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. Author manuscript; available in PMC: 2017 Jan 5.
Published in final edited form as: Cell Rep. 2016 Nov 22;17(9):2312–2325. doi: 10.1016/j.celrep.2016.11.001

Figure 7. Loss of Wnt signaling in AT2s inhibits proliferation and promotes differentiation into AT1s.

Figure 7

(A-C) Proliferation is reduced in SftpcCreERT2:Ctnnb1fl/fl mutant AT2s compared to controls following deletion of β-catenin from P4 to P30. (D-F) Loss of Wnt signaling in SftpcCreERT2:Ctnnb1fl/fl:R26RBr2.1 mutants from P4 to P30 leads to increased differentiation into AT1s during alveologenesis as noted by the increase in clones exhibiting the spread and flattened morphology of AT1 cells. (G-I) These data were confirmed using the R26RmTmG reporter to outline the cell surface of the AT1 cells along with Aqp5 co-immunostaining. (J) Illustration depicting the role of re-emergent Wnt signaling in balancing epithelial growth and differentiation during lung alveologenesis. Quantification of % Ki67+, average % of clone, and % of YFP+ cells is represented by mean ± SEM. Two-tailed student's t-test: *P < 0.05, n > 4 for each group; Two-tailed student's t-test: **P < 0.05, n=133 clones for controls and n=203 clones for SftpcCreERT2:Ctnnb1fl/fl mutants.