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. 2013 Nov 18;210(12):2641–2659. doi: 10.1084/jem.20131141

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© 2013 Abdel-Wahab et al.

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Figure 6. — Combined loss of Asxl1 and Tet2 rescues the impaired self-renewal of Asxl1-deficient HSCs. (A) Enumeration of colonies and serial replating capacity of 20,000 whole BM cells from 6-wk-old littermate mice with hematopoietic-specific deletion of Asxl1 (Vav-cre Asxl1^fl/fl), Tet2 (Vav-cre Tet2^fl/fl), or both (Vav-cre Asxl1^fl/fl Tet2^fl/fl). (B) Schematic depiction of the competitive transplantation experiment. Control, Vav-cre Asxl1^fl/fl, Vav-cre Tet2^fl/fl, and Vav-cre Asxl1^fl/flTet2^fl/fl cells are positive for CD45.2, whereas WT competitor cells are positive for CD45.1. On the right, monthly assessment of donor chimerism in the peripheral blood of recipient animals is shown up to 16 wk after transplant (n = 5 recipient mice were used for each genotype and experiment was performed in biological duplicate). 16-wk chimerism was significantly higher in Tet2^−/− transplanted mice compared with all other genotypes. (C) Representative FACS analysis of peripheral blood of mice transplanted with each genotype at 16 wk. Staining schemes are as indicated and parental gate was live cells. (D) Proportion of CD45.2⁺ peripheral blood cells of each lineage at 16 wk in mice transplanted with each genotype (n = 5 mice analyzed for each genotype) as determined by FACS analysis. Each competitive transplantation experiment was performed in biological duplicate with five recipient mice per genotype in each experiment. Error bars represent ±SD; *, P < 0.05 (Mann–Whitney U test).