Fig 1: BC-2 and BC-1 have distinct behaviors during initiation of repair of the damaged epithelium in mouse models of injury.(A) Diagram: strategy for induction of airway injury by Naphthalene (Nap, intraperitoneal) or Polidocanol (Poli, intratracheal) and analysis at 5dpi post-Nap or 7dpi post-Poli. (B–C) IF of tracheal sections from adult uninjured animals (0dpi, uninjured control, n=4 mice per group) showing typical dorsal-ventral distribution of KRT5 and CC10 (no KRT13 signals) in the basal and luminal layers, respectively. (D–G) Markedly distinct kinetics of repopulation of the airway epithelium by BCs from the ventral (BC-1) compared to dorsal (BC-2) regions at 5dpi (Naphthalene) or 7dpi (Polidocanol) (n=3 mice per group): extensive KRT13 expression in KRT5 + and luminal cells of the dorsal epithelium and low CC10 expression. (H) Morphometric analysis: percentage of proliferating (KI67+) BCs, and luminal (CC10+, SCGB3A2+, FOXJ1+) cells in ventral or dorsal epithelium of 5dpi or 7dpi (see also Figure S10, S11). For KI67 +TRP63+/TRP63+% (far left panel), each dot represents the percentage of proliferating BCs (KI67 +TRP63+) in total BC population (TRP63+) from each view. Graphs: mean ± SEM of 2–20 views per animal; 0dpi-control: n=4 animals; 5dpi-Nap: n=3 animals; 7dpi-Poli: n=3 animals. For CC10+/DAPI%, SCGB3A2+/DAPI%, FOXJ1+/DAPI% (right three panels), each dot represents the percentage of each lineage-committed cells in total epithelial population from each view. Graphs: mean ± SEM of 1–5 views per animal; 0dpi-control: n=4 animals; 5dpi-Nap: n=2–3 animals; 7dpi-Poli: n=3–4 animals. Student’s t-test, **p<0.01, ***p<0.001, ****p<0.0001, n.s., not significant. Scale bars:10µm.