Figure 2.

Loss of Asxl1 Impairs BMSC Self-Renewal and Differentiation in Mice

(A) Quantitation of percentage of CD45⁻CD105⁺CD44⁺CD73⁺CD146⁺CD90⁺ cell populations (BMSCs) in the bone marrow of WT (n = 9 mice) and Asxl1^−/− (n = 10 mice, 3 weeks old) by flow cytometry.

(B and C) The frequencies of CFU-F per femur (B) and per 1 × 10⁶ BMMNCs (C) from WT and Asxl1^−/− mice are shown (n = 6 mice per genotype).

(D) The frequencies of CFU-osteoblast (ALP⁺) per femur are shown (top panel). Representative ALP staining of WT and Asxl1^−/− osteoblastic colonies cultured in osteogenic culture medium from BMMNCs. WT (n = 8 mice) and Asxl1^−/− (n = 7 mice).

(E) The ratio of oil red O⁺ adipocytes to total colonies demonstrates enhanced adipocyte differentiation in Asxl1^−/− BMSCs compared with WT BMSCs (n = 3 mice per genotype). Scale bar represents 200 μm.

(F) Pie chart illustrates that loss of Asxl1 impairs BMSC self-renewal and skews BMSC lineage commitment away from osteoblasts, favoring adipocytes. Data represent the means of four independent experiments.

Data are presented as mean ± SEM. ^∗∗∗p < 0.001. See also Figure S1.