Evidence map›Paper›PMID 21647453›Full record

ArticlePloS one2011

Rtt107 phosphorylation promotes localisation to DNA double-stranded breaks (DSBs) and recombinational repair between sister chromatids.

Pranav Ullal, Felipe Vilella-Mitjana, Adam Jarmuz, Luis Aragón

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.4field-weighted citation impact, top 38% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Pranav UllalCell Cycle Group, Medical Research Council, Clinical Sciences Centre, Imperial College, London, United Kingdom.
Felipe Vilella-Mitjana
Adam Jarmuz
Luis Aragón
Medical Research Council · GBImperial College London · GB

Funding

Medical Research Council MC_U120074328
6 · The paper itself

Abstract

Efficient repair of DNA double-stranded breaks (DSB) requires a coordinated response at the site of lesion. Nucleolytic resection commits repair towards homologous recombination, which preferentially occurs between sister chromatids. DSB resection promotes recruitment of the Mec1 checkpoint kinase to the break. Rtt107 is a target of Mec1 and serves as a scaffold during repair. Rtt107 plays an important role during rescue of damaged replication forks, however whether Rtt107 contributes to the repair of DSBs is unknown. Here we show that Rtt107 is recruited to DSBs induced by the HO endonuclease. Rtt107 phosphorylation by Mec1 and its interaction with the Smc5-Smc6 complex are both required for Rtt107 loading to breaks, while Rtt107 regulators Slx4 and Rtt101 are not. We demonstrate that Rtt107 has an effect on the efficiency of sister chromatid recombination (SCR) and propose that its recruitment to DSBs, together with the Smc5-Smc6 complex is important for repair through the SCR pathway.

Indexed as

DNA Breaks, Double-StrandedCell Cycle ProteinsDNA RepairEndonucleasesIntracellular Signaling Peptides and ProteinsNuclear ProteinsPhosphorylationProtein Serine-Threonine KinasesProtein TransportSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSister Chromatid ExchangeCell Cycle ProteinsEndonucleasesIntracellular Signaling Peptides and ProteinsMEC1 protein, S cerevisiaeNuclear ProteinsProtein Serine-Threonine KinasesRTT107 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsSMC5 protein, S cerevisiaeSMC6 protein, S cerevisiae

Identifiers

PMID21647453
PMCPMC3102082
OpenAlexW2011244647

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.