Evidence map›Paper›PMID 10430580›Full record

ArticleGenetics1999

Repair of endonuclease-induced double-strand breaks in Saccharomyces cerevisiae: essential role for genes associated with nonhomologous end-joining.

L K Lewis, J W Westmoreland, M A Resnick

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Genetics, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Activities of human exonuclease 1 that promote cleavage of transcribed immunoglobulin switch regions.Proceedings of the National Academy of Sciences of the United States of America · 2008
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  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

3 authors at 1 institution in 1 country.

L K LewisLaboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA.
J W Westmoreland
M A Resnick
National Institute of Environmental Health Sciences · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Repair of double-strand breaks (DSBs) in chromosomal DNA by nonhomologous end-joining (NHEJ) is not well characterized in the yeast Saccharomyces cerevisiae. Here we demonstrate that several genes associated with NHEJ perform essential functions in the repair of endonuclease-induced DSBs in vivo. Galactose-induced expression of EcoRI endonuclease in rad50, mre11, or xrs2 mutants, which are deficient in plasmid DSB end-joining and some forms of recombination, resulted in G2 arrest and rapid cell killing. Endonuclease synthesis also produced moderate cell killing in sir4 strains. In contrast, EcoRI caused prolonged cell-cycle arrest of recombination-defective rad51, rad52, rad54, rad55, and rad57 mutants, but cells remained viable. Cell-cycle progression was inhibited in excision repair-defective rad1 mutants, but not in rad2 cells, indicating a role for Rad1 processing of the DSB ends. Phenotypic responses of additional mutants, including exo1, srs2, rad5, and rdh54 strains, suggest roles in recombinational repair, but not in NHEJ. Interestingly, the rapid cell killing in haploid rad50 and mre11 strains was largely eliminated in diploids, suggesting that the cohesive-ended DSBs could be efficiently repaired by homologous recombination throughout the cell cycle in the diploid mutants. These results demonstrate essential but separable roles for NHEJ pathway genes in the repair of chromosomal DSBs that are structurally similar to those occurring during cellular development.

Indexed as

Adenosine TriphosphatasesDNA RepairExodeoxyribonucleasesSaccharomyces cerevisiae ProteinsTyrosine 3-Monooxygenase14-3-3 ProteinsCell CycleDeoxyribonuclease EcoRIDiploidyDNADNA-Binding ProteinsDNA DamageDNA, FungalDNA HelicasesDNA Repair EnzymesEndodeoxyribonucleases14-3-3 ProteinsAdenosine TriphosphatasesDeoxyribonuclease EcoRIDNADNA-Binding ProteinsDNA, FungalDNA HelicasesDNA Repair EnzymesEndodeoxyribonucleasesEndonucleasesExodeoxyribonucleasesFungal Proteinshigh affinity DNA-binding factor, S cerevisiaeLigasesMRE11 protein, S cerevisiaeProteinsRAD10 protein, S cerevisiaeRAD1 protein, S cerevisiaeRAD2 protein, S cerevisiaeRAD50 protein, S cerevisiaeRad52 DNA Repair and Recombination ProteinRAD52 protein, S cerevisiaeRAD5 protein, S cerevisiaeRecombinant Fusion ProteinsSaccharomyces cerevisiae ProteinsSingle-Strand Specific DNA and RNA EndonucleasesTyrosine 3-MonooxygenaseUbiquitin-Conjugating EnzymesXRS2 protein, S cerevisiae

Identifiers

PMID10430580
PMCPMC1460701
OpenAlexW1938372995

What OpenQuestion holds

Textmetadata
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.