Evidence map›Paper›PMID 28419093›Full record

ArticlePLoS genetics2017

Microhomology-mediated end joining induces hypermutagenesis at breakpoint junctions.

Supriya Sinha, Fuyang Li, Diana Villarreal, Jae Hoon Shim, Suhyeon Yoon, Kyungjae Myung, Eun Yong Shim, Sang Eun Lee

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

25 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

8 authors at 5 institutions in 2 countries.

Supriya SinhaDepartment of Molecular Medicine, Institute of Biotechnology, University of Texas Health Science Center at San Antonio, San Antonio, TX, United States of America.ORCID 0000-0001-7315-6063
Fuyang LiDepartment of Molecular Medicine, Institute of Biotechnology, University of Texas Health Science Center at San Antonio, San Antonio, TX, United States of America.
Diana VillarrealChildren's Hospital of San Antonio, Baylor College of Medicine, San Antonio, TX, United States of America.
Jae Hoon ShimKorea Institute of Radiological & Medical Sciences (KIRAMS), 75 Nowon-ro, Nowon-gu, Seoul, Republic of Korea.
Suhyeon YoonDepartment of Biological Science, School of Life Sciences, Ulsan National Institute of Science and Technology (UNIST), Ulsan 44818, Republic of Korea.ORCID 0000-0002-3883-8330
Kyungjae MyungCenter for Genomic Integrity, Institute for Basic Science, Ulsan 44818, Republic of Korea.
Eun Yong ShimDepartment of Radiation Oncology, University of Texas Health Science Center at San Antonio, San Antonio, TX, United States of America.
Sang Eun LeeDepartment of Molecular Medicine, Institute of Biotechnology, University of Texas Health Science Center at San Antonio, San Antonio, TX, United States of America.
The University of Texas Health Science Center at San Antonio · USBaylor College of Medicine · USInstitute for Basic Science · KRKorea Institute of Radiological and Medical Sciences · KRUlsan National Institute of Science and Technology · KR

Funding

Mechanisms of Error Prone Repair of DNA BreaksR01GM071011 · NIGMS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI LEE, SANG EUN · 2004 to 2021
$4.5M
NIGMS NIH HHS R01 GM071011
6 · The paper itself

Abstract

Microhomology (MH) flanking a DNA double-strand break (DSB) drives chromosomal rearrangements but its role in mutagenesis has not yet been analyzed. Here we determined the mutation frequency of a URA3 reporter gene placed at multiple locations distal to a DSB, which is flanked by different sizes (15-, 18-, or 203-bp) of direct repeat sequences for efficient repair in budding yeast. Induction of a DSB accumulates mutations in the reporter gene situated up to 14-kb distal to the 15-bp MH, but more modestly to those carrying 18- and 203-bp or no homology. Increased mutagenesis in MH-mediated end joining (MMEJ) appears coupled to its slower repair kinetics and the extensive resection occurring at flanking DNA. Chromosomal translocations via MMEJ also elevate mutagenesis of the flanking DNA sequences 7.1 kb distal to the breakpoint junction as compared to those without MH. The results suggest that MMEJ could destabilize genomes by triggering structural alterations and increasing mutation burden.

Indexed as

ChromosomesDNADNA-Binding ProteinsDNA Breaks, Double-StrandedDNA End-Joining RepairGalactoseKineticsMutagenesisMutagenesis, InsertionalSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsTranslocation, GeneticDNADNA-Binding ProteinsGalactoseSaccharomyces cerevisiae ProteinsURA3 protein, S cerevisiae

Identifiers

PMID28419093
PMCPMC5413072
OpenAlexW2606011604

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.