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. 2008 Sep 29;205(10):2397–2408. doi: 10.1084/jem.20081297

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© 2008 Chen et al.

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Figure 3. — The Tsc1 deletion causes defective hematopoiesis. (a–d) Serial BMT reveals HSC-intrinsic defects. (a) Diagram of experimental design for data in b–d. (b) Tsc1-deficient BM cells are defective in rescuing lethally irradiated recipients in the second round, which indicate a reduced function of HSCs. 10⁶ WBM cells were used for the first round of BMT, and 3 × 10⁶ WBM cells were used for the second round of BMT. According to Fig. 1 f, 10⁶ WBM cells from Tsc1-deficient mice contain ∼800 HSCs; those from Ctrl mice contain only ∼100 HSCs. For the WBM cells used for the second BMT, the frequency of HSCs was not analyzed. (c) Progressive loss of HSC activity as revealed by reduced replacement of recipient cells. Data shown are means ± SD of the percentage of donor cells in the blood of recipients at 6 wk after BMT (n = 15 for the first BMT, and n = 9 for the second BMT). (d) Reduced reconstitution of multiple lineages of blood cells by Tsc1^fl/flmx-1-cre⁺ BM. Data shown are means ± SD of the relative number of cells in the blood, as measured by CBC. Data are normalized as the percentage of mean counts in mice reconstituted with WT BM. Summary data from two independent experiments involving a total of nine mice per group are presented. LY, lymphocytes; MO, monocytes; NE, neutrophils and eosinophils.