Defective CFU-C activity in the absence of Gab2 is correctable by retroviral complementation. (A) Gab2^−/− and littermate wild-type mice (6 to 8 weeks of age) were humanely killed, and the BM cells were harvested and plated in methylcellulose medium to assay for the CFU-C frequency in response to a cytokine cocktail of SCF, IL-3, and IL-6 in either high-dose (1:01) or 1:10 and 1:50 dilutions. Day-7 BM CFUs-C were assayed in methylcellulose medium after culture with limiting cytokine concentrations. *P > .05 relative to wild-type BM. (B) MSCV-based retroviral vectors expressing Gab2-IRES-GFP or IRES-GFP empty vector were used to test whether CFU-C activity could be restored by retroviral-mediated gene transfer. A total of 3 separate retroviral Gab2 complementation assays were done. In each experiment, 3 Gab2^−/− mice and 3 littermate wild-type mice were used. BM cells were collected and transduced by coculture followed by flow cytometry sorting for GFP⁺ cells. Sorted GFP⁺ cells were plated in methylcellulose medium and then assayed for CFU-C number after 7 days. As a control, BM cells transduced with the empty vector (IRES-GFP) were included. *P = .001 relative to MSCV-Gab2-IRGFP-transduced Gab2^−/− BM, indicating significant correction of the defect. Error bars represent the mean plus or minus a standard deviation.