Evidence map›Paper›PMID 32764605›Full record

ArticleNature communications2020

Dynamic changes in the epigenomic landscape regulate human organogenesis and link to developmental disorders.

Dave T Gerrard, Andrew A Berry, Rachel E Jennings, Matthew J Birket, Peyman Zarrineh, Myles G Garstang, Sarah L Withey, Patrick Short, Sandra Jiménez-Gancedo, Panos N Firbas and 7 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

16 citing papers in PubMed, 27 citations in OpenAlex.

  1. TheiScience · 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

17 authors at 3 institutions in 2 countries.

Dave T Gerrard *Faculty of Biology, Medicine & Health, Manchester Academic Health Sciences Centre, University of Manchester, Oxford Road, Manchester, M13 9PT, UK.ORCID http://orcid.org/0000-0001-6890-7213
Andrew A Berry *Faculty of Biology, Medicine & Health, Manchester Academic Health Sciences Centre, University of Manchester, Oxford Road, Manchester, M13 9PT, UK.
Rachel E JenningsFaculty of Biology, Medicine & Health, Manchester Academic Health Sciences Centre, University of Manchester, Oxford Road, Manchester, M13 9PT, UK.
Matthew J BirketFaculty of Biology, Medicine & Health, Manchester Academic Health Sciences Centre, University of Manchester, Oxford Road, Manchester, M13 9PT, UK.ORCID http://orcid.org/0000-0002-5985-6626
Peyman ZarrinehFaculty of Biology, Medicine & Health, Manchester Academic Health Sciences Centre, University of Manchester, Oxford Road, Manchester, M13 9PT, UK.
Myles G GarstangFaculty of Biology, Medicine & Health, Manchester Academic Health Sciences Centre, University of Manchester, Oxford Road, Manchester, M13 9PT, UK.
Sarah L WitheyFaculty of Biology, Medicine & Health, Manchester Academic Health Sciences Centre, University of Manchester, Oxford Road, Manchester, M13 9PT, UK.
Patrick ShortWellcome Sanger Institute, Wellcome Genome Campus, Hinxton, UK.ORCID http://orcid.org/0000-0002-7626-6177
Sandra Jiménez-GancedoCentro Andaluz de Biología del Desarrollo (CABD), Consejo Superior de Investigacionnes Cientificas/Universidad Pablo de Olavide/Junta de Analucía, Sevilla, Spain.
Panos N FirbasCentro Andaluz de Biología del Desarrollo (CABD), Consejo Superior de Investigacionnes Cientificas/Universidad Pablo de Olavide/Junta de Analucía, Sevilla, Spain.
Ian DonaldsonFaculty of Biology, Medicine & Health, Manchester Academic Health Sciences Centre, University of Manchester, Oxford Road, Manchester, M13 9PT, UK.ORCID http://orcid.org/0000-0002-0032-0931
Andrew D SharrocksFaculty of Biology, Medicine & Health, Manchester Academic Health Sciences Centre, University of Manchester, Oxford Road, Manchester, M13 9PT, UK.
Karen Piper HanleyFaculty of Biology, Medicine & Health, Manchester Academic Health Sciences Centre, University of Manchester, Oxford Road, Manchester, M13 9PT, UK.ORCID http://orcid.org/0000-0001-9473-9647
Matthew E HurlesWellcome Sanger Institute, Wellcome Genome Campus, Hinxton, UK.
José Luis Gomez-SkarmetaCentro Andaluz de Biología del Desarrollo (CABD), Consejo Superior de Investigacionnes Cientificas/Universidad Pablo de Olavide/Junta de Analucía, Sevilla, Spain.
Nicoletta BobolaFaculty of Biology, Medicine & Health, Manchester Academic Health Sciences Centre, University of Manchester, Oxford Road, Manchester, M13 9PT, UK.
Neil A HanleyFaculty of Biology, Medicine & Health, Manchester Academic Health Sciences Centre, University of Manchester, Oxford Road, Manchester, M13 9PT, UK. neil.hanley@manchester.ac.uk.ORCID http://orcid.org/0000-0003-3234-4038
Manchester Academic Health Science Centre · GBCentro Andaluz de Biología del Desarrollo · ESWellcome Sanger Institute · GB

Funding

Medical Research Council G1100420Medical Research Council MR/000638/1Medical Research Council MR/J003352/1Medical Research Council MR/L009986/1Medical Research Council MR/P023541/1Medical Research Council MR/R000638/1Medical Research Council MR/S036121/1Medical Research Council MR/S03613X/1Wellcome Trust 088566Wellcome Trust 097820Wellcome Trust 105610
6 · The paper itself

Abstract

How the genome activates or silences transcriptional programmes governs organ formation. Little is known in human embryos undermining our ability to benchmark the fidelity of stem cell differentiation or cell programming, or interpret the pathogenicity of noncoding variation. Here, we study histone modifications across thirteen tissues during human organogenesis. We integrate the data with transcription to build an overview of how the human genome differentially regulates alternative organ fates including by repression. Promoters from nearly 20,000 genes partition into discrete states. Key developmental gene sets are actively repressed outside of the appropriate organ without obvious bivalency. Candidate enhancers, functional in zebrafish, allow imputation of tissue-specific and shared patterns of transcription factor binding. Overlaying more than 700 noncoding mutations from patients with developmental disorders allows correlation to unanticipated target genes. Taken together, the data provide a comprehensive genomic framework for investigating normal and abnormal human development.

Indexed as

Epigenesis, GeneticAnimalsAnimals, Genetically ModifiedDatabases, GeneticDevelopmental DisabilitiesEnhancer Elements, GeneticGene Expression Regulation, DevelopmentalHistone CodeHumansModels, GeneticMutationOrganogenesisPromoter Regions, GeneticTissue DistributionTranscription FactorsZebrafishTranscription Factors

Identifiers

PMID32764605
PMCPMC7413392
OpenAlexW3047447368

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.