ArticleDevelopment (Cambridge, England)2016
The AP-1 transcription factor component Fosl2 potentiates the rate of myocardial differentiation from the zebrafish second heart field.
Article in Development (Cambridge, England), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed.
- Rapid and robust generation of cardiomyocyte-specific crispants in zebrafish using the cardiodeleter system.Cell reports methods · 2025Article
- Adaptation responses to salt stress in the gut ofAnimal cells and systems · 2025Article
- A novel gene-trap line reveals the dynamic patterns and essential roles of cysteine and glycine-rich protein 3 in zebrafish heart development and regeneration.Cellular and molecular life sciences : CMLS · 2024Article
- The second heart field: the first 20 years.Mammalian genome : official journal of the International Mammalian Genome Society · 2023Review
- RBPMS2 Is a Myocardial-Enriched Splicing Regulator Required for Cardiac Function.Circulation research · 2022Article
- Phylogenetic and Expression Analysis of Fos Transcription Factors in Zebrafish.International journal of molecular sciences · 2022Article
- WhichTF is functionally important in your open chromatin data?PLoS computational biology · 2022Article
- Latent TGFβ-binding proteins 1 and 3 protect the larval zebrafish outflow tract from aneurysmal dilatation.Disease models & mechanisms · 2022Article
- Ruvbl2 Suppresses Cardiomyocyte Proliferation During Zebrafish Heart Development and Regeneration.Frontiers in cell and developmental biology · 2022Article
- KLRD1, FOSL2 and LILRB3 as potential biomarkers for plaques progression in acute myocardial infarction and stable coronary artery disease.BMC cardiovascular disorders · 2021Article
- Getting to the Heart of Left-Right Asymmetry: Contributions from the Zebrafish Model.Journal of cardiovascular development and disease · 2021Review
- From Stripes to a Beating Heart: Early Cardiac Development in Zebrafish.Journal of cardiovascular development and disease · 2021Review
- The emerging roles of circular RNAs in regulating the fate of stem cells.Molecular and cellular biochemistry · 2021Review
- Silencing circRNA_001937 may inhibit cutaneous squamous cell carcinoma proliferation and induce apoptosis by preventing the sponging of the miRNA‑597‑3p/FOSL2 pathway.International journal of molecular medicine · 2020Article
- Endothelial TGF-β signaling instructs smooth muscle cell development in the cardiac outflow tract.eLife · 2020Article
- Cardiac function modulates endocardial cell dynamics to shape the cardiac outflow tract.Development (Cambridge, England) · 2020Article
- MiR-195 enhances cardiomyogenic differentiation of the proepicardium/septum transversum by Smurf1 and Foxp1 modulation.Scientific reports · 2020Article
- Alternative splicing of jnk1a in zebrafish determines first heart field ventricular cardiomyocyte numbers through modulation of hand2 expression.PLoS genetics · 2020Article
- Identifying the key regulators that promote cell-cycle activity in the hearts of early neonatal pigs after myocardial injury.PloS one · 2020Article
- Cardiac Reprogramming Factors Synergistically Activate Genome-wide Cardiogenic Stage-Specific Enhancers.Cell stem cell · 2019Article
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Authors and funding
12 authors.
Funding
Abstract
The vertebrate heart forms through successive phases of cardiomyocyte differentiation. Initially, cardiomyocytes derived from first heart field (FHF) progenitors assemble the linear heart tube. Thereafter, second heart field (SHF) progenitors differentiate into cardiomyocytes that are accreted to the poles of the heart tube over a well-defined developmental window. Although heart tube elongation deficiencies lead to life-threatening congenital heart defects, the variables controlling the initiation, rate and duration of myocardial accretion remain obscure. Here, we demonstrate that the AP-1 transcription factor, Fos-like antigen 2 (Fosl2), potentiates the rate of myocardial accretion from the zebrafish SHF. fosl2 mutants initiate accretion appropriately, but cardiomyocyte production is sluggish, resulting in a ventricular deficit coupled with an accumulation of SHF progenitors. Surprisingly, mutant embryos eventually correct the myocardial deficit by extending the accretion window. Overexpression of Fosl2 also compromises production of SHF-derived ventricular cardiomyocytes, a phenotype that is consistent with precocious depletion of the progenitor pool. Our data implicate Fosl2 in promoting the progenitor to cardiomyocyte transition and uncover the existence of regulatory mechanisms to ensure appropriate SHF-mediated cardiomyocyte contribution irrespective of embryonic stage.
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