Figure 6.
Smc3 haploinsufficiency partially restores HSC quiescence in Yy1−/−mice. (A) Representative gating strategy for Ki67/DAPI cell proliferation assay of LT-HSCs (Lin−Sca1+c-Kit+CD48−CD150+). Cells in the G0 phase were defined as Ki67−DAPI−. Cells in the G1 phase were defined as Ki67+DAPI−. Cells in S/G2/M phase were defined as Ki67+DAPI+. (B-D) Quantification of percentages of LT-HSC, ST-HSC, and MPP cells in G0, G1, and S/G2/M phase. (E) Experimental strategy of BM transplantation (BMT). (F) Quantification of donor-derived contribution in B-cell (Thy1.2−CD19+), T-cell (Thy1.2+CD19−), monocyte (Mac1+Gr1−), and neutrophil (Mac1+Gr1+) populations at 4, 8, 12, 16, and 20 weeks after BMT. N represents the number of mice; data are presented as means ± SD; ∗P < .05, ∗∗P < .01, and ∗∗∗P < .001.

Smc3 haploinsufficiency partially restores HSC quiescence in Yy1−/−mice. (A) Representative gating strategy for Ki67/DAPI cell proliferation assay of LT-HSCs (LinSca1+c-Kit+CD48CD150+). Cells in the G0 phase were defined as Ki67DAPI. Cells in the G1 phase were defined as Ki67+DAPI. Cells in S/G2/M phase were defined as Ki67+DAPI+. (B-D) Quantification of percentages of LT-HSC, ST-HSC, and MPP cells in G0, G1, and S/G2/M phase. (E) Experimental strategy of BM transplantation (BMT). (F) Quantification of donor-derived contribution in B-cell (Thy1.2CD19+), T-cell (Thy1.2+CD19), monocyte (Mac1+Gr1), and neutrophil (Mac1+Gr1+) populations at 4, 8, 12, 16, and 20 weeks after BMT. N represents the number of mice; data are presented as means ± SD; ∗P < .05, ∗∗P < .01, and ∗∗∗P < .001.

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