Fig. 8.

Inactivation of Trip11 in osteoclasts does not result in swelling of ER cisternae and does not disrupt Golgi stack structure. (A) Alcian Blue-stained sections through the humeri of P0 control (Tg:Vav1-Cre;Trip11^cko/+;ROSA26^mTmG/+) and blood cell and osteoclast knockout (Tg:Vav1-Cre;Trip11^cko/−;ROSA26^mTmG/+) pups. Bottom: higher magnification of the primary spongosia of the proximal growth plates. No differences between mutant and control can be observed. (B) µCT of the tibias of 8-week-old control (Tg:Vav1-Cre;Trip11^cko/+;ROSA26^mTmG/+) and mutant (Tg:Vav1-Cre;Trip11^cko/−;ROSA26^mTmG/+) mice. No differences in the density of trabeculae or in the thickness of the bone collar can be observed between mutant and control mice. (C) Transmission electron microscopy pictures of tibial osteoclasts from 8-week-old control, and blood cell and osteoclast knockout mice. Original magnifications: 2900× (left); 9300× (right) Note the presence of normal ER cisternae (arrowheads, top panels) and normal Golgi (arrowheads, bottom panels) in both mice. (D) Western blot analysis of lysates of isolated bone marrow hematopoietic precursor cells from 8-week-old control (lane 1), and blood cell and osteoclast knockout (lane 2) mice. Note the absence of GMAP-210 protein in the knockout mice. Re-probing of the western blot with an anti-actin antibody serves as a loading control. n=3; one representative result is shown.