In contrast to many organs which complete their development in early pregnancy, the lung develops throughout late gestation and the first decade of life. During alveolarization, the final, postnatal stage of lung development, primitive saccules are septated to form over 400,000 million alveoli, and the pulmonary microvascular volume increases 30-fold. However, completion of parenchymal and vascular development after birth renders the immature lung highly susceptible to environmental insults that disrupt this developmental program. My lab is centered on delineating molecular mechanisms that promote alveolarization with a key focus on mechanisms regulating pulmonary angiogenesis, an important driver of alveolarization. We employ single cell transcriptomics, single nuclei ATAC-sequencing, genetic lineage tracing, primary cell culture and cell- and tissue-specific knock out mouse models to identify select lung cell subpopulations with essential functions in lung development and repair after injury.  Although the immaturity of the lung after birth does increase its vulnerability to injuries that can disrupt its development, this same quality appears to offer the immature lung a tremendous capacity for repair and regeneration.  Thus, we delineate transcriptomic alterations, differential chromatin accessibility and response to injury in rodent models at differing stages of development in order to define protective cellular and molecular mechanisms unique to the immature lung. Given that developmental mechanisms are often re-invoked to promote lung regeneration after injury even in the mature lung, our long-term goal is to leverage this knowledge to develop novel therapies to promote lung development and regeneration in infants, children, and adults.