Evidence map›Paper›PMID 30444277›Full record

ArticleDevelopmental dynamics : an official publication of the American Association of Anatomists2019

pouC Regulates Expression of bmp4 During Atrioventricular Canal Formation in Zebrafish.

Minoti Bhakta, Mahesh S Padanad, John P Harris, Christina Lubczyk, James F Amatruda, Nikhil V Munshi

Open access · greenAbstract read
In one paragraph

Article in Developmental dynamics : an official publication of the American Association of Anatomists, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 45% 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

3 citing papers in PubMed, 4 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

6 authors at 1 institution in 1 country.

Minoti BhaktaDepartment of Internal Medicine - Cardiology, UT Southwestern Medical Center, Dallas, Texas.
Mahesh S PadanadDepartment of Internal Medicine - Cardiology, UT Southwestern Medical Center, Dallas, Texas.
John P HarrisDepartment of Internal Medicine - Cardiology, UT Southwestern Medical Center, Dallas, Texas.
Christina LubczykDepartment of Internal Medicine - Cardiology, UT Southwestern Medical Center, Dallas, Texas.
James F AmatrudaDepartment of Pediatrics, UT Southwestern Medical Center, Dallas, Texas.
Nikhil V MunshiDepartment of Internal Medicine - Cardiology, UT Southwestern Medical Center, Dallas, Texas.ORCID 0000-0002-8397-100X
Southwestern Medical Center · US

Funding

Diversity Supplement- Analysis of transcriptional and chromatin accessibility during atrioventricular node formatR01HL136604 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI MUNSHI, NIKHIL VILAS · 2017 to 2021
$2.1M
Molecular Dissection of Cardiac Conduction System DevelopmentK08HL094699 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI MUNSHI, NIKHIL VILAS · 2009 to 2014
$650k
Diversity Supplement - Magid MohamedR03HL133642 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI MUNSHI, NIKHIL VILAS · 2016 to 2017
$284k
Defining process control parameters for cardiac reprogrammingR03HL135217 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI MUNSHI, NIKHIL VILAS · 2016 to 2017
$162k
NHLBI NIH HHS K08 HL094699NHLBI NIH HHS R01 HL136604NHLBI NIH HHS R03 HL133642NHLBI NIH HHS R03 HL135217
6 · The paper itself

Abstract

backgroundMany human gene mutations have been linked to congenital heart disease (CHD), yet CHD remains a major health issue worldwide due in part to an incomplete understanding of the molecular basis for cardiac malformation.

resultsHere we identify the orthologous mouse Pou6f1 and zebrafish pouC as POU homeodomain transcription factors enriched in the developing heart. We find that pouC is a multi-functional transcriptional regulator containing separable activation, repression, protein-protein interaction, and DNA binding domains. Using zebrafish heart development as a model system, we demonstrate that pouC knockdown impairs cardiac morphogenesis and affects cardiovascular function. We also find that levels of pouC expression must be fine-tuned to enable proper heart formation. At the cellular level, we demonstrate that pouC knockdown disrupts atrioventricular canal (AVC) cardiomyocyte maintenance, although chamber myocyte specification remains intact. Mechanistically, we show that pouC binds a bmp4 intronic regulatory element to mediate transcriptional activation.

conclusionsTaken together, our study establishes pouC as a novel transcriptional input into the regulatory hierarchy that drives AVC morphogenesis in zebrafish. We anticipate that these findings will inform future efforts to explore functional conservation in mammals and potential association with atrioventricular septal defects in humans. Developmental Dynamics 248:173-188, 2019. © 2018 Wiley Periodicals, Inc.

Indexed as

Gene Expression Regulation, DevelopmentalAnimalsBone Morphogenetic Protein 4HeartHeart Septal DefectsHeart SeptumMicePOU Domain FactorsProtein BindingTranscription FactorsZebrafishZebrafish Proteinsbmp4 protein, zebrafishBone Morphogenetic Protein 4Pou6f1 protein, mousepou6f1 protein, zebrafishPOU Domain FactorsTranscription FactorsZebrafish Proteinsatrioventricular canalcardiac developmentmorphogenesispouCtranscription factor

Identifiers

PMID30444277
PMCPMC6340724
OpenAlexW2901633648

What OpenQuestion holds

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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.