Figure 6. Lung mesenchymal knockout of Myocd did not cause any branching abnormalities or lung cysts.

(A) The expression of Myocd in Bmpr1a conditional knockout (CKO) lungs was substantially decreased, as measured by real-time PCR, **p<0.01. (B) Deficiency in airway smooth muscle cells (SMCs) was observed in embryonic day (E)15.5 mesenchyme-specific Myocd CKO lungs, as shown by co-immunofluorescence staining of Cdh1, Acta2, and elastin. (C) Comparison of Bmpr1a expression between E15.5 Myocd CKO and wildtype (WT) control lungs by immunofluorescence staining. (D) Comparison of the lungs between WT and Myocd CKO mice at the end of gestation (E18.5) did not reveal any significant morphological changes by gross view. No histological difference was found between the WT and the Myocd CKO lungs by examining their hematoxylin and eosin (H&E)-stained lung tissue sections.

Figure 6—figure supplement 1. Schematic representation of the lung mesenchyme-specific knockout of Myocd by Tbx4-rtTA/Teto-Cre driver line.