of Cell Biology, School of Biological Sciences, University of Edinburgh, Edinburgh, UK smakovet@staffmail.ed.ac.uk.ORCID 0000-0002-0226-2093
University of Edinburgh · GBMasaryk University · CZ

Funding

Medical Research Council G0900500
6 · The paper itself

Abstract

Cells use homology-dependent DNA repair to mend chromosome breaks and restore broken replication forks, thereby ensuring genome stability and cell survival. DNA break repair via homology-based mechanisms involves nuclease-dependent DNA end resection, which generates long tracts of single-stranded DNA required for checkpoint activation and loading of homologous recombination proteins Rad52/51/55/57. While recruitment of the homologous recombination machinery is well characterized, it is not known how its presence at repair loci is coordinated with downstream re-synthesis of resected DNA We show that Rad51 inhibits recruitment of proliferating cell nuclear antigen (PCNA), the platform for assembly of the DNA replication machinery, and that unloading of Rad51 by Srs2 helicase is required for efficient PCNA loading and restoration of resected DNA As a result, srs2Δ mutants are deficient in DNA repair correlating with extensive DNA processing, but this defect in srs2Δ mutants can be suppressed by inactivation of the resection nuclease Exo1. We propose a model in which during re-synthesis of resected DNA, the replication machinery must catch up with the preceding processing nucleases, in order to close the single-stranded gap and terminate further resection.

Indexed as

DNA DamageHomologous RecombinationRecombinational DNA RepairDNADNA Repair EnzymesModels, BiologicalProliferating Cell Nuclear AntigenRecombinasesSaccharomyces cerevisiaeDNADNA Repair EnzymesProliferating Cell Nuclear AntigenRecombinasesDNA re‐synthesisPCNARad51recombination machinerySrs2

Identifiers

PMID27932447
PMCPMC5239998
OpenAlexW2560401628

What OpenQuestion holds

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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.