Evidence map›Paper›PMID 20041164›Full record

ArticlePloS one2009

Extraordinary molecular evolution in the PRDM9 fertility gene.

James H Thomas, Ryan O Emerson, Jay Shendure

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

54 citing papers in PubMed, 76 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Pinpointing theFrontiers in genetics · 2021
    Article
  6. Article
  7. Discovery of a chemical probe for PRDM9.Nature communications · 2019
    Article
  8. Molecular evolution of the meiotic recombination pathway in mammals.Evolution; international journal of organic evolution · 2019
    Article
  9. Article
  10. Review
  11. PRDM9 and Its Role in Genetic Recombination.Trends in genetics : TIG · 2018
    Review
  12. 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
  13. Article
  14. Article
  15. Article
  16. The long zinc finger domain of PRDM9 forms a highly stable and long-lived complex with its DNA recognition sequence.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2017
    Article
  17. Article
  18. Article
  19. Article
  20. 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 1 institution in 1 country.

James H ThomasDepartment of Genome Sciences, University of Washington, Seattle, Washington, United States of America. jht@u.washington.edu
Ryan O Emerson
Jay Shendure
University of Washington · US

Funding

SeattleSeqR01HL094976 · NHLBI · UNIVERSITY OF WASHINGTON · PI EICHLER, EVAN, GREEN, PHILIP P · 2008 to 2009
$4.0M
Molecular Tools for Genome PartitioningR21HG004749 · NHGRI · UNIVERSITY OF WASHINGTON · PI SHENDURE, JAY ASHOK · 2008 to 2009
$405k
NHGRI NIH HHS 1R21HG004749-01NHGRI NIH HHS R21 HG004749NHLBI NIH HHS 5R01HL094976-02NHLBI NIH HHS R01 HL094976
6 · The paper itself

Abstract

Recent work indicates that allelic incompatibility in the mouse PRDM9 (Meisetz) gene can cause hybrid male sterility, contributing to genetic isolation and potentially speciation. The only phenotype of mouse PRDM9 knockouts is a meiosis I block that causes sterility in both sexes. The PRDM9 gene encodes a protein with histone H3(K4) trimethyltransferase activity, a KRAB domain, and a DNA-binding domain consisting of multiple tandem C2H2 zinc finger (ZF) domains. We have analyzed human coding polymorphism and interspecies evolutionary changes in the PRDM9 gene. The ZF domains of PRDM9 are evolving very rapidly, with compelling evidence of positive selection in primates. Positively selected amino acids are predominantly those known to make nucleotide specific contacts in C2H2 zinc fingers. These results suggest that PRDM9 is subject to recurrent selection to change DNA-binding specificity. The human PRDM9 protein is highly polymorphic in its ZF domains and nearly all polymorphisms affect the same nucleotide contact residues that are subject to positive selection. ZF domain nucleotide sequences are strongly homogenized within species, indicating that interfinger recombination contributes to their evolution. PRDM9 has previously been assumed to be a transcription factor required to induce meiosis specific genes, a role that is inconsistent with its molecular evolution. We suggest instead that PRDM9 is involved in some aspect of centromere segregation conflict and that rapidly evolving centromeric DNA drives changes in PRDM9 DNA-binding domains.

Indexed as

Evolution, MolecularAmino Acid SequenceAnimalsBase SequenceFertilityHistone-Lysine N-MethyltransferaseHumansMiceMolecular Sequence DataPolymorphism, Single NucleotidePrimatesSelection, GeneticZinc FingersHistone-Lysine N-MethyltransferasePRDM9 protein, human

Identifiers

PMID20041164
PMCPMC2794550
OpenAlexW2132496832

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.