Evidence map›Paper›PMID 23071463›Full record

ArticlePLoS genetics2012

Complex chromosomal rearrangements mediated by break-induced replication involve structure-selective endonucleases.

Benjamin Pardo, Andrés Aguilera

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

37 citing papers in PubMed, 54 citations in OpenAlex.

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  4. Recurrent DNA nicks drive massive expansions of (GAA)Proceedings of the National Academy of Sciences of the United States of America · 2024
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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

2 authors at 1 institution in 1 country.

Benjamin PardoCentro Andaluz de Biología Molecular y Medicina Regenerativa CABIMER, Universidad de Sevilla, Sevilla, Spain.
Andrés Aguilera
Centro Andaluz de Biología Molecular y Medicina Regenerativa · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA double-strand break (DSB) repair occurring in repeated DNA sequences often leads to the generation of chromosomal rearrangements. Homologous recombination normally ensures a faithful repair of DSBs through a mechanism that transfers the genetic information of an intact donor template to the broken molecule. When only one DSB end shares homology to the donor template, conventional gene conversion fails to occur and repair can be channeled to a recombination-dependent replication pathway termed break-induced replication (BIR), which is prone to produce chromosome non-reciprocal translocations (NRTs), a classical feature of numerous human cancers. Using a newly designed substrate for the analysis of DSB-induced chromosomal translocations, we show that Mus81 and Yen1 structure-selective endonucleases (SSEs) promote BIR, thus causing NRTs. We propose that Mus81 and Yen1 are recruited at the strand invasion intermediate to allow the establishment of a replication fork, which is required to complete BIR. Replication template switching during BIR, a feature of this pathway, engenders complex chromosomal rearrangements when using repeated DNA sequences dispersed over the genome. We demonstrate here that Mus81 and Yen1, together with Slx4, also promote template switching during BIR. Altogether, our study provides evidence for a role of SSEs at multiple steps during BIR, thus participating in the destabilization of the genome by generating complex chromosomal rearrangements.

Indexed as

DNA RepairDNA ReplicationChromosome AberrationsChromosomes, FungalDNA-Binding ProteinsDNA, FungalElectrophoresis, Gel, Pulsed-FieldEndodeoxyribonucleasesEndonucleasesGene ConversionGenetic LociHolliday Junction ResolvasesMutationRecombination, GeneticSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsDNA-Binding ProteinsDNA, FungalEndodeoxyribonucleasesEndonucleasesHolliday Junction ResolvasesMUS81 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsSLX4 protein, S cerevisiaeYen1 protein, S cerevisiae

Identifiers

PMID23071463
PMCPMC3459980
OpenAlexW1978005916

What OpenQuestion holds

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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.