Skip to main content
. 2024 Jun 10;12:RP91876. doi: 10.7554/eLife.91876

Figure 1. Lung mesenchyme-specific deletion of Bmpr1a caused abnormal lung morphogenesis and prenatal airway cystic lesions beginning in mid-gestation.

(A) Brightfield images of whole wildtype (WT) and Bmpr1a conditional knockout (CKO) mouse lungs at different embryonic stages. (B and C) Quantitative measurement and comparison of terminal airway branching numbers and sizes. (D) Hematoxylin and eosin (H&E)-stained Bmpr1a CKO lungs at different embryonic stages. (E and F) EdU incorporation study for cell proliferation analysis in lung mesenchymal and cytokeratin-positive epithelial cells (n=6). (G) Apoptosis analysis by TUNEL assay. The positive control slides for apoptosis were generated by treating the tissue sections with DNase I. Pictures are representative of at least five samples in each condition.

Figure 1.

Figure 1—figure supplement 1. Bmpr1a was specifically deleted in lung mesenchymal cells.

Figure 1—figure supplement 1.

(A) Schematic representation of the lung mesenchyme-specific knockout of Bmpr1a by Tbx4-rtTA/Teto-Cre driver line. (B) Verification of Bmpr1a genetic deletion at the mRNA level. △E2: exon 2 deletion. (C) Immunostaining of Bmpr1a (green) and Cdh1 (red). The airways are highlighted with dot lines.
Figure 1—figure supplement 1—source data 1. Original file for the mRNA analysis in Figure 1—figure supplement 1B (exon 2 deletion of Bmpr1a).
Figure 1—figure supplement 1—source data 2. PDF containing Figure 1—figure supplement 1B and original image of the relevant mRNA analysis (exon 2 deletion of Bmpr1a).