Number and proliferation of hematopoietic progenitor cells were compromised due to Cited2 deficiency. Fetal liver cells were prepared and 2 × 10⁴ fetal liver cells from each sample were plated in triplicate cultures of methylcellulose-based medium supplemented with 3 units/mL Epo, 10 ng/mL mouse recombinant IL-3, 10 ng/mL human recombinant IL-6, and 50 ng/mL mouse recombinant stem cell factor. The frequency of BFU-Es, CFU-GMs, and CFU-GEMMs was determined after 7 to 12 days of culture. Total number of BFU-Es, CFU-GMs, and CFU-GEMMs per fetal liver was obtained by multiplying the frequency of BFU-Es, CFU-GMs, and CFU-GEMMs per 2 × 10⁴ cells by the total fetal liver cell number. The data were expressed as average (± SD). (A) At 13.5 dpc, the number of BFU-Es, CFU-GMs, and CFU-GEMMs was reduced in Cited2^−/− fetal liver (n = 5) compared with the wild-type littermate control (n = 5). Cited2^+/− fetal liver (n = 4) had fewer numbers of BFU-Es, CFU-GMs, and CFU-GEMMs as well. (B) At 14.5 dpc, decreased number of BFU-Es, CFU-GMs, and CFU-GEMMs was observed in Cited2^−/− fetal liver (n = 4) compared with the wild-type littermate control (n = 3). Cited2^+/− fetal liver (n = 5) showed decreased number of BFU-Es and CFU-GMs. (C) Decreased number of BFU-Es, CFU-GMs, and CFU-GEMMs was observed in Cited2^−/− fetal liver (n = 4) compared with the wild-type littermate control (n = 6) at 15.5 dpc. Cited2^+/− fetal liver (n = 4) showed decreased number of BFU-Es, CFU-GMs, and CFU-GEMMs. All comparisons were relative to wild-type controls (^# indicates P < .05, *P < .01).