In situ deletion of SHIP does not compromise homing and secondary repopulating capacity of HSCs. (A) Flow cytometric quantitation of the relative contribution to KLSCD48 HSC by MxCreSHIP^flox/flox (CD45.2) or WT-Ly5.1 (CD45.1) cells in the BM of MxCreSHIP^flox/flox (CD45.2):WT-Ly5.1 (CD45.1) chimeras 5 months after poly I:C treatment (n ≥ 3). BM cells were stained with markers for the Lineage^−/lowc-Kit⁺Sca1⁺CD48⁻ (KLSCD48) phenotype.⁴  (B) Flow cytometric quantitation of the relative contribution to KLSCD48 HSCs by MxCreSHIP^flox/flox (CD45.2) cells in the BM of MxCreSHIP^flox/flox (CD45.2):WT-Ly5.1 (CD45.1) chimeras versus SHIP^flox/flox (CD45.2) cells in SHIP^flox/flox (CD45.2):WT-Ly5.1 (CD45.1) control chimeras. Both sets of chimeras were analyzed 5 months after poly I:C treatment (n ≥ 3). (C) Percentage global repopulation of PB at the indicated times by MxCreSHIP^flox/flox (CD45.2) and WT-Ly5.1 (CD45.1) HSCs after serial transplantation of 10⁶ WBM cells from MxCreSHIP^flox/flox (CD45.2):WT-Ly5.1 (CD45.1) chimeras 5 months after poly I:C treatment (n ≥ 3). Significance was established using the unpaired Student t test. Errors shown represent the SEM; ■, cells derived from MxCreSHIP^flox/flox BM (Cre⁺); , cells derived from WT-Ly5.1 BM (WT) or SHIP^flox/flox (Cre⁻).