Rescue of the skeletal phenotype in CasR-deficient mice by transfer onto the Gcm2 null background
J. Clin. Invest. Qisheng Tu, et al. 111:1029 doi:10.1172/JCI17054 [Go to this article.]

Figure 3
Alizarin red S/Alcian blue–stained skeletal regions of CasR- and Gcm2-deficient mice. (a–c) Heterozygous Gcm2^+/– and wild-type mice. (d–f) Homozygous CasR-deficient mice. (g–i) Homozygous Gcm2-deficient mice. (j–l) Double homozygous CasR- and Gcm2-deficient mice. (m–o) Heterozygous CasR^+/– and double heterozygous Gcm2^+/–/CasR^+/– mice. (p–r) Heterozygous CasR^+/– and homozygous Gcm2-deficient mice. Normal appearance of the wrist from a group I control mouse (a) is compared to the widening of the growth plate of the wrist in a 1-week-old group II homozygous CasR-deficient littermate (d). These abnormalities are rescued in group IV double knockout mice (j) and are not present in the other groups (g, m, and p). Mineralization in the epiphysis cartilage of the femur is present in group I control mice (b) but not in the CasR^–/– mice (e). Secondary centers of ossification are restored in group IV homozygous CasR- and Gcm2-deficient mice (k). No abnormalities of ossification centers were observed in the other groups (h, n, and q). Endochondral mineralization, as assessed by the number of alizarin red–positive mineralized caudal vertebrae, is reduced in 1-week-old group II CasR^–/– mice (f) as compared with group I controls (c), whereas group IV homozygous CasR- and Gcm2-deficient mice (l) as well as the other groups (i, o, and r) show the same number of alizarin red–positive mineralized caudal vertebrae, consistent with a normal temporal and spatial pattern of endochondral bone formation.