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Tevosian, Sergei G; Deconinck, Anne E; Tanaka, Makoto; Schinke, Martina; Litovsky, Silvio H; Izumo, Seigo; Fujiwara, Yuko; Orkin, Stuart H
Cell, 06/2000, Letnik: 101, Številka: 7Journal Article
We disrupted the FOG-2 gene in mice to define its requirement in vivo. FOG-2−/− embryos die at midgestation with a cardiac defect characterized by a thin ventricular myocardium, common atrioventricular canal, and the tetralogy of Fallot malformation. Remarkably, coronary vasculature is absent in FOG-2−/− hearts. Despite formation of an intact epicardial layer and expression of epicardium-specific genes, markers of cardiac vessel development (ICAM-2 and FLK-1) are not detected, indicative of failure to activate their expression and/or to initiate the epithelial to mesenchymal transformation of epicardial cells. Transgenic reexpression of FOG-2 in cardiomyocytes rescues the FOG-2−/− vascular phenotype, demonstrating that FOG-2 function in myocardium is required and sufficient for coronary vessel development. Our findings provide the molecular inroad into the induction of coronary vasculature by myocardium in the developing heart.
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