Figure 1.
PU.1 knock-out fetal liver HSCs are arrested at the transition to the common myeloid and lymphoid progenitor stages. Multicolor FACS analysis was performed in E14.5 fetal livers from PU.1+/+, PU.1–/+, and PU.1–/– embryos. (A) The top panels demonstrate the Sca-1/c-Kit profile of Lin– cells. PU.1–/– fetal liver has a decreased number of Lin–Sca-1+c-Kit+CD34+ HSCs. PU.1–/– fetal liver lacks CMPs and GMPs as well as their progeny, mature monocytic (CD11b+/Gr-1lo) and granulocytic (CD11b+/Gr-1hi) populations. (B) PU.1+/+, PU.1–/+, and PU.1–/– fetal livers have almost equal numbers of Lin–IL-7Rα+ cells. PU.1–/– fetal liver lacks Lin–IL-7Rα+Sca-1loc-Kitlo CLPs and CD19+ early B cells. In both analyses, PU.1–/+ fetal liver has intermediate numbers of myeloid and lymphoid progenitors. Numbers in each panel represent percentages of the gated population in whole fetal liver cells. FSC indicates forward scatter; Gra, granulocytes; Mo, monocytes; and Lin, lineage.