My research program investigates the role of cell-extracellular matrix (ECM) interactions during lung development, alveolar homeostasis, and repair.  We have developed organ specific mouse models that are combined with state-of-the-art cell biological techniques to define fundamental mechanisms whereby integrins regulate epithelial cell behavior in both health and disease. My laboratory has previously shown that lung epithelial deletion of the ECM receptor β1 integrin results in branching morphogenesis defects and impaired alveolarization, delayed epithelial cell differentiation, and increased lung inflammation during lung development. Current work focuses on discriminating the role of the 3 different laminin receptors, integrins a3β1, a6β1, a6β4, during lung morphogenesis. The goal of my research program is to define the mechanisms whereby laminin-binding integrins modulate epithelial differentiation and migration during alveolarization and identify disruptions in ECM-epithelial signaling that phenocopy human developmental lung diseases.