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. 2015 Apr 1;142(7):1357–1367. doi: 10.1242/dev.118802

Fig. 5.

Fig. 5.

Augmentation of BMP signaling leads to increased levels of cell death and p53 protein in developing nasal cartilage of E12.5 mice and newborns. (A) tdTomato distribution in E12.5 P0-Cre transgenic mice crossed with ROSA-tdTomato Cre reporter mice. The right panel is the tdTomato image merged with DAPI staining, which is shown in blue. (B-D) Frontal sections of E12.5 control, mutant and ca-Bmpr1a:P0-Cre:Bmpr1a+/− (rescue) mice were stained using H&E. Control and rescue mice had comparable nasal septum morphology; however, mutants had shorter nasal septa. lv, lateral ventricle; ns, nasal septum. (E-G) TUNEL assay was performed to detect apoptosis. E12.5 mutants exhibited increased numbers of apoptotic cells shown in green (F). Blue indicates DAPI staining. (H-J) Immunohistochemistry using p53 antibody revealed increased p53 levels in mutant nasal septa (I). (K-P) Frontal sections of newborn controls, type 1 and type 2 mutants were stained using H&E. Boxed areas in K-P are shown at high magnification in Q-V, respectively. (Q-S) TUNEL assay was performed to detect apoptosis. Both type 1 and type 2 newborn mutants exhibited more apoptotic cells, which are shown in green (R,S). (T-V) Immunohistochemistry using p53 antibody revealed increased p53 levels in both mutant nasal septa (U,V). (W) Quantification of TUNEL assay results in newborns. All data are represented as mean±s.d. (n=3); *P<0.01 (Student's t-test). Scale bars: 500 µm in A,B,K,N; 100 µm in E,H,Q,T.