ArticleDevelopment (Cambridge, England)2013
Nkx genes are essential for maintenance of ventricular identity.
Article in Development (Cambridge, England), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed.
- Nr2f1a and Isl1 repress acquisition of epicardial identity in venous atrial cardiomyocytes.Development (Cambridge, England) · 2026Article
- In Vivo Models of Cardiovascular Disease:Biomedicines · 2025Review
- Review
- A systems genetics approach identifies roles for proteasome factors in heart development and congenital heart defects.PLoS genetics · 2025Article
- Nkx2.7 is a conserved regulator of craniofacial development.Nature communications · 2025Article
- Zebrafish as a Versatile Model for Cardiovascular Research: Peering into the Heart of the Matter.Cells · 2025Review
- A Foxf1-Wnt-Nr2f1 cascade promotes atrial cardiomyocyte differentiation in zebrafish.PLoS genetics · 2024Article
- From promoter motif to cardiac function: a single DPE motif affects transcription regulation and organ function in vivo.Development (Cambridge, England) · 2024Article
- Retinoic acid modulation guides human-induced pluripotent stem cell differentiation towards left or right ventricle-like cardiomyocytes.Stem cell research & therapy · 2024Article
- Nkx2.3 transcription factor is a key regulator of mucous cell identity in salivary glands.Developmental biology · 2024Article
- A Foxf1-Wnt-Nr2f1 cascade promotes atrial cardiomyocyte differentiation in zebrafish.bioRxiv : the preprint server for biology · 2024Article
- The MEK-ERK signaling pathway promotes maintenance of cardiac chamber identity.Development (Cambridge, England) · 2024Article
- In-Depth Genomic Analysis: The New Challenge in Congenital Heart Disease.International journal of molecular sciences · 2024Review
- Genetic and Molecular Underpinnings of Atrial Fibrillation.NPJ cardiovascular health · 2024Article
- Tbx5 maintains atrial identity in post-natal cardiomyocytes by regulating an atrial-specific enhancer network.Nature cardiovascular research · 2023Article
- Nr2f1a maintains atrialeLife · 2023Article
- Sin3a Associated Protein 130kDa, sap130, plays an evolutionary conserved role in zebrafish heart development.bioRxiv : the preprint server for biology · 2023Article
- In Vivo Dissection of Chamber-Selective Enhancers Reveals Estrogen-Related Receptor as a Regulator of Ventricular Cardiomyocyte Identity.Circulation · 2023Article
- Activation of Nkx2.5 transcriptional program is required for adult myocardial repair.Nature communications · 2022Article
- Stage-specific regulation of signalling pathways to differentiate pluripotent stem cells to cardiomyocytes with ventricular lineage.Stem cell research & therapy · 2022Article
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Authors and funding
7 authors.
Funding
Abstract
Establishment of specific characteristics of each embryonic cardiac chamber is crucial for development of a fully functional adult heart. Despite the importance of defining and maintaining unique features in ventricular and atrial cardiomyocytes, the regulatory mechanisms guiding these processes are poorly understood. Here, we show that the homeodomain transcription factors Nkx2.5 and Nkx2.7 are necessary to sustain ventricular chamber attributes through repression of atrial chamber identity. Mutation of nkx2.5 in zebrafish yields embryos with diminutive ventricular and bulbous atrial chambers. These chamber deformities emerge gradually during development, with a severe collapse in the number of ventricular cardiomyocytes and an accumulation of excess atrial cardiomyocytes as the heart matures. Removal of nkx2.7 function from nkx2.5 mutants exacerbates the loss of ventricular cells and the gain of atrial cells. Moreover, in these Nkx-deficient embryos, expression of vmhc, a ventricular gene, fades, whereas expression of amhc, an atrial gene, expands. Cell-labeling experiments suggest that ventricular cardiomyocytes can transform into atrial cardiomyocytes in the absence of Nkx gene function. Through suggestion of transdifferentiation from ventricular to atrial fate, our data reveal a pivotal role for Nkx genes in maintaining ventricular identity and highlight remarkable plasticity in differentiated myocardium. Thus, our results are relevant to the etiologies of fetal and neonatal cardiac pathology and could direct future innovations in cardiac regenerative medicine.
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