Fig. 2.
Fig. 2. Induction of erythroid burst formation from day-12.5 fetal liver BFU-E progenitors. (A) Fetal liver cells were infected with retroviruses encoding gp55-P, gp55-A, gp55-AAP, or gp55-APA or with virus encoding β-galactosidase (control). Formation of BFU-E colonies was scored 7 to 9 days after infection in complete methylcellulose medium containing plasma-derived serum, SCM, and SF (see the Materials and Methods). Data represent the mean of the indicated number of assays ± 1 standard deviation. Treatment with 3 U/mL Epo resulted in the formation of 230.5 ± 16.1 BFU-E colonies per 100,000 fetal liver cells (N = 4). (B) BFU-E colonies induced either by 3 U/mL Epo or after infection with SFFV-gp55-P and culture in the absence of Epo. Scale bar = 50 μm.

Induction of erythroid burst formation from day-12.5 fetal liver BFU-E progenitors. (A) Fetal liver cells were infected with retroviruses encoding gp55-P, gp55-A, gp55-AAP, or gp55-APA or with virus encoding β-galactosidase (control). Formation of BFU-E colonies was scored 7 to 9 days after infection in complete methylcellulose medium containing plasma-derived serum, SCM, and SF (see the Materials and Methods). Data represent the mean of the indicated number of assays ± 1 standard deviation. Treatment with 3 U/mL Epo resulted in the formation of 230.5 ± 16.1 BFU-E colonies per 100,000 fetal liver cells (N = 4). (B) BFU-E colonies induced either by 3 U/mL Epo or after infection with SFFV-gp55-P and culture in the absence of Epo. Scale bar = 50 μm.

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