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???displayArticle.abstract??? Ets1 is an important transcription factor that is expressed in both the cardiac neural crest (NC) and heartmesoderm of vertebrate embryos. Moreover, Ets1 deletion in humans results in congenital heart abnormalities. To clarify the functional contributions of Ets1 in cardiac NC vs. heartmesoderm, we performed tissue-targeted loss-of-function analysis to compare the relative roles of Ets1 in these two tissues during heart formation using Xenopus embryos as a model system. We confirmed by in situ hybridization analysis that Ets1 is expressed in NC and heartmesoderm during embryogenesis. Using a translation-blocking antisense morpholino to knockdown Ets1 protein selectively in the NC, we observed defects in NC delamination from the neural tube, collective cell migration, as well as segregation of NC streams in the cranial and cardiac regions. Many cardiac NC cells failed to reach their destination in the heart, resulting in defective aortic archartery formation. A different set of defects was noted when Ets1 knockdown was targeted to heartmesoderm. The formation of the primitive heart tube was dramatically delayed and the endocardial tissue appeared depleted. As a result, the conformation of the heart was severely disrupted. In addition, the outflow tractseptum was missing, and trabeculae formation in the ventricle was abolished. Our study shows that Ets1 is required in both the cardiac NC and heartmesoderm, albeit for different aspects of heart formation. Our results reinforce the suggestion that proper interaction between these tissues is critical for normal heart development.
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???displayArticle.pmcLink???PMC4447785 ???displayArticle.link???Cardiovasc Res ???displayArticle.grants???[+]
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