Midline defects of the body wall account for approximately 5% of congenital abnormalities observed at birth. Defects in closure thoracic body wall lead to conditions such as ectopia cordis (exposed heart), anomalous sternum as well as affect the normal development of the lungs. The molecular mechanisms underlying the formation of the ventral body are poorly understood.

We are currently studying models wherein perturbation to Wnt ligand secretion (by deletion of Wls) or Wnt ligand reception (deletion of Lrp5 and Lrp6) prevents the closure of the thoracic body wall, resulting in malformed sternum, exposed heart and abnormal pulmonary morphology. These studies will provide insights into the normal development of the body wall and the pathogenesis of conditions resulting in defecting closure of the body wall.