Evidence map›Paper›PMID 23586741›Full record

ArticleBMC genomics2013

A multistep genomic screen identifies new genes required for repair of DNA double-strand breaks in Saccharomyces cerevisiae.

Jennifer Summers McKinney, Sunaina Sethi, Jennifer DeMars Tripp, Thuy N Nguyen, Brian A Sanderson, James W Westmoreland, Michael A Resnick, L Kevin Lewis

Open access · goldAbstract read
In one paragraph

Article in BMC genomics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

11 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Consider the workhorse: Nonhomologous end-joining in budding yeast.Biochemistry and cell biology = Biochimie et biologie cellulaire · 2016
    Review
  10. Article
  11. Review
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 3 institutions in 1 country.

Jennifer Summers McKinneyDepartment of Chemistry and Biochemistry, Texas State University, San Marcos, TX 78666, USA.
Sunaina Sethi
Jennifer DeMars Tripp
Thuy N Nguyen
Brian A Sanderson
James W Westmoreland
Michael A Resnick
L Kevin Lewis
Texas State University · USNational Institute of Environmental Health Sciences · USNational Institutes of Health · US

Funding

Double Strand Break Repair And RecombinationZIAES021016 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI MENENDEZ RENDON, DANIEL · 2009 to 2018
$5.6M
Genome-wide analysis identifies genes required for repair of DNA strand breaksR15GM099049 · NIGMS · TEXAS STATE UNIVERSITY · PI LEWIS, LYSLE KEVIN · 2012 to 2012
$293k
NIGMS NIH HHS 1R15GM09904901NIGMS NIH HHS R15 GM099049
6 · The paper itself

Abstract

backgroundEfficient mechanisms for rejoining of DNA double-strand breaks (DSBs) are vital because misrepair of such lesions leads to mutation, aneuploidy and loss of cell viability. DSB repair is mediated by proteins acting in two major pathways, called homologous recombination and nonhomologous end-joining. Repair efficiency is also modulated by other processes such as sister chromatid cohesion, nucleosome remodeling and DNA damage checkpoints. The total number of genes influencing DSB repair efficiency is unknown.

resultsTo identify new yeast genes affecting DSB repair, genes linked to gamma radiation resistance in previous genome-wide surveys were tested for their impact on repair of site-specific DSBs generated by in vivo expression of EcoRI endonuclease. Eight members of the RAD52 group of DNA repair genes (RAD50, RAD51, RAD52, RAD54, RAD55, RAD57, MRE11 and XRS2) and 73 additional genes were found to be required for efficient repair of EcoRI-induced DSBs in screens utilizing both MATa and MATα deletion strain libraries. Most mutants were also sensitive to the clastogenic chemicals MMS and bleomycin. Several of the non-RAD52 group genes have previously been linked to DNA repair and over half of the genes affect nuclear processes. Many proteins encoded by the protective genes have previously been shown to associate physically with each other and with known DNA repair proteins in high-throughput proteomics studies. A majority of the proteins (64%) share sequence similarity with human proteins, suggesting that they serve similar functions.

conclusionsWe have used a genetic screening approach to detect new genes required for efficient repair of DSBs in Saccharomyces cerevisiae. The findings have spotlighted new genes that are critical for maintenance of genome integrity and are therefore of greatest concern for their potential impact when the corresponding gene orthologs and homologs are inactivated or polymorphic in human cells.

Indexed as

DNA Breaks, Double-StrandedGenomicsAnimalsAntineoplastic AgentsBleomycinDNA RepairGamma RaysGenes, PlantHumansMethyl MethanesulfonateMiceRatsSaccharomyces cerevisiaeAntineoplastic AgentsBleomycinMethyl Methanesulfonate

Identifiers

PMID23586741
PMCPMC3637596
OpenAlexW2080036268

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.