Evidence map›Paper›PMID 19189942›Full record

ArticleGenetics2009

Suppression of the double-strand-break-repair defect of the Saccharomyces cerevisiae rad57 mutant.

Cindy W Fung, Amy M Mozlin, Lorraine S Symington

Abstract read
In one paragraph

Article in Genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
–field-weighted citation impact
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

29 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Rad54 and Rdh54 prevent Srs2-mediated disruption of Rad51 presynaptic filaments.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Mediators of homologous DNA pairing.Cold Spring Harbor perspectives in biology · 2014
    Review
  18. Activation of aflatoxin B1 by expression of human CYP1A2 polymorphisms in Saccharomyces cerevisiae.Mutation research. Genetic toxicology and environmental mutagenesis · 2014
    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.

Cindy W FungDepartment of Microbiology, Columbia University College of Physicians and Surgeons, New York, New York 10032, USA.
Amy M Mozlin
Lorraine S Symington

Funding

MECHANISMS OF DOUBLE STRAND BREAK REPAIR IN YEASTR01GM054099 · NIGMS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI SYMINGTON, LORRAINE S · 1997 to 2009
$2.5M
TRAINING PROGRAM IN MICROBIOLOGY FOR INFECTIOUS DISEASEST32AI007161 · NIAID · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI FIDOCK, DAVID A · 1985 to 2008
$1.9M
NIAID NIH HHS T32 AI007161NIAID NIH HHS T32 AI07161NIGMS NIH HHS GM054099NIGMS NIH HHS R01 GM054099
6 · The paper itself

Abstract

The Rad51 paralogs Rad55 and Rad57 form a heterodimer required to mediate the formation and/or stabilization of the Rad51 filament. To further characterize the function of Rad55-Rad57, we used a combination of rad57 partial suppressors to determine whether the DNA repair and recombination defects of the rad57 mutant could be completely suppressed. The combination of all suppressors, elevated temperature, srs2, rad51-I345T, and mating-type (MAT) heterozygosity resulted in almost complete suppression of the rad57 mutant defect in the recruitment of Rad51 to DNA-damaged sites, as well as survival in response to ionizing radiation and camptothecin. In a physical assay to monitor the kinetics of double-strand-break (DSB)-induced gene conversion, the rad57 mutant defect was effectively suppressed by srs2 and MAT heterozygosity, but these same suppressors failed to suppress the spontaneous recombination defect. Thus the Rad55-Rad57 heterodimer appears to have a unique function in spontaneous recombination that is not essential for DSB repair. Furthermore, we investigated the currently unknown mechanism of rad57 suppression by MAT heterozygosity and found that it is independent of DNL4.

Indexed as

DNA Breaks, Double-StrandedAdenosine TriphosphatasesDNA-Binding ProteinsDNA HelicasesDNA RepairDNA Repair EnzymesDown-RegulationGene ConversionGenes, Mating Type, FungalHeterozygoteModels, BiologicalMutant ProteinsOrganisms, Genetically ModifiedProtein MultimerizationRecombination, GeneticSaccharomyces cerevisiaeAdenosine TriphosphatasesDNA-Binding ProteinsDNA HelicasesDNA Repair EnzymesMutant ProteinsRAD55 protein, S cerevisiaeRAD57 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsSRS2 protein, S cerevisiae

Identifiers

PMID19189942
PMCPMC2666491

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.