Evidence map›Paper›PMID 20838427›Full record

ArticlePLoS genetics2010

Commercially available outbred mice for genome-wide association studies.

Binnaz Yalcin, Jérôme Nicod, Amarjit Bhomra, Stuart Davidson, James Cleak, Laurent Farinelli, Magne Østerås, Adam Whitley, Wei Yuan, Xiangchao Gan and 8 more

Abstract read
In one paragraph

Article in PLoS genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed, 3 pooled it
–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

78 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
  2. Genome-wide association study for age-related hearing loss (AHL) in the mouse: a meta-analysis.Journal of the Association for Research in Otolaryngology : JARO · 2014
    Pooled it
  3. Pooled it
  4. Article
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  10. Article
  11. Characterization of Two MouseInternational journal of molecular sciences · 2022
    Article
  12. Review
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  15. Design and Immunological Validation ofFrontiers in immunology · 2021
    Article
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  19. Article
  20. MHC-II alleles shape the CDR3 repertoires of conventional and regulatory naïve CD4Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article

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

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

18 authors.

Binnaz YalcinWellcome Trust Centre for Human Genetics, University of Oxford, Oxford, United Kingdom.
Jérôme Nicod
Amarjit Bhomra
Stuart Davidson
James Cleak
Laurent Farinelli
Magne Østerås
Adam Whitley
Wei Yuan
Xiangchao Gan
Martin Goodson
Paul Klenerman
Ansu Satpathy
Diane Mathis
Christophe Benoist
David J Adams
Richard Mott
Jonathan Flint

Funding

Medical Research Council G0800024Wellcome Trust 079912
6 · The paper itself

Abstract

Genome-wide association studies using commercially available outbred mice can detect genes involved in phenotypes of biomedical interest. Useful populations need high-frequency alleles to ensure high power to detect quantitative trait loci (QTLs), low linkage disequilibrium between markers to obtain accurate mapping resolution, and an absence of population structure to prevent false positive associations. We surveyed 66 colonies for inbreeding, genetic diversity, and linkage disequilibrium, and we demonstrate that some have haplotype blocks of less than 100 Kb, enabling gene-level mapping resolution. The same alleles contribute to variation in different colonies, so that when mapping progress stalls in one, another can be used in its stead. Colonies are genetically diverse: 45% of the total genetic variation is attributable to differences between colonies. However, quantitative differences in allele frequencies, rather than the existence of private alleles, are responsible for these population differences. The colonies derive from a limited pool of ancestral haplotypes resembling those found in inbred strains: over 95% of sequence variants segregating in outbred populations are found in inbred strains. Consequently it is possible to impute the sequence of any mouse from a dense SNP map combined with inbred strain sequence data, which opens up the possibility of cataloguing and testing all variants for association, a situation that has so far eluded studies in completely outbred populations. We demonstrate the colonies' potential by identifying a deletion in the promoter of H2-Ea as the molecular change that strongly contributes to setting the ratio of CD4+ and CD8+ lymphocytes.

Indexed as

Genome-Wide Association StudyAnimalsAnimals, LaboratoryAnimals, Outbred StrainsChromosome MappingGenetic DriftGenetic MarkersGenetics, PopulationGenetic VariationHaplotypesInbreedingLinkage DisequilibriumMicePhenotypePhylogenyQuantitative Trait LociGenetic Markers

Identifiers

PMID20838427
PMCPMC2932682

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.