Evidence map›Paper›PMID 31989924›Full record

ArticleeLife2020

GLI transcriptional repression regulates tissue-specific enhancer activity in response to Hedgehog signaling.

Rachel K Lex, Zhicheng Ji, Kristin N Falkenstein, Weiqiang Zhou, Joanna L Henry, Hongkai Ji, Steven A Vokes

Open access · goldAbstract read
In one paragraph

Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

26 citing papers in PubMed, 40 citations in OpenAlex.

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  13. Timing is everything: Transcriptional repression is not the default mode for regulating Hedgehog signaling.BioEssays : news and reviews in molecular, cellular and developmental biology · 2022
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  20. TheProceedings of the National Academy of Sciences of the United States of America · 2021
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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

7 authors at 2 institutions in 1 country.

Rachel K Lex *Department of Molecular Biosciences, The University of Texas at Austin, Austin, United States.
Zhicheng Ji *Department of Biostatistics, Johns Hopkins Bloomberg School of Public Health, Baltimore, United States.
Kristin N Falkenstein *Department of Molecular Biosciences, The University of Texas at Austin, Austin, United States.
Weiqiang ZhouDepartment of Biostatistics, Johns Hopkins Bloomberg School of Public Health, Baltimore, United States.
Joanna L HenryDepartment of Molecular Biosciences, The University of Texas at Austin, Austin, United States.
Hongkai JiDepartment of Biostatistics, Johns Hopkins Bloomberg School of Public Health, Baltimore, United States.
Steven A VokesDepartment of Molecular Biosciences, The University of Texas at Austin, Austin, United States.ORCID https://orcid.org/0000-0002-1724-0102
The University of Texas at Austin · USJohns Hopkins University · US

Funding

Cis-regulatory circuitry underlying Hedgehog mediated limb developmentR01HD073151 · NICHD · UNIVERSITY OF TEXAS AT AUSTIN · PI Steven Alexander Vokes · 2012 to 2026
$5.1M
Big Data Methods for Decoding Gene RegulationR01HG009518 · NHGRI · JOHNS HOPKINS UNIVERSITY · PI JI, HONGKAI · 2018 to 2021
$1.7M
Defining the epigenetic mechanisms underlying GLI-mediated transcriptional repressionF31DE027597 · NIDCR · UNIVERSITY OF TEXAS AT AUSTIN · PI LEX, RACHEL K · 2017 to 2020
$122k
Eunice Kennedy Shriver National Institute of Child Health and Human Development R01HD073151NHGRI NIH HHS R01 HG009518NICHD NIH HHS R01 HD073151NIDCR NIH HHS F31 DE027597NIDCR NIH HHS F31DE027597NIH HHS R01HG009518
6 · The paper itself

Abstract

Transcriptional repression needs to be rapidly reversible during embryonic development. This extends to the Hedgehog pathway, which primarily serves to counter GLI repression by processing GLI proteins into transcriptional activators. In investigating the mechanisms underlying GLI repression, we find that a subset of GLI binding regions, termed HH-responsive enhancers, specifically loses acetylation in the absence of HH signaling. These regions are highly enriched around HH target genes and primarily drive HH-specific transcriptional activity in the mouse limb bud. They also retain H3K27ac enrichment in limb buds devoid of GLI activator and repressor, indicating that their activity is primarily regulated by GLI repression. Furthermore, the Polycomb repression complex is not active at most of these regions, suggesting it is not a major mechanism of GLI repression. We propose a model for tissue-specific enhancer activity in which an HDAC-associated GLI repression complex regulates target genes by altering the acetylation status at enhancers.

Indexed as

AnimalsEmbryonic DevelopmentGene Expression Regulation, DevelopmentalHedgehog ProteinsHistonesLimb BudsMiceMice, KnockoutNerve Tissue ProteinsNIH 3T3 CellsTrans-ActivatorsZinc Finger Protein Gli3Gli3 protein, mouseHedgehog Proteinshistone H3 trimethyl Lys4HistonesNerve Tissue ProteinsShh protein, mouseTrans-ActivatorsZinc Finger Protein Gli3chromatindevelopmental biologyenhancersgeneticsgenomicsGLIHedgehoglimb budmousetranscriptional repression

Identifiers

PMID31989924
PMCPMC6986877
OpenAlexW3003728324

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.