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Growth factor independence 1b (GFI1B) is a DNA binding repressor of transcription with vital functions in hematopoiesis.  Gfi1b -null embryos die at midgestation very likely due to defects in erythro- and megakaryopoiesis. To analyze the full functionality of  Gfi1b , we used conditionally deficient mice that harbor floxed  Gfi1b  alleles and inducible ( Mx -Cre, Cre-ERT) or erythroid specific ( EpoR -Cre) Cre expressing transgenes. In contrast to the germline knockout,  EpoR -Cre mediated erythroid specific ablation of  Gfi1b  allows full gestation, but causes perinatal lethality with very few mice surviving to adulthood. Both the embryonic deletion of  Gfi1b  by  EpoR -Cre and the deletion in adult mice by  Mx -Cre or Cre-ERT leads to reduced numbers of erythroid precursors, perturbed and delayed erythroid maturation, anemia and extramedullary erythropoiesis. Global expression analyses showed that the  Hba-x ,  Hbb-bh1  and  Hbb-y  embryonic globin genes were upregulated in  Gfi1b  deficient TER119 +  fetal liver cells over the gestation period from day 12.5–17.5 p.c. and an increased level of  Hbb-bh1  and  Hbb-y  embryonic globin gene expression was even maintained in adult  Gfi1b  deficient mice. While the expression of  Bcl11a , a regulator of embryonic globin expression was not affected by  Gfi1b  deficiency, the expression of  Gata1  was reduced and the expression of  Sox6 , also involved in globin switch, was almost entirely lost when  Gfi1b  was absent. These findings establish  Gfi1b  as a regulator of embryonic globin expression and embryonic and adult erythroid maturation.

Growth Factor Independence 1b (Gfi1b) Is Important for the Maturation of Erythroid Cells and the Regulation of Embryonic Globin Expression