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FAM20C  mutations in humans cause Raine syndrome and our previous studies showed that global inactivation of mouse  Fam20C  led to bone and dental defects. By crossbreeding  2.3    kb Col 1a1-Cre  mice with  Fam20C    flox/flox   mice, we created  2.3    kb Col 1a1-Cre;Fam20C    foxl/flox   (cKO) mice, in which  Fam20C  was inactivated in cells expressing Type I collagen. This study showed that the long bones of cKO mice were shorter and had a lower level of mineralization compared to the normal mice. The collagen fibrils in  Fam20C -deficient bone were disorganized and thicker while the growth plate cartilage in cKO mice was disorganized and wider compared to the normal mice. The  Fam20C -deficient bone had a lower level of dentin matrix protein 1, and higher levels of osteopontin and bone sialoprotein than the normal. The blood of cKO mice had an elevated level of fibroblast growth factor 23 and reduced level of phosphorus. These findings indicate that inactivation of  Fam20C  in cells expressing type I collagen led to skeletal defects and hypophosphatemia. The altered levels of dentin matrix protein 1 and osteopontin in  Fam20C -deficient bone may be significant contributors to the mineralized tissue defects in human patients and animals suffering from the functional loss of FAM20C.

Specific ablation of mouse Fam20C in cells expressing type I collagen leads to skeletal defects and hypophosphatemia