Evidence map›Paper›PMID 25527838›Full record

ArticleGenome biology and evolution2014

Germline methylation patterns determine the distribution of recombination events in the dog genome.

Jonas Berglund, Javier Quilez, Peter F Arndt, Matthew T Webster

Open access · goldAbstract read
In one paragraph

Article in Genome biology and evolution, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

14 citing papers in PubMed, 25 citations in OpenAlex.

  1. Why recombination hotspots?PLoS genetics · 2026
    Review
  2. Fine-scale recombination rates inferred using the canFam4 assembly are strongly correlated with previous maps of dog recombination.Mammalian genome : official journal of the International Mammalian Genome Society · 2025
    Article
  3. Article
  4. Article
  5. High prevalence of PRDM9-independent recombination hotspots in placental mammals.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  6. De Novo Mutation Rates in Sticklebacks.Molecular biology and evolution · 2023
    Article
  7. Article
  8. Review
  9. The consequences of sequence erosion in the evolution of recombination hotspots.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017
    Review
  10. Coevolution between transposable elements and recombination.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017
    Review
  11. Article
  12. Article
  13. Review
  14. 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 3 institutions in 2 countries.

Jonas BerglundScience for Life Laboratory, Department of Medical Biochemistry and Microbiology, Uppsala University, Sweden.
Javier QuilezScience for Life Laboratory, Department of Medical Biochemistry and Microbiology, Uppsala University, Sweden.
Peter F ArndtDepartment of Computational Molecular Biology, Max Planck Institute for Molecular Genetics, Berlin, Germany.
Matthew T WebsterScience for Life Laboratory, Department of Medical Biochemistry and Microbiology, Uppsala University, Sweden matthew.webster@imbim.uu.se.
Science for Life Laboratory · SEMax Planck Institute for Molecular Genetics · DEUppsala University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The positive-regulatory domain containing nine gene, PRDM9, which strongly associates with the location of recombination events in several vertebrates, is inferred to be inactive in the dog genome. Here, we address several questions regarding the control of recombination and its influence on genome evolution in dogs. First, we address whether the association between CpG islands (CGIs) and recombination hotspots is generated by lack of methylation, GC-biased gene conversion (gBGC), or both. Using a genome-wide dog single nucleotide polymorphism data set and comparisons of the dog genome with related species, we show that recombination-associated CGIs have low CpG mutation rates, and that CpG mutation rate is negatively correlated with recombination rate genome wide, indicating that nonmethylation attracts the recombination machinery. We next use a neighbor-dependent model of nucleotide substitution to disentangle the effects of CpG mutability and gBGC and analyze the effects that loss of PRDM9 has on these rates. We infer that methylation patterns have been stable during canid genome evolution, but that dog CGIs have experienced a drastic increase in substitution rate due to gBGC, consistent with increased levels of recombination in these regions. We also show that gBGC is likely to have generated many new CGIs in the dog genome, but these mostly occur away from genes, whereas the number of CGIs in gene promoter regions has not increased greatly in recent evolutionary history. Recombination has a major impact on the distribution of CGIs that are detected in the dog genome due to the interaction between methylation and gBGC. The results indicate that germline methylation patterns are the main determinant of recombination rates in the absence of PRDM9.

Indexed as

GenomeRecombination, GeneticAnimalsBase CompositionCpG IslandsDNA MethylationDogsGerm CellsPolymorphism, Single NucleotideUrsidaebiased gene conversionCpG islanddog genomemethylationrecombination

Identifiers

PMID25527838
PMCPMC4350167
OpenAlexW2131979324

What OpenQuestion holds

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LicenceCC BY-NC
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.