Evidence map›Paper›PMID 28372944›Full record

ArticleDevelopmental biology2017

Histone demethylases Kdm6ba and Kdm6bb redundantly promote cardiomyocyte proliferation during zebrafish heart ventricle maturation.

Alexander A Akerberg, Astra Henner, Scott Stewart, Kryn Stankunas

Abstract read
In one paragraph

Article in Developmental biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

18 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
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  4. Review
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  7. The Roles of Histone Lysine Methyltransferases in Heart Development and Disease.Journal of cardiovascular development and disease · 2023
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Roles and regulation of histone methylation in animal development.Nature reviews. Molecular cell biology · 2019
    Review
  18. 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

4 authors at 1 institution in 1 country.

Alexander A AkerbergInstitute of Molecular Biology, University of Oregon, Eugene, OR 97403-1229, United States; Department of Biology, University of Oregon, Eugene, OR 97403-1229, United States.
Astra HennerInstitute of Molecular Biology, University of Oregon, Eugene, OR 97403-1229, United States.
Scott StewartInstitute of Molecular Biology, University of Oregon, Eugene, OR 97403-1229, United States.
Kryn StankunasInstitute of Molecular Biology, University of Oregon, Eugene, OR 97403-1229, United States; Department of Biology, University of Oregon, Eugene, OR 97403-1229, United States. Electronic address: kryn@uoregon.edu.
University of Oregon · US

Funding

DEVELOPMENTAL BIOLOGY TRAINING PROGRAMT32HD007348 · NICHD · UNIVERSITY OF OREGON · PI Chris Q Doe, KRYN STANKUNAS · 1989 to 2026
$6.8M
Chromatin Regulation of Heart Valve DevelopmentR01HL115294 · NHLBI · UNIVERSITY OF OREGON · PI STANKUNAS, KRYN · 2014 to 2018
$1.8M
NHLBI NIH HHS R01 HL115294NICHD NIH HHS T32 HD007348
6 · The paper itself

Abstract

Trimethylation of lysine 27 on histone 3 (H3K27me3) by the Polycomb repressive complex 2 (PRC2) contributes to localized and inherited transcriptional repression. Kdm6b (Jmjd3) is a H3K27me3 demethylase that can relieve repression-associated H3K27me3 marks, thereby supporting activation of previously silenced genes. Kdm6b is proposed to contribute to early developmental cell fate specification, cardiovascular differentiation, and/or later steps of organogenesis, including endochondral bone formation and lung development. We pursued loss-of-function studies in zebrafish to define the conserved developmental roles of Kdm6b. kdm6ba and kdm6bb homozygous deficient zebrafish are each viable and fertile. However, loss of both kdm6ba and kdm6bb shows Kdm6b proteins share redundant and pleiotropic roles in organogenesis without impacting initial cell fate specification. In the developing heart, co-expressed Kdm6b proteins promote cardiomyocyte proliferation coupled with the initial stages of cardiac trabeculation. While newly formed trabecular cardiomyocytes display a striking transient decrease in bulk cellular H3K27me3 levels, this demethylation is independent of collective Kdm6b. Our results indicate a restricted and likely locus-specific role for Kdm6b demethylases during heart ventricle maturation rather than initial cardiogenesis.

Indexed as

AnimalsAnimals, Genetically ModifiedCell DifferentiationCell ProliferationGene Expression Regulation, DevelopmentalGene Knockout TechniquesHeart VentriclesHistone DemethylasesHistonesJumonji Domain-Containing Histone DemethylasesMethylationMyocytes, CardiacOrganogenesisZebrafishZebrafish ProteinsHistone DemethylasesHistonesJumonji Domain-Containing Histone Demethylaseskdm6bb protein, zebrafishlysine (K)-specific demethylase 6B, zebrafishZebrafish ProteinsCardiogenesisH3K27me3Histone demethylaseKdm6bTrabeculationVentricle

Identifiers

PMID28372944
PMCPMC5607060
OpenAlexW2601144754

What OpenQuestion holds

Textmetadata
LicenceTDM
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.