Evidence map›Paper›PMID 37830496›Full record

ArticleeLife2023

Down the Penrose stairs, or how selection for fewer recombination hotspots maintains their existence.

Zachary Baker, Molly Przeworski, Guy Sella

Open access · goldAbstract read
In one paragraph

Article in eLife, 2023. 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
2.5field-weighted citation impact, top 11% 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, 16 citations in OpenAlex.

  1. Article
  2. On the origin of PRDM9-guided recombination hotspots.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Why recombination hotspots?PLoS genetics · 2026
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. 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
  10. Review
  11. Article
  12. Article
  13. Article
  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

3 authors at 2 institutions in 2 countries.

Zachary BakerDepartment of Systems Biology, Columbia University, New York, United States.ORCID 0000-0002-1540-0731
Molly PrzeworskiDepartment of Systems Biology, Columbia University, New York, United States.ORCID 0000-0002-5369-9009
Guy SellaDepartment of Biological Sciences, Columbia University, New York, United States.ORCID 0000-0002-5239-7930
Genomics (United Kingdom) · GBColumbia University · US

Funding

Recombination rate variation and evolution in vertebratesR01GM083098 · NIGMS · UNIVERSITY OF CHICAGO · PI PRZEWORSKI, MOLLY F · 2007 to 2024
$4.6M
The population genetics of disease risk and other quantitative traitsR01GM115889 · NIGMS · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI SELLA, GUY · 2015 to 2025
$2.9M
NIGMS NIH HHS R01 GM083098NIGMS NIH HHS R01 GM115889NIH HHS R01 GM115889NIH HHS R01 GM83098
6 · The paper itself

Abstract

In many species, meiotic recombination events tend to occur in narrow intervals of the genome, known as hotspots. In humans and mice, double strand break (DSB) hotspot locations are determined by the DNA-binding specificity of the zinc finger array of the PRDM9 protein, which is rapidly evolving at residues in contact with DNA. Previous models explained this rapid evolution in terms of the need to restore PRDM9 binding sites lost to gene conversion over time, under the assumption that more PRDM9 binding always leads to more DSBs. This assumption, however, does not align with current evidence. Recent experimental work indicates that PRDM9 binding on both homologs facilitates DSB repair, and that the absence of sufficient symmetric binding disrupts meiosis. We therefore consider an alternative hypothesis: that rapid PRDM9 evolution is driven by the need to restore symmetric binding because of its role in coupling DSB formation and efficient repair. To this end, we model the evolution of PRDM9 from first principles: from its binding dynamics to the population genetic processes that govern the evolution of the zinc finger array and its binding sites. We show that the loss of a small number of strong binding sites leads to the use of a greater number of weaker ones, resulting in a sharp reduction in symmetric binding and favoring new PRDM9 alleles that restore the use of a smaller set of strong binding sites. This decrease, in turn, drives rapid PRDM9 evolutionary turnover. Our results therefore suggest that the advantage of new PRDM9 alleles is in

Indexed as

DNA Breaks, Double-StrandedHistone-Lysine N-MethyltransferaseAnimalsDNADNA RepairHomologous RecombinationHumansMeiosisMiceDNAHistone-Lysine N-MethyltransferasePRDM9 protein, humanDSB repairevolutionary biologygene conversiongeneticsgenomicshotspothumanmeiosismousePRDM9recombination

Identifiers

PMID37830496
PMCPMC10703446
OpenAlexW4387597662

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.