My laboratory is interested in understanding how congenital heart defects occur. In particular I am focused on defects of the conotruncus (or arterial pole) which include persistent truncus arteriosus, double outlet right ventricle, and tetralogy of Fallot. During early stages of heart development the secondary heart field, a population of cardiac stem cells, forms the smooth muscle and myocardial junction of the arterial pole. Another cell population important for arterial pole formation are the cardiac neural crest. These cells migrate into the arterial pole and form a septum to divide the systemic and pulmonary circulations. Disruption of secondary heart field or cardiac neural crest development results in conotruncal defects. My research focuses on the understanding the integration of the cell signaling mechanisms that influence the secondary heart field progenitor cells and cardiac neural crest to form the arterial pole. We have shown that modulation of fibroblast growth factor 8 (FGF8) signaling by cardiac neural crest in the pharynx is required for normal heart development and that too much or too little FGF8 signaling results in secondary heart field defects that lead to arterial pole defects. Current work in the lab focuses on the integration of FGF8 signaling with other signaling pathways including retinoic acid, sonic hedgehog (Shh), and BMP to effect normal arterial pole development.
