Figure 4.
Arhgef2−/− fetal liver and bone marrow insufficiently reconstitute the blood system and show productive deficits at the HSC level. (A) Experimental schematic of non-competitive and competitive transplantations. (B) Kaplan-Meier survival curves demonstrating higher mortality among recipients of Arhgef2−/− E14.5 fetal liver cells (n = 6 recipients with n = 2 biological Arhgef2fl/fl and n = 3 Arhgef2−/− fetal liver donors). (C) Decreased levels of peripheral blood engraftment and granulocytic populations as measured in the 2 remaining mice that received Arhgef2−/− E14.5 fetal liver cells at day 10 posttransplantation. (D) Insufficient and/or delayed hematopoietic recovery in the peripheral blood of primary transplanted mouse recipients of Arhgef2−/− bone marrow. (E) Kaplan-Meier survival curves demonstrating higher mortality among recipients of non-competitively transplanted Arhgef2−/− bone marrow. (F) Comparable homing efficiencies from 5 × 104 Lin–Arhgef2−/− bone marrow cells. (G) Lower levels of Arhgef2−/− Lin–CD150+CD48– HSCs in secondary non-competitively transplanted bone marrow grafts. (H) Poorer engraftment levels from competing 1:1 and 2:1 Arhgef2−/−:wild-type doses of bone marrow among primary recipients. (I) Increased percentage of HSCs in the primary grafts of competitively transplanted Arhgef2−/− bone marrow. (J) Increased proportion of LSK CD150+CD48– LT-HSCs within secondary grafts among competitively transplanted recipients. Primary non-competitive transplants and homing experiments initiated with 6 recipients per condition using 3 biological replicates of bone marrow samples. Secondary noncompetitive transplants completed with 7 Arhgef2fl/fl and 4 Arhgef2−/− recipients (data from 2 representative experiments). Primary competitive transplants initiated with 3 recipients per dose and secondary competitive analyses conducted with 3 recipients from 2 primary mice. Error bars represent SEM.*P < .05; **P < .01. PB, peripheral blood; SSC, side scatter.

Arhgef2−/− fetal liver and bone marrow insufficiently reconstitute the blood system and show productive deficits at the HSC level. (A) Experimental schematic of non-competitive and competitive transplantations. (B) Kaplan-Meier survival curves demonstrating higher mortality among recipients of Arhgef2−/− E14.5 fetal liver cells (n = 6 recipients with n = 2 biological Arhgef2fl/fl and n = 3 Arhgef2−/− fetal liver donors). (C) Decreased levels of peripheral blood engraftment and granulocytic populations as measured in the 2 remaining mice that received Arhgef2−/− E14.5 fetal liver cells at day 10 posttransplantation. (D) Insufficient and/or delayed hematopoietic recovery in the peripheral blood of primary transplanted mouse recipients of Arhgef2−/− bone marrow. (E) Kaplan-Meier survival curves demonstrating higher mortality among recipients of non-competitively transplanted Arhgef2−/− bone marrow. (F) Comparable homing efficiencies from 5 × 104 LinArhgef2−/− bone marrow cells. (G) Lower levels of Arhgef2−/− LinCD150+CD48 HSCs in secondary non-competitively transplanted bone marrow grafts. (H) Poorer engraftment levels from competing 1:1 and 2:1 Arhgef2−/−:wild-type doses of bone marrow among primary recipients. (I) Increased percentage of HSCs in the primary grafts of competitively transplanted Arhgef2−/− bone marrow. (J) Increased proportion of LSK CD150+CD48 LT-HSCs within secondary grafts among competitively transplanted recipients. Primary non-competitive transplants and homing experiments initiated with 6 recipients per condition using 3 biological replicates of bone marrow samples. Secondary noncompetitive transplants completed with 7 Arhgef2fl/fl and 4 Arhgef2−/− recipients (data from 2 representative experiments). Primary competitive transplants initiated with 3 recipients per dose and secondary competitive analyses conducted with 3 recipients from 2 primary mice. Error bars represent SEM.*P < .05; **P < .01. PB, peripheral blood; SSC, side scatter.

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