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. Author manuscript; available in PMC: 2021 Apr 6.
Published in final edited form as: Dev Cell. 2020 Mar 5;53(1):73–85.e5. doi: 10.1016/j.devcel.2020.02.001

Figure 4.

Figure 4.

Loss of airway smooth muscle differentiation led to disrupted cartilage segmentation. (A,B) Whole mount alcian blue staining showed cartilage segmentation defects in MyocdCKO E18.5 tracheas. Scalebar: 50 μm. (C,D) Col2a1 wholemount RNA in situ hybridization revealed reduced chondrocytes in MyocdCKO E14.5 tracheas. Scalebar: 100 μm. (E-J) Immunofluorescent detection of ACTA2 (magenta) and cartilage marker SOX9 (green) expression in transverse sections of tracheas of control and MyocdCKO at E13.5 (E,F), E14.5 (G,H), and E17.5 (I,J). Scalebar: 50 μm for E-H and 100 μm for I,J. “t” indicates trachea and “e” indicates esophagus. (K) Heatmap of RNA-seq data showing groups of significantly downregulated genes, by an adjusted p-value less than 0.05, in the MyocdCKO E18.5 tracheas. (L) qRT-PCR quantification of relative mRNA levels of mechanosensitive genes Runx2, Spp1, Hapln1, and Itgbl1 in control and MyocdCKO tracheas at E18.5. *: p<0.05, **: p<0.005. (M) qRT-PCR quantification of relative mRNA levels of Sox9 and mechanosensitive genes Runx2, Spp1, and Hapln1 in control and MyocdCKO tracheas at E13.5. *: p<0.05. Data are represented as individual points for each biological sample ± SD.