Previous studies have provided evidence for two types of airway epithelial progenitors, one randomly distributed in the airways that maintains normal epithelial homeostasis and responds to minor injuries of the epithelium, and a second, associated with previously described progenitor cell niches that can renew depleted Clara cells upon severe epithelial injury [38, 56] . The randomly distributed eGFP neg -BrdU pos cells detected in the developing lungs ( Figure 7A ) could represent the former type whereas the eGFP pos epithelial cells could represent the latter type of progenitors. Once lung development is completed, the homeostatic, low turnover, maintenance of the epithelial population can be supported by the distributed Clara cells [38, 56] and thus active BMP signaling may not be required any longer. The decline in eGFP expression in the lungs of the adult BRE-eGFP transgenics may reflect just that. Reactivation of the BRE-eGFP reporter in adult lung after tissue injury suggests an active role of BMP-signaling in adult lung repair after injury