Fig. 1: ASXL1-MT causes dysfunction of HSPCs associated with increased apoptosis and altered cell cycle status. | Nature Communications

Fig. 1: ASXL1-MT causes dysfunction of HSPCs associated with increased apoptosis and altered cell cycle status.

From: Mutant ASXL1 induces age-related expansion of phenotypic hematopoietic stem cells through activation of Akt/mTOR pathway

Fig. 1

a Enumeration of white blood cells (WBC), hemoglobin (Hb), and platelets (Plt) in peripheral blood of young Vav-Cre ASXL1-MT KI mice (n = 13 (Control), 11 (ASXL1-MT)). b Frequency of myeloid cells (CD11b+), B cells (B220+), and T cells (CD3+) in peripheral white blood cells of young Vav-Cre ASXL1-MT KI mice (n = 13 (Control), 11 (ASXL1-MT)). c Absolute numbers of bone marrow cells per leg in young Vav-Cre ASXL1-MT KI mice (n = 5). d Frequency of LSK cells, multipotent progenitors (MPPs), short-term HSCs (ST-HSCs) and long-term HSCs (LT-HSCs) in bone marrow cells of young Vav-Cre ASXL1-MT KI mice (n = 5). e The experimental design for competitive transplantation assays. 3000 MPPs or 200 LT-HSCs isolated from young control or young Vav-Cre ASXL1-MT KI mice were transplanted into lethally irradiated recipient mice with 4 × 105 whole bone marrow cells. f Levels of donor chimerism in peripheral blood were analyzed at the indicated weeks after transplantation (n = 3 (Control), 4 (ASXL1-MT)). Data are mean ± s.e.m. g Apoptosis analysis of HSPCs of young Vav-Cre ASXL1-MT KI mice (n = 7). h Cell cycle analysis with Ki-67/DAPI staining of MPPs (left panel) and LT-HSCs (right panel) of young Vav-Cre ASXL1-MT KI mice (n = 5). Data are mean ± s.d. unless otherwise noted. *P ≤ 0.05, **P ≤ 0.01, ***P ≤ 0.001; two-tailed Student’s t-test.

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