Evidence map›Paper›PMID 22006216›Full record

ArticleGenome research2012

Death of PRDM9 coincides with stabilization of the recombination landscape in the dog genome.

Erik Axelsson, Matthew T Webster, Abhirami Ratnakumar, LUPA Consortium, Chris P Ponting, Kerstin Lindblad-Toh

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Genome research, 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 97 papers.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed
–field-weighted citation impact
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

97 citing papers in PubMed, 147 citations in OpenAlex.

  1. Why recombination hotspots?PLoS genetics · 2026
    Review
  2. Article
  3. Article
  4. Meiotic Recombination in Teleosts.Advances in experimental medicine and biology · 2026
    Review
  5. 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
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. 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
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  15. Article
  16. Article
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  19. Article
  20. Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article

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

4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

6 authors at 3 institutions in 3 countries.

Erik AxelssonScience for Life Laboratory, Department of Medical Biochemistry and Microbiology, Uppsala University, 75237 Uppsala, Sweden. Erik.Axelsson@imbim.uu.se
Matthew T Webster
Abhirami Ratnakumar
LUPA Consortium
Chris P Ponting
Kerstin Lindblad-Toh
Uppsala University · SEBroad Institute · USUniversity of Oxford · GB

Funding

Medical Research Council MC_U137761446
6 · The paper itself

Abstract

Analysis of diverse eukaryotes has revealed that recombination events cluster in discrete genomic locations known as hotspots. In humans, a zinc-finger protein, PRDM9, is believed to initiate recombination in >40% of hotspots by binding to a specific DNA sequence motif. However, the PRDM9 coding sequence is disrupted in the dog genome assembly, raising questions regarding the nature and control of recombination in dogs. By analyzing the sequences of PRDM9 orthologs in a number of dog breeds and several carnivores, we show here that this gene was inactivated early in canid evolution. We next use patterns of linkage disequilibrium using more than 170,000 SNP markers typed in almost 500 dogs to estimate the recombination rates in the dog genome using a coalescent-based approach. Broad-scale recombination rates show good correspondence with an existing linkage-based map. Significant variation in recombination rate is observed on the fine scale, and we are able to detect over 4000 recombination hotspots with high confidence. In contrast to human hotspots, 40% of canine hotspots are characterized by a distinct peak in GC content. A comparative genomic analysis indicates that these peaks are present also as weaker peaks in the panda, suggesting that the hotspots have been continually reinforced by accelerated and strongly GC biased nucleotide substitutions, consistent with the long-term action of biased gene conversion on the dog lineage. These results are consistent with the loss of PRDM9 in canids, resulting in a greater evolutionary stability of recombination hotspots. The genetic determinants of recombination hotspots in the dog genome may thus reflect a fundamental process of relevance to diverse animal species.

Indexed as

Evolution, MolecularPolymorphism, Single NucleotideAnimalsDogsGC Rich SequenceGenomeGenomic InstabilityHistone-Lysine N-MethyltransferaseHumansRecombination, GeneticHistone-Lysine N-Methyltransferase

Identifiers

PMID22006216
PMCPMC3246206
OpenAlexW2170301165

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.