Evidence map›Paper›PMID 14668445›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2003

Positional cloning and characterization of Mei1, a vertebrate-specific gene required for normal meiotic chromosome synapsis in mice.

Brian J Libby, Laura G Reinholdt, John C Schimenti

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

81 citing papers in PubMed, 139 citations in OpenAlex.

  1. Controlling Meiotic Double-Strand Break Formation in Mice: A Web of Multivalent Protein-Protein Interactions.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026
    Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. The Impact ofAnimals : an open access journal from MDPI · 2025
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Advances in the genetic etiology of female infertility.Journal of assisted reproduction and genetics · 2024
    Review
  16. Review
  17. Article
  18. Article
  19. In vivo versus in silico assessment of potentially pathogenic missense variants in human reproductive genes.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Brian J LibbyThe Jackson Laboratory, Bar Harbor, ME 04609, USA.
Laura G Reinholdt
John C Schimenti
Jackson Laboratory · USUniversity of Oregon · US

Funding

Shared Resource ManagementP30CA034196 · NCI · JACKSON LABORATORY · PI William Carl Skarnes · 1985 to 2026
$61.9M
Genetics of recombination/genomic instability in miceR01GM045415 · NIGMS · JACKSON LABORATORY · PI SCHIMENTI, JOHN C · 1992 to 2016
$4.9M
NCI NIH HHS CA34196NCI NIH HHS P30 CA034196NIGMS NIH HHS GM45415NIGMS NIH HHS R01 GM045415
6 · The paper itself

Abstract

The mouse meiotic mutant Mei1 was isolated in a screen for infertile mice descended from chemically mutagenized embryonic stem cells. Homozygotes of both sexes are sterile due to meiotic arrest caused by defects in chromosome synapsis. Notably, RAD51 protein does not load onto Mei1 mutant meiotic chromosomes, suggesting that there is a defect in either recombinational repair or the production of double-strand breaks (DSBs) that require such repair. Here, we show that treatment of mutant males with cisplatin restores RAD51 loading, suggesting that mutant spermatocytes have intact recombinational repair mechanisms. Levels of histone H2AX phosphorylation (gammaH2AX) at leptonema are significantly reduced compared with wild-type controls but comparable to that seen in animals deficient for SPO11, the molecule required for catalyzing DSB formation during meiosis. These observations provide evidence that genetically programmed DSB induction is defective in Mei1 leptotene spermatocytes. We also report the positional cloning of Mei1, which encodes a product without significant homology to any known protein. Expressed almost exclusively in gonads, Mei1 has no apparent homologs in yeast, worms, or flies. However, Mei1 orthologs are present in the genomes of mammals, chickens, and zebrafish. Thus, Mei1 is required for vertebrate meiosis. To our knowledge, Mei1 is the first meiosis-specific mutation identified by forward genetic approaches in mammals.

Indexed as

Amino Acid SequenceAnimalsBase SequenceCell Cycle ProteinsChickensChromosomesCisplatinCloning, MolecularConsensus SequenceDNA PrimersHumansMeiosisMiceMolecular Sequence DataPolymerase Chain ReactionProteinsCell Cycle ProteinsCisplatinDNA PrimersMei1 protein, mouseProteins

Identifiers

PMID14668445
PMCPMC307632
OpenAlexW1986800638

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.