Fig. 2.

Tsc1 deficiency and premature aging of HSC from young mice. A. six week old Tsc1^flox/flox (WT) and Tsc1^flox/flox; Mx1-cre⁺ (KO) mice were treated 7 times with pIpC every other day for 14 days and sacrificed 10 days after the last treatment. The abundance of p16Ink4a, p19Arf, and p21Cip1 mRNAs in FACS-sorted HSCs was measured by real-time PCR and normalized to hypoxanthine-guanine phosphoribosyltransferase (Hprt). n=5. B–E. 50 HSCs were mixed with 2×10⁵ recipient-type total BM cells (WBM) and transplanted into lethally irradiated B6Ly5.2 recipients. The donor and recipient-type cells were identified by congenic CD45 markers. B. Diagram of the experimental design for C–D. C. Hematopoiesis by WT and Tsc1^−/− HSCs. Left shown the representative dot plots of the recipient peripheral blood at 16-weeks after transplantation with WT (top) or Tsc1^−/− cells (bottom). Data on the right summarize two independent experiments with a total of 10 recipients for each group. D. The percent of the donor HSC-derived and B220⁺ (B) and Mac-1⁺ (M) cells in the recipient peripheral blood at 4 weeks after transplantation. E. The percentage of B and M cells in total white blood cells.