Fig. 7

Loss of SMN in chondrocytes caused retardation of bone development. a Experimental design involves the retro-orbital injection of AAV9-Vector/AAV9-Col2a1p-shSmn1 (2 ×10¹¹ vg/g) into WT mice at P3, with daily weight monitoring until P12. b Weight measurements of control and Smn1-cKD mice from P3 to P12 (n = 6 per group). P-value was derived from two-tailed unpaired Student’s t test. Representative micro-CT images of L2 vertebra (c) and femur (d) from control and Smn- cKD mice at P12. The pseudocolor represents the thickness of bone trabecula. Quantitative analysis of trabecular bone microarchitecture (BV/TV, Tb.Th, and Tb.Pf) in vertebra (e–g) and femur (h–j) from control and Smn1-cKD mice at P12 (n = 3 per group). P-value was derived from Wilcoxon rank-sum test. k HE staining of growth plates from control and Smn1-cKD mice at P12. Histograms show ratio of HZ area and HZ height in growth plates (n = 6 per group). P-value was derived from two-tailed unpaired Student’s t test. l SF staining of hypertrophic chondrocytes from control and Smn1-cKD mice at P12. Histograms show cell size and cell density of hypertrophic chondrocytes in HZ (n = 6 per group). P-value was derived from two-tailed unpaired Student’s t test. m VK staining of growth plates and metaphysis from control and Smn1-cKD mice at P12. Histograms show ratio of calcification in HZ and metaphysis (n = 6 per group). P-value was derived from two-tailed unpaired Student’s t test. Immunofluorescence staining of SMN (n), YBX1 (o), SOX9 (p), RUNX2 (q), COL X (r), and SP7 (s) in hypertrophic zone or metaphysis of control and Smn1-cKD mice at P12. The regions outlined with yellow boxes in the upper panels are shown at higher magnification in the corresponding lower panels. Full-length views of the growth plates and their associated MFI data are provided in Fig. S12a–f. Data are presented as the mean ± SD. ^*P < 0.05, ^**P < 0.01, ^***P < 0.001