ArticleHuman molecular genetics2022
ETS1 loss in mice impairs cardiac outflow tract septation via a cell migration defect autonomous to the neural crest.
Article in Human molecular genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 14 citations in OpenAlex.
- Neural signaling contributes to heart formation and growth in the invertebrate chordate, Ciona robusta.PLoS biology · 2026Article
- Ets1-regulated endothelial-secreted factors promote compact myocardial growth and contribute to the pathogenesis of ventricular non-compaction.Cardiovascular research · 2026Article
- Discovery ofDiagnostics (Basel, Switzerland) · 2025Article
- ETS1, a Target Gene of the EWSR1::FLI1 Fusion Oncoprotein, Regulates the Expression of the Focal Adhesion Protein TENSIN3.Molecular cancer research : MCR · 2024Article
- ETS1, a target gene of the EWSR1::FLI1 fusion oncoprotein, regulates the expression of the focal adhesion protein TENSIN3.bioRxiv : the preprint server for biology · 2023Article
- Isolated Absent Aortic Valves: A Unique Fetal Case With Echocardiographic, Pathologic, and Genetic Correlation.JACC. Case reports · 2023Article
- Use of Frogs as a Model to Study the Etiology of HLHS.Journal of cardiovascular development and disease · 2023Article
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Authors and funding
12 authors at 6 institutions in 2 countries.
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Abstract
Ets1 deletion in some mouse strains causes septal defects and has been implicated in human congenital heart defects in Jacobsen syndrome, in which one copy of the Ets1 gene is missing. Here, we demonstrate that loss of Ets1 in mice results in a decrease in neural crest (NC) cells migrating into the proximal outflow tract cushions during early heart development, with subsequent malalignment of the cushions relative to the muscular ventricular septum, resembling double outlet right ventricle (DORV) defects in humans. Consistent with this, we find that cultured cardiac NC cells from Ets1 mutant mice or derived from iPS cells from Jacobsen patients exhibit decreased migration speed and impaired cell-to-cell interactions. Together, our studies demonstrate a critical role for ETS1 for cell migration in cardiac NC cells that are required for proper formation of the proximal outflow tracts. These data provide further insights into the molecular and cellular basis for development of the outflow tracts, and how perturbation of NC cells can lead to DORV.
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