We have found that in mutant mice in which a Notch ligand Dlk1 was deleted in alveolar type II cells, the type II cells had a dis-regulated Notch signaling and were unable to function as stem cells in the lung. Instead, the mutant cells were trapped at an intermediate stage in between type II to type I cell transition. We will continue to study the intermediate cells and determine if these cells will cause chronic lung disease in the mutant mice. In addition, we will identify novel signaling mechanism that cross-talk with the Notch signals in type II cells during lung repair.
– Dlk1-Mediated Temporal Regulation of Notch Signaling Is Required for Differentiation of Alveolar Type II to Type I Cells during Repair.