Evidence map›Paper›PMID 7635279›Full record

ArticleGenetics1995

Suppression of a new allele of the yeast RAD52 gene by overexpression of RAD51, mutations in srs2 and ccr4, or mating-type heterozygosity.

D Schild

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
2.2field-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

72 citing papers in PubMed, 132 citations in OpenAlex.

  1. Article
  2. Article
  3. Regulation of recombination and genomic maintenance.Cold Spring Harbor perspectives in biology · 2015
    Review
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  6. Article
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  8. Article
  9. Article
  10. Review
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  12. Presynaptic filament dynamics in homologous recombination and DNA repair.Critical reviews in biochemistry and molecular biology · 2011
    Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Nej1 recruits the Srs2 helicase to DNA double-strand breaks and supports repair by a single-strand annealing-like mechanism.Proceedings of the National Academy of Sciences of the United States of America · 2009
    Article
  20. Article

12 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

D SchildLife Sciences Division, Lawrence Berkeley Laboratory, California 94720, USA.
Lawrence Berkeley National Laboratory · US

Funding

YEAST RAD GENES IN REPAIR, RECOMBINATION, AND MEIOSISR01GM030990 · NIGMS · UNIVERSITY OF CALIFORNIA BERKELEY · PI SCHILD, DAVID · 1985 to 2001
$718k
NIGMS NIH HHS GM-30990
6 · The paper itself

Abstract

The RAD52 gene of Saccharomyces cerevisiae is involved both in the recombinational repair of DNA damage and in mitotic and meiotic recombination. A new allele of rad52 has been isolated that has unusual properties. Unlike other alleles of rad52, this allele (rad52-20) is partially suppressed by an srs2 deletion; srs2 mutations normally act to suppress only rad6 and rad18 mutations. In addition, although haploid rad52-20 strains are very X-ray sensitive, diploids homozygous for this allele are only slightly X-ray sensitive and undergo normal meiosis and meiotic recombination. Because rad52-20 diploids homozygous for mating type are very X-ray sensitive, mating-type heterozygosity is acting to suppress rad52-20. Mating-type heterozygosity suppresses this allele even in haploids, because sir mutations, which result in expression of the normally silent mating-type cassettes, were identified among the extragenic revertants of rad52-20. A new allele of srs2 and alleles of the transcriptional regulatory genes ccr4 and caf1 were among the other extragenic revertants of rad52-20. Because other researchers have shown that the RAD51 and RAD52 proteins interact, RAD51 on a high copy number plasmid was tested and found to suppress the rad52-20 allele, but RAD54, 55 and 57 did not suppress. The RAD51 plasmid did not suppress rad52-1. The rad52-20 allele may encode a protein that has low affinity binding to the RAD51 protein. To test whether the selected revertants suppressed rad52-20 by elevating the expression of RAD51, an integrated RAD51-lacZ fusion was genetically crossed into each revertant. Because none of the revertants increased the level of RAD51-lacZ, the revertants must exert their effect by one or more mechanisms that are not mediated by RAD51.

Indexed as

AllelesGene Expression Regulation, FungalGenes, FungalHistone DeacetylasesHomeodomain ProteinsRecombination, GeneticRibonucleasesSaccharomyces cerevisiae ProteinsSilent Information Regulator Proteins, Saccharomyces cerevisiaeSuppression, GeneticDNA-Binding ProteinsDNA HelicasesFungal ProteinsHeterozygoteMating FactorPeptidesCCR4 protein, S cerevisiaeDNA-Binding ProteinsDNA HelicasesFungal ProteinsHistone DeacetylasesHomeodomain ProteinsMATA2 protein, S cerevisiaeMating FactorPeptidesPOP2 protein, S cerevisiaeRecombinant Fusion ProteinsRepressor ProteinsRibonucleasesSaccharomyces cerevisiae ProteinsSilent Information Regulator Proteins, Saccharomyces cerevisiaeSIR1 protein, S cerevisiaeSIR2 protein, S cerevisiaeSIR3 protein, S cerevisiaeSIR4 protein, S cerevisiaeSirtuin 2SirtuinsTrans-ActivatorsTranscription Factors

Identifiers

PMID7635279
PMCPMC1206541
OpenAlexW1840794711

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.