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.