Evidence map›Paper›PMID 31056477›Full record

ArticleStem cell reports2019

Enhancer Chromatin and 3D Genome Architecture Changes from Naive to Primed Human Embryonic Stem Cell States.

Stephanie L Battle, Naresh Doni Jayavelu, Robert N Azad, Jennifer Hesson, Faria N Ahmed, Eliah G Overbey, Joseph A Zoller, Julie Mathieu, Hannele Ruohola-Baker, Carol B Ware and 1 more

Open access · goldAbstract read
In one paragraph

Article in Stem cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.7field-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

24 citing papers in PubMed, 40 citations in OpenAlex.

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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

11 authors at 2 institutions in 1 country.

Stephanie L BattleDivision of Medical Genetics, Department of Medicine, Department of Genome Sciences, University of Washington School of Medicine, Seattle, WA, USA; Institute for Stem Cell and Regenerative Medicine, University of Washington School of Medicine, Seattle, WA, USA.
Naresh Doni JayaveluDivision of Medical Genetics, Department of Medicine, Department of Genome Sciences, University of Washington School of Medicine, Seattle, WA, USA; Institute for Stem Cell and Regenerative Medicine, University of Washington School of Medicine, Seattle, WA, USA.
Robert N AzadDivision of Medical Genetics, Department of Medicine, Department of Genome Sciences, University of Washington School of Medicine, Seattle, WA, USA; Institute for Stem Cell and Regenerative Medicine, University of Washington School of Medicine, Seattle, WA, USA.
Jennifer HessonInstitute for Stem Cell and Regenerative Medicine, University of Washington School of Medicine, Seattle, WA, USA; Department of Comparative Medicine, University of Washington School of Medicine, Seattle, WA, USA.
Faria N AhmedDivision of Medical Genetics, Department of Medicine, Department of Genome Sciences, University of Washington School of Medicine, Seattle, WA, USA; Institute for Stem Cell and Regenerative Medicine, University of Washington School of Medicine, Seattle, WA, USA.
Eliah G OverbeyDivision of Medical Genetics, Department of Medicine, Department of Genome Sciences, University of Washington School of Medicine, Seattle, WA, USA; Institute for Stem Cell and Regenerative Medicine, University of Washington School of Medicine, Seattle, WA, USA.
Joseph A ZollerDivision of Medical Genetics, Department of Medicine, Department of Genome Sciences, University of Washington School of Medicine, Seattle, WA, USA.
Julie MathieuInstitute for Stem Cell and Regenerative Medicine, University of Washington School of Medicine, Seattle, WA, USA; Department of Biochemistry, University of Washington School of Medicine, Seattle, WA, USA.
Hannele Ruohola-BakerInstitute for Stem Cell and Regenerative Medicine, University of Washington School of Medicine, Seattle, WA, USA; Department of Biochemistry, University of Washington School of Medicine, Seattle, WA, USA.
Carol B WareInstitute for Stem Cell and Regenerative Medicine, University of Washington School of Medicine, Seattle, WA, USA; Department of Biochemistry, University of Washington School of Medicine, Seattle, WA, USA.
R David HawkinsDivision of Medical Genetics, Department of Medicine, Department of Genome Sciences, University of Washington School of Medicine, Seattle, WA, USA; Institute for Stem Cell and Regenerative Medicine, University of Washington School of Medicine, Seattle, WA, USA. Electronic address: rdhawk@uw.edu.
University of Washington · USUniversity of Washington Medical Center · US

Funding

Vector and Transgenic Mouse CoreP30DK017047 · NIDDK · UNIVERSITY OF WASHINGTON · PI Sakeneh Zraika · 1986 to 2026
$41.4M
Functional assessment of distal regulatory SNPs associated with type 1 diabetes.R01DK103667 · NIDDK · UNIVERSITY OF WASHINGTON · PI HAWKINS, RAYMOND DAVID · 2015 to 2019
$2.5M
Functional validation of Rheumatoid Arthritis-associated distal regulatory SNPs iR01AR065952 · NIAMS · UNIVERSITY OF WASHINGTON · PI HAWKINS, RAYMOND DAVID · 2015 to 2018
$1.8M
Molecular Medicine Training ProgramT32GM095421 · NIGMS · UNIVERSITY OF WASHINGTON · PI HAWN, THOMAS R, LILES, W. CONRAD · 2011 to 2020
$1.6M
University of Washington PhD Training in Big Data for Genomics and NeuroscienceT32LM012419 · NLM · UNIVERSITY OF WASHINGTON · PI DANIEL, THOMAS L., FAIRHALL, ADRIENNE L · 2016 to 2019
$1.1M
NIAMS NIH HHS R01 AR065952NIDDK NIH HHS P30 DK017047NIDDK NIH HHS R01 DK103667NIGMS NIH HHS T32 GM095421NLM NIH HHS T32 LM012419
6 · The paper itself

Abstract

During mammalian embryogenesis, changes in morphology and gene expression are concurrent with epigenomic reprogramming. Using human embryonic stem cells representing the preimplantation blastocyst (naive) and postimplantation epiblast (primed), our data in 2iL/I/F naive cells demonstrate that a substantial portion of known human enhancers are premarked by H3K4me1, providing an enhanced open chromatin state in naive pluripotency. The 2iL/I/F enhancer repertoire occupies 9% of the genome, three times that of primed cells, and can exist in broad chromatin domains over 50 kb. Enhancer chromatin states are largely poised. Seventy-seven percent of 2iL/I/F enhancers are decommissioned in a stepwise manner as cells become primed. While primed topologically associating domains are largely unaltered upon differentiation, naive 2iL/I/F domains expand across primed boundaries, affecting three-dimensional genome architecture. Differential topologically associating domain edges coincide with 2iL/I/F H3K4me1 enrichment. Our results suggest that naive-derived 2iL/I/F cells have a unique chromatin landscape, which may reflect early embryogenesis.

Indexed as

AnimalsBlastocystCell DifferentiationChromatinEmbryo, MammalianEmbryonic DevelopmentEnhancer Elements, GeneticGene Expression Regulation, DevelopmentalGerm LayersHuman Embryonic Stem CellsHumansChromatin3D genome architectureembryogenesisenhancersnaive hESCs

Identifiers

PMID31056477
PMCPMC6524944
OpenAlexW2943661585

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.