Evidence map›Paper›PMID 12871899›Full record

ArticleGenetics2003

The mitotic DNA damage checkpoint proteins Rad17 and Rad24 are required for repair of double-strand breaks during meiosis in yeast.

Miki Shinohara, Kazuko Sakai, Tomoko Ogawa, Akira Shinohara

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Genetics, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
1.3field-weighted citation impact, top 23% 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

47 citing papers in PubMed, 84 citations in OpenAlex.

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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

4 authors at 3 institutions in 1 country.

Miki ShinoharaDepartment of Biology, Graduate School of Science, Osaka University, Toyonaka, Japan.
Kazuko Sakai
Tomoko Ogawa
Akira Shinohara
Osaka University · JPHiroshima University · JPIwate College of Nursing · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We show here that deletion of the DNA damage checkpoint genes RAD17 and RAD24 in Saccharomyces cerevisiae delays repair of meiotic double-strand breaks (DSBs) and results in an altered ratio of crossover-to-noncrossover products. These mutations also decrease the colocalization of immunostaining foci of the RecA homologs Rad51 and Dmc1 and cause a delay in the disappearance of Rad51 foci, but not of Dmc1. These observations imply that RAD17 and RAD24 promote efficient repair of meiotic DSBs by facilitating proper assembly of the meiotic recombination complex containing Rad51. Consistent with this proposal, extra copies of RAD51 and RAD54 substantially suppress not only the spore inviability of the rad24 mutant, but also the gamma-ray sensitivity of the mutant. Unexpectedly, the entry into meiosis I (metaphase I) is delayed in the checkpoint single mutants compared to wild type. The control of the cell cycle in response to meiotic DSBs is also discussed.

Indexed as

Gamma RaysGene DeletionBlotting, SouthernCell Cycle ProteinsCrossing Over, GeneticDNA-Binding ProteinsDNA DamageDNA RepairElectrophoresis, Agar GelIntracellular Signaling Peptides and ProteinsMeiosisMicroscopy, FluorescenceNuclear ProteinsPlasmidsRad51 RecombinaseSaccharomyces cerevisiaeCell Cycle ProteinsDNA-Binding ProteinsIntracellular Signaling Peptides and ProteinsNuclear ProteinsRAD17 protein, S cerevisiaeRAD24 protein, S cerevisiaeRAD51 protein, S cerevisiaeRad51 RecombinaseSaccharomyces cerevisiae Proteins

Identifiers

PMID12871899
PMCPMC1462628
OpenAlexW1931669830

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.