FOG-2, a Cofactor for GATA Transcription Factors, Is Essential for Heart Morphogenesis and Development of Coronary Vessels from Epicardium
Copyright policy )FOG-2, a Cofactor for GATA Transcription Factors, Is Essential for Heart Morphogenesis and Development of Coronary Vessels from Epicardium
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.
- Beth Israel Deaconess Medical Center United States
- Dana-Farber Cancer Institute United States
- Harvard University United States
- Howard Hughes Medical Institute United States
Biochemistry, Genetics and Molecular Biology(all), Gene Expression Regulation, Developmental, Heart, Mice, Transgenic, Zinc Fingers, Coronary Vessels, DNA-Binding Proteins, Embryonic and Fetal Development, Mice, Morphogenesis, Animals, Pericardium, Transcription Factors
Biochemistry, Genetics and Molecular Biology(all), Gene Expression Regulation, Developmental, Heart, Mice, Transgenic, Zinc Fingers, Coronary Vessels, DNA-Binding Proteins, Embryonic and Fetal Development, Mice, Morphogenesis, Animals, Pericardium, Transcription Factors
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