Skip to main content
. 2024 May 1;12:RP91883. doi: 10.7554/eLife.91883

Figure 7. Inhibition of PKA signaling blocks microtia development in Bmpr1a-deficient mice.

(A) Diagram showing the schedule of Tamoxifen (TAM) and H89 administration. (B) Immunostaining results of p-Creb in ear sections of the H89-treated mutant and control mice. Scale bars=50 μm. (C) The rescue of the microtia phenotype in the mutant mice by H89. Right panels: Quantitation data. n=3. (D) H/E staining results. Right panels: the thickness of the cartilage and the size of the chondrocytes in the ear of the mutant and control mice. n=3. Right panels: Quantitation data. Scale bars=50 μm. n=3. (E) Immunostaining results for Col1α1 in the ear sections of the H89-treated mutant and control mice. Scale bars=20 μm. Arrows: positive signals. (F) Alkaline phosphatase (ALP) activity was greatly suppressed by H89 in the auricle of the Prrx1CreERT; Bmpr1af/f mice compared to the control mice. Scale bars=50 μm. Arrows: positive signals. G. WB blot also showed that H89 rescued the expression of the osteoblast marker genes Runx2 and osteocalcin in the mutant mice. Right panel: quantitation data. n=3. One-way ANOVA (and nonparametric or mixed) multiple comparisons were applied to evaluate the correlation data in (C, D, and G). p<0.05 was considered as statistically significant.

Figure 7—source data 1. Original file for the western blot in Figure 7G.

Figure 7.

Figure 7—figure supplement 1. Analysis of scRNA-seq data of human microtia pinna samples.

Figure 7—figure supplement 1.

(A) tSNE results of the cell populations in the pinna samples of microtia patients. (B) The expression of marker genes in various cell populations. (C) Analysis of osteoblast and chondrocyte signature genes. (D) KEGG and Gene Ontology (GO) analysis of the osteoblast (Chon_Ost) population. (E) KEGG and GO analysis of the chondrocyte population.