Evidence map›Paper›PMID 27074148›Full record

ArticlePLoS genetics2016

Role of Double-Strand Break End-Tethering during Gene Conversion in Saccharomyces cerevisiae.

Suvi Jain, Neal Sugawara, James E Haber

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.3field-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

17 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
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  3. Review
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  5. Article
  6. Review
  7. Article
  8. Frequency of DNA end joiningProceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  9. Review
  10. Article
  11. Article
  12. DNA Repair: The Search for Homology.BioEssays : news and reviews in molecular, cellular and developmental biology · 2018
    Review
  13. Review
  14. Article
  15. Article
  16. Break-induced replication links microsatellite expansion to complex genome rearrangements.BioEssays : news and reviews in molecular, cellular and developmental biology · 2017
    Review
  17. Article
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.

Suvi JainDepartment of Biology and Rosenstiel Medical Center, Brandeis University, Waltham, Massachusetts, United States of America.
Neal SugawaraDepartment of Biology and Rosenstiel Medical Center, Brandeis University, Waltham, Massachusetts, United States of America.
James E HaberDepartment of Biology and Rosenstiel Medical Center, Brandeis University, Waltham, Massachusetts, United States of America.
Brandeis University · US

Funding

Arrest, Recovery, and Adaptation from DNA DamageR01GM061766 · NIGMS · BRANDEIS UNIVERSITY · PI HABER, JAMES E · 2001 to 2016
$4.6M
Analysis of Break-Induced ReplicationR01GM076020 · NIGMS · BRANDEIS UNIVERSITY · PI HABER, JAMES E · 2006 to 2017
$3.4M
NIGMS NIH HHS GM22056NIGMS NIH HHS GM61766NIGMS NIH HHS R01 GM061766NIGMS NIH HHS R01 GM076020
6 · The paper itself

Abstract

Correct repair of DNA double-strand breaks (DSBs) is critical for maintaining genome stability. Whereas gene conversion (GC)-mediated repair is mostly error-free, repair by break-induced replication (BIR) is associated with non-reciprocal translocations and loss of heterozygosity. We have previously shown that a Recombination Execution Checkpoint (REC) mediates this competition by preventing the BIR pathway from acting on DSBs that can be repaired by GC. Here, we asked if the REC can also determine whether the ends that are engaged in a GC-compatible configuration belong to the same break, since repair involving ends from different breaks will produce potentially deleterious translocations. We report that the kinetics of repair are markedly delayed when the two DSB ends that participate in GC belong to different DSBs (termed Trans) compared to the case when both DSB ends come from the same break (Cis). However, repair in Trans still occurs by GC rather than BIR, and the overall efficiency of repair is comparable. Hence, the REC is not sensitive to the "origin" of the DSB ends. When the homologous ends for GC are in Trans, the delay in repair appears to reflect their tethering to sequences on the other side of the DSB that themselves recombine with other genomic locations with which they share sequence homology. These data support previous observations that the two ends of a DSB are usually tethered to each other and that this tethering facilitates both ends encountering the same donor sequence. We also found that the presence of homeologous/repetitive sequences in the vicinity of a DSB can distract the DSB end from finding its bona fide homologous donor, and that inhibition of GC by such homeologous sequences is markedly increased upon deleting Sgs1 but not Msh6.

Indexed as

DNA Breaks, Double-StrandedCell SurvivalChromosomes, FungalDNA, FungalGene ConversionGenomic InstabilityRecombinational DNA RepairSaccharomyces cerevisiaeSequence Homology, Nucleic AcidDNA, Fungal

Identifiers

PMID27074148
PMCPMC4830573
OpenAlexW2338376743

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.