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- W2055124799 abstract "Development of the heart requires recruitment of cardiovascular progenitor cells (CPCs) to the future heart-forming region. CPCs are the building blocks of the heart, and have the potential to form all the major cardiac lineages. However, little is known regarding what regulates CPC fate and behavior. Activity of GATA4, SMARCD3 and TBX5 - the `cardiac BAF' (cBAF) complex, can promote myocardial differentiation in embryonic mouse mesoderm. Here, we exploit the advantages of the zebrafish embryo to gain mechanistic understanding of cBAF activity. Overexpression of smarcd3b and gata5 in zebrafish results in an enlarged heart, whereas combinatorial loss of cBAF components inhibits cardiac differentiation. In transplantation experiments, cBAF acts cell autonomously to promote cardiac fate. Remarkably, cells overexpressing cBAF migrate to the developing heart and differentiate as cardiomyocytes, endocardium and smooth muscle. This is observed even in host embryos that lack endoderm or cardiac mesoderm. Our results reveal an evolutionarily conserved role for cBAF activity in cardiac differentiation. Importantly, they demonstrate that Smarcd3b and Gata5 can induce a primitive, CPC-like state." @default.
- W2055124799 created "2016-06-24" @default.
- W2055124799 creator A5014732782 @default.
- W2055124799 creator A5036049307 @default.
- W2055124799 creator A5054970085 @default.
- W2055124799 creator A5086227409 @default.
- W2055124799 date "2011-08-01" @default.
- W2055124799 modified "2023-10-18" @default.
- W2055124799 title "Smarcd3b and Gata5 promote a cardiac progenitor fate in the zebrafish embryo" @default.
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- W2055124799 doi "https://doi.org/10.1242/dev.064279" @default.
- W2055124799 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21715426" @default.
- W2055124799 hasPublicationYear "2011" @default.
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