Evidence map›Paper›PMID 21462316›Full record

ArticleJournal of experimental zoology. Part B, Molecular and developmental evolution2011

Evolution of pleiotropy: epistatic interaction pattern supports a mechanistic model underlying variation in genotype-phenotype map.

Mihaela Pavlicev, Elizabeth A Norgard, Gloria L Fawcett, James M Cheverud

Abstract read
In one paragraph

Article in Journal of experimental zoology. Part B, Molecular and developmental evolution, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

21 citing papers in PubMed, 54 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Review
  5. [Evolutionary cardiology and experimental research].Archivos de cardiologia de Mexico · 2022
    Article
  6. Review
  7. Article
  8. Review
  9. Why does allometry evolve so slowly?Integrative and comparative biology · 2019
    Article
  10. Plastic responses to novel environments are biased towards phenotype dimensions with high additive genetic variation.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  11. Article
  12. Article
  13. Article
  14. Modularity: genes, development and evolution.Annual review of ecology, evolution, and systematics · 2016
    Article
  15. Complex constraints on allometry revealed by artificial selection on the wing of Drosophila melanogaster.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  16. Article
  17. Integrated phenotypes: understanding trait covariation in plants and animals.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014
    Review
  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

4 authors at 3 institutions in 2 countries.

Mihaela PavlicevCenter for Ecological and Evolutionary Synthesis, Department of Biology, University of Oslo, Norway. mihaela.pavlicev@bio.uio.no
Elizabeth A Norgard
Gloria L Fawcett
James M Cheverud
Washington University in St. Louis · USBaylor College of Medicine · USUniversity of Oslo · NO

Funding

GENETIC VARIATION IN MURINE LONG BONE GROWTH AND DEVELOPMENTR01AR053224 · NIAMS · WASHINGTON UNIVERSITY · PI CHEVERUD, JAMES M · 2006 to 2010
$1.6M
NIAMS NIH HHS AR053224NIAMS NIH HHS R01 AR053224
6 · The paper itself

Abstract

The genotype-phenotype (GP) map consists of developmental and physiological mechanisms mapping genetic onto phenotypic variation. It determines the distribution of heritable phenotypic variance on which selection can act. Comparative studies of morphology as well as of gene regulatory networks show that the GP map itself evolves, yet little is known about the actual evolutionary mechanisms involved. The study of such mechanisms requires exploring the variation in GP maps at the population level, which presently is easier to quantify by statistical genetic methods rather than by regulatory network structures. We focus on the evolution of pleiotropy, a major structural aspect of the GP map. Pleiotropic genes affect multiple traits and underlie genetic covariance between traits, often causing evolutionary constraints. Previous quantitative genetic studies have demonstrated population-level variation in pleiotropy in the form of loci, at which genotypes differ in the genetic covariation between traits. This variation can potentially fuel evolution of the GP map under selection and/or drift. Here, we propose a developmental mechanism underlying population genetic variation in covariance and test its predictions. Specifically, the mechanism predicts that the loci identified as responsible for genetic variation in pleiotropy are involved in trait-specific epistatic interactions. We test this prediction for loci affecting allometric relationships between traits in an advanced intercross between inbred mouse strains. The results consistently support the prediction. We further find a high degree of sign epistasis in these interactions, which we interpret as an indication of adaptive gene complexes within the diverged parental lines.

Indexed as

Biological EvolutionEpistasis, GeneticGenetic PleiotropyModels, GeneticPhenotypeQuantitative Trait LociAnimalsCrosses, GeneticEvolution, MolecularGene Regulatory NetworksGenetic VariationGenotypeMiceMice, Inbred Strains

Identifiers

PMID21462316
PMCPMC3112255
OpenAlexW2043387802

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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.