Embigin deficiency leads to delayed embryonic lung development and high neonatal mortality in mice

Embigin (Gp70), a receptor for fibronectin and an ancillary protein for monocarboxylate transporters, is known to regulate stem cell niches in sebaceous gland and bone marrow. Here, we show that embigin expression is at high level during early mouse embryogenesis and that embigin is essential for lung development. Markedly increased neonatal mortality of Emb−/− mice can be explained by the compromised lung maturation: in Emb−/− mice (E17.5) the number and the size of the small airways and distal airspace are significantly smaller, there are fewer ATI and ATII cells, and the alkaline phosphatase activity in amniotic fluid is lower. Emb−/− lungs show less peripheral branching already at E12.5, and embigin is highly expressed in lung primordium. Thus, embigin function is essential at early pseudoglandular stage or even earlier. Furthermore, our RNA-seq analysis and Ki67 staining results support the idea that the development of Emb−/− lungs is rather delayed than defected. [Display omitted] •Embigin expression is high at early embryogenesis including the lung primordium•Maturation of the Emb−/− mice lung is delayed explaining high neonatal mortality•Embigin may execute its biological function in primordial lung cells•Embigin is detected in stem-like club cells lining bronchioles in adult mouse lungs Developmental genetics; Developmental biology; Transcriptomics