Evidence map›Paper›PMID 10388811›Full record

ArticleGenetics1999

Radiosensitive and mitotic recombination phenotypes of the Saccharomyces cerevisiae dun1 mutant defective in DNA damage-inducible gene expression.

M Fasullo, J Koudelik, P AhChing, P Giallanza, C Cera

Open access · bronzeAbstract read
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 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

17 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Regulation of ribosomal DNA amplification by the TOR pathway.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  3. Nucleotide salvage deficiencies, DNA damage and neurodegeneration.International journal of molecular sciences · 2015
    Review
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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

5 authors at 2 institutions in 1 country.

M FasulloDepartment of Biochemistry and Molecular Biology, The Albany Medical College, Albany, New York 12208, USA. mfasullo@ccgateway.amc.edu
J Koudelik
P AhChing
P Giallanza
C Cera
Albany Medical Center Hospital · USUniversity of Chicago · US

Funding

RADIATION INDUCTION OF GENOMIC REARRANGEMENTS IN YEASTR01CA070105 · NCI · ORDWAY RESEARCH INSTITUTE, INC. · PI FASULLO, MICHAEL THOMAS · 2000 to 2004
$1.1M
RADIATION INDUCTION OF GENOMIC REARRANGEMENTS IN YEASTR29CA070105 · NCI · LOYOLA UNIVERSITY CHICAGO · PI FASULLO, MICHAEL THOMAS · 1995 to 1999
–
NCI NIH HHS CA70105
6 · The paper itself

Abstract

The biological significance of DNA damage-induced gene expression in conferring resistance to DNA-damaging agents is unclear. We investigated the role of DUN1-mediated, DNA damage-inducible gene expression in conferring radiation resistance in Saccharomyces cerevisiae. The DUN1 gene was assigned to the RAD3 epistasis group by quantitating the radiation sensitivities of dun1, rad52, rad1, rad9, rad18 single and double mutants, and of the dun1 rad9 rad52 triple mutant. The dun1 and rad52 single mutants were similar in terms of UV sensitivities; however, the dun1 rad52 double mutant exhibited a synergistic decrease in UV resistance. Both spontaneous intrachromosomal and heteroallelic gene conversion events between two ade2 alleles were enhanced in dun1 mutants, compared to DUN1 strains, and elevated recombination was dependent on RAD52 but not RAD1 gene function. Spontaneous sister chromatid exchange (SCE), as monitored between truncated his3 fragments, was not enhanced in dun1 mutants, but UV-induced SCE and heteroallelic recombination were enhanced. Ionizing radiation and methyl methanesulfonate (MMS)-induced DNA damage did not exhibit greater recombinogenicity in the dun1 mutant compared to the DUN1 strain. We suggest that one function of DUN1-mediated DNA damage-induced gene expression is to channel the repair of UV damage into a nonrecombinogenic repair pathway.

Indexed as

Saccharomyces cerevisiae ProteinsCell Cycle ProteinsDNA-Binding ProteinsDNA DamageDose-Response Relationship, RadiationGene ExpressionGenotypeMitosisModels, GeneticPhenotypeProtein KinasesProtein Serine-Threonine KinasesRad52 DNA Repair and Recombination ProteinRecombination, GeneticSaccharomyces cerevisiaeSister Chromatid ExchangeCell Cycle ProteinsDNA-Binding ProteinsDUN1 protein, S cerevisiaeProtein KinasesProtein Serine-Threonine KinasesRad52 DNA Repair and Recombination ProteinRAD52 protein, S cerevisiaerad9 proteinSaccharomyces cerevisiae Proteins

Identifiers

PMID10388811
PMCPMC1460661
OpenAlexW1917273705

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.