FOG-2, a cofactor for GATA transcription factors, is essential for heart morphogenesis and development of coronary vessels from epicardium

Academic 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.
  • Authors

    Published In

  • Cell  Journal
  • Digital Object Identifier (doi)

    Author List

  • Tevosian SG; Deconinck AE; Tanaka M; Schinke M; Litovsky SH; Izumo S; Fujiwara Y; Orkin SH
  • Start Page

  • 729
  • End Page

  • 739
  • Volume

  • 101
  • Issue

  • 7