Evidence map›Paper›PMID 12072452›Full record

ArticleGenetics2002

Replication protein A is required for meiotic recombination in Saccharomyces cerevisiae.

Christine Soustelle, Michèle Vedel, Richard Kolodner, Alain Nicolas

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

38 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
  2. Article
  3. Molecular mechanisms and regulation of recombination frequency and distribution in plants.TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. Meiotic Chromosome Dynamics in Zebrafish.Frontiers in cell and developmental biology · 2021
    Review
  8. Pathogenic Variations of Homologous Recombination GeneFrontiers in cell and developmental biology · 2021
    Article
  9. Article
  10. Meiotic Recombination Defects and Premature Ovarian Insufficiency.Frontiers in cell and developmental biology · 2021
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Meiotic Recombination: The Essence of Heredity.Cold Spring Harbor perspectives in biology · 2015
    Review
  17. Replication protein A prevents promiscuous annealing between short sequence homologies: Implications for genome integrity.BioEssays : news and reviews in molecular, cellular and developmental biology · 2015
    Review
  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

4 authors at 2 institutions in 2 countries.

Christine SoustelleInstitut Curie, Section de recherche, CNRS UMR144, 75248 Paris Cedex 05, France.
Michèle Vedel
Richard Kolodner
Alain Nicolas
Centre National de la Recherche Scientifique · FRUniversity of California San Diego · US

Funding

ENZYMATIC MECHANISMS OF GENETIC RECOMBINATIONR01GM026017 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Richard D Kolodner · 1985 to 2026
$10.5M
ENZYMATIC MECHANISMS OF GENETIC RECOMBINATIONR37GM026017 · NIGMS · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI KOLODNER, RICHARD D · 1992 to 2001
$759k
NIGMS NIH HHS GM-26017
6 · The paper itself

Abstract

In Saccharomyces cerevisiae, meiotic recombination is initiated by transient DNA double-stranded breaks (DSBs). These DSBs undergo a 5' --> 3' resection to produce 3' single-stranded DNA ends that serve to channel DSBs into the RAD52 recombinational repair pathway. In vitro studies strongly suggest that several proteins of this pathway--Rad51, Rad52, Rad54, Rad55, Rad57, and replication protein A (RPA)--play a role in the strand exchange reaction. Here, we report a study of the meiotic phenotypes conferred by two missense mutations affecting the largest subunit of RPA, which are localized in the protein interaction domain (rfa1-t11) and in the DNA-binding domain (rfa1-t48). We find that both mutant diploids exhibit reduced sporulation efficiency, very poor spore viability, and a 10- to 100-fold decrease in meiotic recombination. Physical analyses indicate that both mutants form normal levels of meiosis-specific DSBs and that the broken ends are processed into 3'-OH single-stranded tails, indicating that the RPA complex present in these rfa1 mutants is functional in the initial steps of meiotic recombination. However, the 5' ends of the broken fragments undergo extensive resection, similar to what is observed in rad51, rad52, rad55, and rad57 mutants, indicating that these RPA mutants are defective in the repair of the Spo11-dependent DSBs that initiate homologous recombination during meiosis.

Indexed as

Recombination, GeneticCrossing Over, GeneticDNA-Binding ProteinsGene ConversionMeiosisMutationReplication Protein ASaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSpores, FungalDNA-Binding ProteinsReplication Protein ASaccharomyces cerevisiae Proteins

Identifiers

PMID12072452
PMCPMC1462150
OpenAlexW2136145320

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.