Evidence map›Paper›PMID 29782925›Full record

ReviewSeminars in cell & developmental biology2019

The developmental-genetics of canalization.

Benedikt Hallgrimsson, Rebecca M Green, David C Katz, Jennifer L Fish, Francois P Bernier, Charles C Roseman, Nathan M Young, James M Cheverud, Ralph S Marcucio

Abstract readReview
In one paragraph

Review in Seminars in cell & developmental biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 1 pooled it
8.1field-weighted citation impact, top 2% 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

51 citing papers in PubMed, 1 synthesis or guideline pooled it, 111 citations in OpenAlex.

  1. Pooled it
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  15. Downstream branches of receptor tyrosine kinase signaling act interdependently to shape the face.Developmental dynamics : an official publication of the American Association of Anatomists · 2025
    Article
  16. Review
  17. Dosage-dependent effects of FGFR2Anatomical record (Hoboken, N.J. : 2007) · 2025
    Article
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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

9 authors at 6 institutions in 2 countries.

Benedikt HallgrimssonDept. of Cell Biology & Anatomy, Alberta Children's Hospital Research Institute and McCaig Bone and Joint Institute, Cumming School of Medicine, University of Calgary, Calgary, AB, T2N 4N1, Canada. Electronic address: bhallgri@ucalgary.ca.
Rebecca M GreenDept. of Cell Biology & Anatomy, Alberta Children's Hospital Research Institute and McCaig Bone and Joint Institute, Cumming School of Medicine, University of Calgary, Calgary, AB, T2N 4N1, Canada.
David C KatzDept. of Cell Biology & Anatomy, Alberta Children's Hospital Research Institute and McCaig Bone and Joint Institute, Cumming School of Medicine, University of Calgary, Calgary, AB, T2N 4N1, Canada.
Jennifer L FishDept. of Biological Sciences, University of Massachusetts Lowell, Lowell, MA, 01854, USA.
Francois P BernierDept of Medical Genetics, Alberta Children's Hospital Research Institute Cumming School of Medicine, University of Calgary, Calgary, AB, T2N 4N1, Canada.
Charles C RosemanDept. of Animal Biology, University of Illinois Urbana Champaign, Urbana, IL, 61801, USA.
Nathan M YoungDept. of Orthopaedic Surgery, School of Medicine, University of California San Francisco, San Francisco, CA, 94110, USA.
James M CheverudDept. of Biology, Loyola University Chicago, Chicago, IL, 60660, USA.
Ralph S MarcucioDept. of Orthopaedic Surgery, School of Medicine, University of California San Francisco, San Francisco, CA, 94110, USA. Electronic address: Ralph.Marcucio@ucsf.edu.
Alberta Children's Hospital · CAUniversity of Calgary · CAUniversity of California, San Francisco · USLoyola University Chicago · USUniversity of Illinois Urbana-Champaign · USUniversity of Massachusetts Lowell · US

Funding

The role of continuous phenotypic variation in structural defects of the faceR01DE019638 · NIDCR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Benedikt Hallgrimsson, Ralph S Marcucio · 2010 to 2026
$7.3M
NIDCR NIH HHS R01 DE019638
6 · The paper itself

Abstract

Canalization, or robustness to genetic or environmental perturbations, is fundamental to complex organisms. While there is strong evidence for canalization as an evolved property that varies among genotypes, the developmental and genetic mechanisms that produce this phenomenon are very poorly understood. For evolutionary biology, understanding how canalization arises is important because, by modulating the phenotypic variation that arises in response to genetic differences, canalization is a determinant of evolvability. For genetics of disease in humans and for economically important traits in agriculture, this subject is important because canalization is a potentially significant cause of missing heritability that confounds genomic prediction of phenotypes. We review the major lines of thought on the developmental-genetic basis for canalization. These fall into two groups. One proposes specific evolved molecular mechanisms while the other deals with robustness or canalization as a more general feature of development. These explanations for canalization are not mutually exclusive and they overlap in several ways. General explanations for canalization are more likely to involve emergent features of development than specific molecular mechanisms. Disentangling these explanations is also complicated by differences in perspectives between genetics and developmental biology. Understanding canalization at a mechanistic level will require conceptual and methodological approaches that integrate quantitative genetics and developmental biology.

Indexed as

Biological EvolutionEpigenesis, GeneticEpistasis, GeneticGenetic Association StudiesGenotypePhenotypeAdaptation, PhysiologicalAnimalsDevelopmental BiologyGene-Environment InteractionGene Regulatory NetworksGeneticsGenetic TechniquesGenetic VariationHumansPlantsCanalizationEpistasisGenotype-phenotype mapsNonlinearityRobustness

Identifiers

PMID29782925
PMCPMC6251770
OpenAlexW2804486271

What OpenQuestion holds

Textmetadata
LicenceTDM
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.