Osteopetrosis and thalamic hypomyelinosis with synaptic degeneration in DAP12-deficient mice
J. Clin. Invest. Tomonori Kaifu, et al. 111:323 doi:10.1172/JCI16923 [Go to this article.]

Figure 3
In vitro development of osteoclasts from DAP12^–/– mice is impaired. (a) TRAP staining of cultured osteoclasts induced in vitro in the presence of M-CSF and RANKL. Reduction of multinucleated TRAP⁺ osteoclasts is evident in cells from DAP12^–/– mice. Original magnification: ×100. Multinucleated osteoclasts are developed from DAP12^–/– bone marrow cells as seen at higher magnification (original magnification: ×400). (b) Comparison of the number of multinucleated (having more than two nuclei) TRAP⁺ osteoclasts induced by RANKL (left) or TNF-α (right). *P < 0.05, **P < 0.01. n = 3. (c) Actin ring formation by osteoclasts. DAP12^–/– osteoclasts did not form actin rings. (d) Formation of resorption pits by osteoclasts induced in wild-type or DAP12^–/– mice. DAP12^–/– osteoclasts did not form significant pits. *P < 0.05. n = 3. (e) Immunoblot analysis of DAP12 expression in osteoclasts induced from bone marrow cells. Osteoclasts (10 μg protein per lane) from wild-type mice showed DAP12 expression, although at lower levels than were measured in bone marrow–derived cultured mast cells (BMMCs) (10 μg protein per lane) from wild-type mice.