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

Cell. 2000 Jun 23;101(7):729-39. doi: 10.1016/s0092-8674(00)80885-5.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Coronary Vessels / embryology*
  • Coronary Vessels / physiology
  • DNA-Binding Proteins / physiology*
  • Embryonic and Fetal Development
  • Gene Expression Regulation, Developmental / physiology
  • Heart / embryology*
  • Heart / physiology
  • Mice
  • Mice, Transgenic
  • Morphogenesis
  • Pericardium / embryology
  • Transcription Factors / physiology*
  • Zinc Fingers


  • DNA-Binding Proteins
  • Transcription Factors
  • Zfpm2 protein, mouse