Figure 3. YAP/TAZ deletion prior to bleomycin injury leads to altered epithelial cell populations, activated fibroblast, and disrupted immune response.

(A) Schematic of experimental strategy to generate single-cell RNA-Seq analysis from mouse lungs. (B and C) UMAP embedding demonstrating clustering of the 29 cell types identified in the mouse lungs (B) and depicting cells recovered from respective genotype and treatment groups (C). (D–F) Relative proportions of each cell types/states within total cell populations (D), epithelial cell populations (E), and fibroblast cell populations between each treatment group (F). (G and H) Dot plot showing expression levels of AT2 cell lineage markers (G) and intermediate epithelial cell marker expression (H) in each treatment group. (I) Violin plot showing relative expression of activated fibroblast markers in WT or YT^del bleomycin-treated mice. (J) Output from LIANA demonstrating loss of Factor 4 ligand-receptor signaling in YT^del mice. (K) Gene ontology–associated programs identified as misregulated by LIANA. (L) Relative proportions of immune cell populations from each treatment group. (M) Flow cytometry analysis of immune cell subpopulations present in mice 7 days after bleomycin injury. n = 3 WT saline- and YT^del saline-, n = 5 WT bleomycin- and YT^del bleomycin-treated mice. (N) Dot plot showing expression of Ccl2 in intermediate alveolar epithelial cells and activated (including both intermediate and activated from F) fibroblast population.