Pip5k1c loss impairs osteoblast, but promotes adipogenic, formation and differentiation.A, colony forming unit-fibroblast (CFU-F) assays. B, the number of CFU-F was counted under a microscope. Results were expressed as mean ± SD; N = 11 mice for control, N = 10 mice for cKO. ∗∗p < 0.01 versus control; Unpaired two-tailed t test. C, colony forming unit-osteoblast (CFU-OB) assays. D, the number of CFU-OB was counted under a microscope. Results were expressed as mean ± SD; N = 10 mice for control, N = 11 mice for cKO. ∗∗p < 0.01 versus control; unpaired two-tailed t test. E and F, primary BMSC isolated from 4-month-old control and cKO male mice and cultured with osteoblast differentiation medium for 14 days, followed by alizarin red staining (E) and RT-qPCR analyses (F). Results were expressed as mean ± SD; N = 3 biologically independent experiments. ∗p < 0.05, ∗∗p < 0.01 versus control; unpaired two-tailed t test. G and H, primary BMSCs isolated from 4-month-old control, and cKO male mice were cultured with adipogenic medium for 14 days, followed by Oil Red O staining (G) and RT-qPCR analyses (H). Results were expressed as mean ± SD; N = 3 biologically independent experiments. ∗p < 0.05, versus control; unpaired two-tailed t test. I, bone marrow adiposity. Tibial sections of 4-month-old control, and cKO male mice were subjected to H/E staining. BMSCs, bone marrow stromal cells. Runx2, Runt-related transcription factor 2; Osx, Osterix; Col1a1, type 1 collagen a1; Alp, alkaline phosphatase; Ocn, Osteocalcin; Pref-1, preadipocyte factor 1; Pparg2, peroxisome proliferator-activated receptor gamma 2; Cebp/α, CCAAT/enhancer-binding protein (C/EBP), alpha; Cebp/β, CCAAT/enhancer-binding protein (C/EBP), beta; Ap2, adipocyte protein 2.