The methylation of non-histone proteins in bone diseases

我们建立并分析了PRMT5常规基因敲除(KO)小鼠和破骨细胞特异性条件性KO(CKO)小鼠。PRMT5 Homo KO小鼠在胚胎发育的非常早期就死于子宫。PRMT5异种KO小鼠自发形成多器官肿瘤。这些表明PRMT5在发育和肿瘤发生中具有非多余的作用。另一方面，破骨细胞特异性的PRMT5 CKO小鼠表现出正常的骨骼发育和骨量，提示PRMT7可能弥补了PRMT5在破骨细胞形成中的缺失。

We generated and analyzed PRMT5 conventional knockout (KO) mice and osteoclast-specific conditional KO (cKO) mice. PRMT5 homo KO mice died in uterus at the very early stage of embryo development. PRMT5 hetero KO mice spontaneously developed tumor in various organs. These suggested that PRMT5 had role a non-redundant role in development and tumorigenesis. On the other hand, osteoclast-specific PRMT5 cKO mice exhibited normal skeletal development and bone volume, suggesting that other member of Type II PRMT family, PRMT7 may compensated the lack of PRMT5 in osteoclastogenesis.