Congenital organ anomalies are the leading cause of infant mortality in North America.

The disease mechanisms responsible for causing congenital organ anomalies are poorly understood. Though many are caused by known risk genes discovered after genetic sequencing of an individual with a congenital organ anomaly, how sequence variants in these genes affect the underlying cell and developmental biology during organogenesis is not known.

Our lab is particularly interested in how disruptions to cell and tissue fusion-separation events in organogenesis underlie many common congenital malformations. We currently focus on tissue splitting events in the embryonic gut tube, like how the trachea and esophagus split from a single anterior foregut tube.

To approach this challenge, our lab uses research animal models including Xenopus (African clawed frog) and mice. Xenopus and mice have all of the same organs as humans, including a trachea and esophagus, and their organ development is similar, making them excellent models to study human development and disease.

We also use pluripotent stem cell-derived digestive and respiratory tissue to understand how the underlying cell biology is disrupted.