Evidence map›Paper›PMID 23028340›Full record

ArticlePLoS genetics2012

A genetic basis for a postmeiotic X versus Y chromosome intragenomic conflict in the mouse.

Julie Cocquet, Peter J I Ellis, Shantha K Mahadevaiah, Nabeel A Affara, Daniel Vaiman, Paul S Burgoyne

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 115 papers.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed
10.5field-weighted citation impact, top 1% 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

115 citing papers in PubMed, 193 citations in OpenAlex.

  1. Signatures of sex ratio distortion in humans.bioRxiv : the preprint server for biology · 2026
    Article
  2. The evolutionary genomics of meiotic drive.Molecular biology and evolution · 2026
    Article
  3. Article
  4. Article
  5. Article
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  7. Article
  8. Article
  9. Sex ratio drive in mice: A binding competition between sex-linked genes.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  10. Reenacting a mouse genetic evolutionary arms race in yeast reveals that SLXL1/SLX compete with SLY1/2 for binding to Spindlins.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  11. Review
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  15. Article
  16. New perspectives on the causes and consequences of male meiotic drive.Current opinion in genetics & development · 2023
    Review
  17. Article
  18. Review
  19. Article
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 2 countries.

Julie CocquetInserm, U1016, Institut Cochin, Paris, France. julie.cocquet@inserm.fr
Peter J I Ellis
Shantha K Mahadevaiah
Nabeel A Affara
Daniel Vaiman
Paul S Burgoyne
Délégation Paris 5 · FRUniversity of Cambridge · GB

Funding

Biotechnology and Biological Sciences Research Council BB/F007434/1Medical Research Council MC_U117532009Medical Research Council U117532009
6 · The paper itself

Abstract

Intragenomic conflicts arise when a genetic element favours its own transmission to the detriment of others. Conflicts over sex chromosome transmission are expected to have influenced genome structure, gene regulation, and speciation. In the mouse, the existence of an intragenomic conflict between X- and Y-linked multicopy genes has long been suggested but never demonstrated. The Y-encoded multicopy gene Sly has been shown to have a predominant role in the epigenetic repression of post meiotic sex chromatin (PMSC) and, as such, represses X and Y genes, among which are its X-linked homologs Slx and Slxl1. Here, we produced mice that are deficient for both Sly and Slx/Slxl1 and observed that Slx/Slxl1 has an opposite role to that of Sly, in that it stimulates XY gene expression in spermatids. Slx/Slxl1 deficiency rescues the sperm differentiation defects and near sterility caused by Sly deficiency and vice versa. Slx/Slxl1 deficiency also causes a sex ratio distortion towards the production of male offspring that is corrected by Sly deficiency. All in all, our data show that Slx/Slxl1 and Sly have antagonistic effects during sperm differentiation and are involved in a postmeiotic intragenomic conflict that causes segregation distortion and male sterility. This is undoubtedly what drove the massive gene amplification on the mouse X and Y chromosomes. It may also be at the basis of cases of F1 male hybrid sterility where the balance between Slx/Slxl1 and Sly copy number, and therefore expression, is disrupted. To the best of our knowledge, our work is the first demonstration of a competition occurring between X and Y related genes in mammals. It also provides a biological basis for the concept that intragenomic conflict is an important evolutionary force which impacts on gene expression, genome structure, and speciation.

Indexed as

Adaptor Proteins, Signal TransducingAdaptor Proteins, Vesicular TransportAnimalsEpigenesis, GeneticFemaleGene DosageGene Expression RegulationGenetic SpeciationInfertility, MaleMaleMeiosisMiceMice, TransgenicNuclear ProteinsProteinsSex ChromatinAdaptor Proteins, Signal TransducingAdaptor Proteins, Vesicular TransportNuclear ProteinsProteinsSlx-like1 protein, mouseSlx protein, mouseSLY1 protein, mouse

Identifiers

PMID23028340
PMCPMC3441658
OpenAlexW1967001182

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.