Evidence map›Paper›PMID 28536180›Full record

ArticleGenome research2017

YY1 and CTCF orchestrate a 3D chromatin looping switch during early neural lineage commitment.

Jonathan A Beagan, Michael T Duong, Katelyn R Titus, Linda Zhou, Zhendong Cao, Jingjing Ma, Caroline V Lachanski, Daniel R Gillis, Jennifer E Phillips-Cremins

Open access · bronzeAbstract read
In one paragraph

Article in Genome research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 209 papers.

0numbers the graph read from it
0cells of the map it votes in
209citing papers in PubMed
–field-weighted citation impact
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

209 citing papers in PubMed, 329 citations in OpenAlex.

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149 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Jonathan A BeaganDepartment of Bioengineering, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.
Michael T DuongDepartment of Bioengineering, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.
Katelyn R TitusDepartment of Bioengineering, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.
Linda ZhouDepartment of Bioengineering, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.
Zhendong CaoDepartment of Bioengineering, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.
Jingjing MaDepartment of Bioengineering, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.
Caroline V LachanskiDepartment of Bioengineering, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.
Daniel R GillisDepartment of Bioengineering, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.
Jennifer E Phillips-CreminsDepartment of Bioengineering, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.
University of Pennsylvania · US

Funding

Training Program in Computational GenomicsT32HG000046 · NHGRI · UNIVERSITY OF PENNSYLVANIA · PI JUNHYONG KIM, Mingyao Li · 1999 to 2026
$9.5M
Engineering and visualizing genome folding at high spatiotemporal resolutionU01HL129998 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI BLOBEL, GERD A, PHILLIPS-CREMINS, JENNIFER ELIZABETH · 2015 to 2019
$4.2M
Engineering 3-D Epigenome Topology with LightDP2MH110247 · NIMH · UNIVERSITY OF PENNSYLVANIA · PI PHILLIPS-CREMINS, JENNIFER ELIZABETH · 2015 to 2015
$2.4M
NHGRI NIH HHS T32 HG000046NHLBI NIH HHS U01 HL129998NIMH NIH HHS DP2 MH110247
6 · The paper itself

Abstract

CTCF is an architectural protein with a critical role in connecting higher-order chromatin folding in pluripotent stem cells. Recent reports have suggested that CTCF binding is more dynamic during development than previously appreciated. Here, we set out to understand the extent to which shifts in genome-wide CTCF occupancy contribute to the 3D reconfiguration of fine-scale chromatin folding during early neural lineage commitment. Unexpectedly, we observe a sharp decrease in CTCF occupancy during the transition from naïve/primed pluripotency to multipotent primary neural progenitor cells (NPCs). Many pluripotency gene-enhancer interactions are anchored by CTCF, and its occupancy is lost in parallel with loop decommissioning during differentiation. Conversely, CTCF binding sites in NPCs are largely preexisting in pluripotent stem cells. Only a small number of CTCF sites arise de novo in NPCs. We identify another zinc finger protein, Yin Yang 1 (YY1), at the base of looping interactions between NPC-specific genes and enhancers. Putative NPC-specific enhancers exhibit strong YY1 signal when engaged in 3D contacts and negligible YY1 signal when not in loops. Moreover, siRNA knockdown of

Indexed as

Cell DifferentiationChromatin Assembly and DisassemblyCCCTC-Binding FactorCell LineChromatinEnhancer Elements, GeneticGenome-Wide Association StudyHuman Embryonic Stem CellsHumansNeural Stem CellsYY1 Transcription FactorCCCTC-Binding FactorChromatinCTCF protein, humanYY1 protein, humanYY1 Transcription Factor

Identifiers

PMID28536180
PMCPMC5495066
OpenAlexW2616964127

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.