Evidence map›Paper›PMID 32058623›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2020

Histone ChIP-Seq identifies differential enhancer usage during chondrogenesis as critical for defining cell-type specificity.

Kathleen Cheung, Matthew J Barter, Julia Falk, Carole J Proctor, Louise N Reynard, David A Young

Open access · hybridAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 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
2.8field-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

16 citing papers in PubMed, 21 citations in OpenAlex.

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  16. Histone ChIP-Seq identifies differential enhancer usage during chondrogenesis as critical for defining cell-type specificity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    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

6 authors at 1 institution in 1 country.

Kathleen CheungSkeletal Research Group, Institute of Genetic Medicine, Newcastle University, Central Parkway, Newcastle upon Tyne, UK.
Matthew J BarterSkeletal Research Group, Institute of Genetic Medicine, Newcastle University, Central Parkway, Newcastle upon Tyne, UK.
Julia FalkSkeletal Research Group, Institute of Genetic Medicine, Newcastle University, Central Parkway, Newcastle upon Tyne, UK.
Carole J ProctorSkeletal Research Group, Institute of Genetic Medicine, Newcastle University, Central Parkway, Newcastle upon Tyne, UK.
Louise N ReynardSkeletal Research Group, Institute of Genetic Medicine, Newcastle University, Central Parkway, Newcastle upon Tyne, UK.
David A YoungSkeletal Research Group, Institute of Genetic Medicine, Newcastle University, Central Parkway, Newcastle upon Tyne, UK.
Newcastle University · GB

Funding

Arthritis Research UK 18746Arthritis Research UK 19424Department of HealthMedical Research Council MR/P020941/1The Dunhill Medical Trust R476/0516Versus Arthritis 18746Versus Arthritis 19424
6 · The paper itself

Abstract

Epigenetic mechanisms are known to regulate gene expression during chondrogenesis. In this study, we have characterized the epigenome during the in vitro differentiation of human mesenchymal stem cells (hMSCs) into chondrocytes. Chromatin immunoprecipitation followed by next-generation sequencing (ChIP-seq) was used to assess a range of N-terminal posttranscriptional modifications (marks) to histone H3 lysines (H3K4me3, H3K4me1, H3K27ac, H3K27me3, and H3K36me3) in both hMSCs and differentiated chondrocytes. Chromatin states were characterized using histone ChIP-seq and cis-regulatory elements were identified in chondrocytes. Chondrocyte enhancers were associated with chondrogenesis-related gene ontology (GO) terms. In silico analysis and integration of DNA methylation data with chondrogenesis chromatin states revealed that enhancers marked by histone marks H3K4me1 and H3K27ac were de-methylated during in vitro chondrogenesis. Similarity analysis between hMSC and chondrocyte chromatin states defined in this study with epigenomes of cell-types defined by the Roadmap Epigenomics project revealed that enhancers are more distinct between cell-types compared to other chromatin states. Motif analysis revealed that the transcription factor SOX9 is enriched in chondrocyte enhancers. Luciferase reporter assays confirmed that chondrocyte enhancers characterized in this study exhibited enhancer activity which may be modulated by DNA methylation and SOX9 overexpression. Altogether, these integrated data illustrate the cross-talk between different epigenetic mechanisms during chondrocyte differentiation.

Indexed as

ChondrogenesisEnhancer Elements, GeneticEpigenesis, GeneticAdultCell DifferentiationCell LineageCells, CulturedChondrocytesChromatinChromatin Immunoprecipitation SequencingDNA MethylationEpigenomicsFemaleHistonesHumansPromoter Regions, GeneticChromatinHistonesSOX9 protein, humanSOX9 Transcription Factorcartilagechondrocyte developmentchromatin

Identifiers

PMID32058623
PMCPMC7187454
OpenAlexW3006007721

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.