Evidence map›Paper›PMID 24752179›Full record

ArticleGenome research2014

Tissue-specific SMARCA4 binding at active and repressed regulatory elements during embryogenesis.

Catia Attanasio, Alex S Nord, Yiwen Zhu, Matthew J Blow, Simon C Biddie, Eric M Mendenhall, Jesse Dixon, Crystal Wright, Roya Hosseini, Jennifer A Akiyama and 9 more

Open access · greenAbstract read
In one paragraph

Article in Genome research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing 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

42 citing papers in PubMed, 66 citations in OpenAlex.

  1. Trial
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  8. iScience · 2021
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  18. The role of ARID1B, a BAF chromatin remodeling complex subunit, in neural development and behavior.Progress in neuro-psychopharmacology & biological psychiatry · 2019
    Review
  19. Article
  20. 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

19 authors at 5 institutions in 3 countries.

Catia AttanasioGenomics Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA;
Alex S NordGenomics Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA;
Yiwen ZhuGenomics Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA;
Matthew J BlowUS Department of Energy Joint Genome Institute, Walnut Creek, California 94598, USA;
Simon C BiddieUS Department of Energy Joint Genome Institute, Walnut Creek, California 94598, USA; Addenbrooke's Hospital, Cambridge University NHS Trust, Cambridge CB2 0QQ, United Kingdom;
Eric M MendenhallHHMI and Department of Pathology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA;
Jesse DixonLudwig Institute for Cancer Research, UCSD School of Medicine, La Jolla, California 92093, USA.
Crystal WrightUS Department of Energy Joint Genome Institute, Walnut Creek, California 94598, USA;
Roya HosseiniGenomics Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA;
Jennifer A AkiyamaGenomics Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA;
Amy HoltGenomics Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA;
Ingrid Plajzer-FrickGenomics Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA;
Malak ShoukryGenomics Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA;
Veena AfzalGenomics Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA;
Bing RenLudwig Institute for Cancer Research, UCSD School of Medicine, La Jolla, California 92093, USA.
Bradley E BernsteinHHMI and Department of Pathology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA;
Edward M RubinGenomics Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA; US Department of Energy Joint Genome Institute, Walnut Creek, California 94598, USA;
Axel ViselGenomics Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA; US Department of Energy Joint Genome Institute, Walnut Creek, California 94598, USA;
Len A PennacchioGenomics Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA; US Department of Energy Joint Genome Institute, Walnut Creek, California 94598, USA;
Lawrence Berkeley National Laboratory · USHarvard University · USJoint Genome Institute · USLudwig Cancer Research · BEUnited States Department of Energy · US

Funding

Generation of an In Vivo Human Genome Transcriptional Enhancer DatasetR01HG003988 · NHGRI · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI Len Alexander Pennacchio · 2006 to 2026
$24.1M
Center for Mammalian Regulatory GenomicsU54HG006997 · NHGRI · LUDWIG INSTITUTE FOR CANCER RES LTD · PI REN, BING · 2012 to 2016
$14.3M
Genomic, Transgenic and Knockout Resources for Craniofacial Enhancer StudiesU01DE024427 · NIDCR · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI VISEL, AXEL · 2014 to 2018
$3.7M
Developmental and evolutionary dynamics of tissue-specific mammalian enhancers.F32GM105202 · NIGMS · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI NORD, ALEXANDER · 2013 to 2014
$60k
NHGRI NIH HHS HG003988NHGRI NIH HHS R01 HG003988NHGRI NIH HHS U54 HG006997NHGRI NIH HHS U54HG006997NIDCR NIH HHS U01 DE024427NIGMS NIH HHS F32 GM105202NIGMS NIH HHS GM105202
6 · The paper itself

Abstract

The SMARCA4 (also known as BRG1 in humans) chromatin remodeling factor is critical for establishing lineage-specific chromatin states during early mammalian development. However, the role of SMARCA4 in tissue-specific gene regulation during embryogenesis remains poorly defined. To investigate the genome-wide binding landscape of SMARCA4 in differentiating tissues, we engineered a Smarca4(FLAG) knock-in mouse line. Using ChIP-seq, we identified ∼51,000 SMARCA4-associated regions across six embryonic mouse tissues (forebrain, hindbrain, neural tube, heart, limb, and face) at mid-gestation (E11.5). The majority of these regions was distal from promoters and showed dynamic occupancy, with most distal SMARCA4 sites (73%) confined to a single or limited subset of tissues. To further characterize these regions, we profiled active and repressive histone marks in the same tissues and examined the intersection of informative chromatin states and SMARCA4 binding. This revealed distinct classes of distal SMARCA4-associated elements characterized by activating and repressive chromatin signatures that were associated with tissue-specific up- or down-regulation of gene expression and relevant active/repressed biological pathways. We further demonstrate the predicted active regulatory properties of SMARCA4-associated elements by retrospective analysis of tissue-specific enhancers and direct testing of SMARCA4-bound regions in transgenic mouse assays. Our results indicate a dual active/repressive function of SMARCA4 at distal regulatory sequences in vivo and support its role in tissue-specific gene regulation during embryonic development.

Indexed as

Gene Expression Regulation, DevelopmentalRegulatory Elements, TranscriptionalAnimalsBrainChromatinDNA HelicasesExtremitiesGenomeHeartHistonesMiceMyocardiumNuclear ProteinsOrgan SpecificityProtein BindingTranscription FactorsChromatinDNA HelicasesHistonesNuclear ProteinsSmarca4 protein, mouseTranscription Factors

Identifiers

PMID24752179
PMCPMC4032856
OpenAlexW1970495742

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.