Evidence map›Paper›PMID 25781962›Full record

ArticlePLoS genetics2015

Gene networks underlying convergent and pleiotropic phenotypes in a large and systematically-phenotyped cohort with heterogeneous developmental disorders.

Tallulah Andrews, Stephen Meader, Anneke Vulto-van Silfhout, Avigail Taylor, Julia Steinberg, Jayne Hehir-Kwa, Rolph Pfundt, Nicole de Leeuw, Bert B A de Vries, Caleb Webber

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.5field-weighted citation impact, top 16% 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

8 citing papers in PubMed, 16 citations in OpenAlex.

  1. Shared and distinct phenotypic profiles among neurodevelopmental disorder genes.medRxiv : the preprint server for health sciences · 2026
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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

10 authors at 3 institutions in 2 countries.

Tallulah AndrewsMRC Functional Genomics Unit, Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom.
Stephen MeaderMRC Functional Genomics Unit, Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom.
Anneke Vulto-van SilfhoutDepartment of Human Genetics, Radboud University Medical Center, Nijmegen, the Netherlands.
Avigail TaylorMRC Functional Genomics Unit, Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom.
Julia SteinbergMRC Functional Genomics Unit, Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom; Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, United Kingdom.
Jayne Hehir-KwaDepartment of Human Genetics, Radboud University Medical Center, Nijmegen, the Netherlands.
Rolph PfundtDepartment of Human Genetics, Radboud University Medical Center, Nijmegen, the Netherlands.
Nicole de LeeuwDepartment of Human Genetics, Radboud University Medical Center, Nijmegen, the Netherlands.
Bert B A de VriesDepartment of Human Genetics, Radboud University Medical Center, Nijmegen, the Netherlands.
Caleb WebberMRC Functional Genomics Unit, Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom.
University of Oxford · GBRadboud University Nijmegen · NLRadboud University Medical Center · NL

Funding

Medical Research Council MC_UP_A320_1004Medical Research Council MC_UU_12021/4
6 · The paper itself

Abstract

Readily-accessible and standardised capture of genotypic variation has revolutionised our understanding of the genetic contribution to disease. Unfortunately, the corresponding systematic capture of patient phenotypic variation needed to fully interpret the impact of genetic variation has lagged far behind. Exploiting deep and systematic phenotyping of a cohort of 197 patients presenting with heterogeneous developmental disorders and whose genomes harbour de novo CNVs, we systematically applied a range of commonly-used functional genomics approaches to identify the underlying molecular perturbations and their phenotypic impact. Grouping patients into 408 non-exclusive patient-phenotype groups, we identified a functional association amongst the genes disrupted in 209 (51%) groups. We find evidence for a significant number of molecular interactions amongst the association-contributing genes, including a single highly-interconnected network disrupted in 20% of patients with intellectual disability, and show using microcephaly how these molecular networks can be used as baits to identify additional members whose genes are variant in other patients with the same phenotype. Exploiting the systematic phenotyping of this cohort, we observe phenotypic concordance amongst patients whose variant genes contribute to the same functional association but note that (i) this relationship shows significant variation across the different approaches used to infer a commonly perturbed molecular pathway, and (ii) that the phenotypic similarities detected amongst patients who share the same inferred pathway perturbation result from these patients sharing many distinct phenotypes, rather than sharing a more specific phenotype, inferring that these pathways are best characterized by their pleiotropic effects.

Indexed as

AnimalsDevelopmental DisabilitiesDNA Copy Number VariationsGene ExpressionGenetic Association StudiesGenome, HumanGenotypeHumansMetabolic Networks and PathwaysMicePhenotypeProtein Interaction MappingProtein Interaction Maps

Identifiers

PMID25781962
PMCPMC4362763
OpenAlexW2027508727

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.