Abstract
Erythroid progenitor cells in +/+ and Sl/Sld fetal livers manifested as burst-forming units-erythroid (BFU-E) and colony-forming units- erythroid (CFU-E) were assayed in vitro during early development. The proportion of BFU-E was higher as mutant than in normal fetal livers. On the other hand, the proportion of CFU-E was less in the mutant than in the normal. These results suggest that the defect in Sl/Sld fetal hepatic erythropoiesis is expressed at the steps of differentiation that effect the transition from BFU-E to CFU-E.
Key Points
Transient expansion of fetal megaerythroid progenitors in ERG/Gata1s mouse is biologically similar to Down syndrome TMD. The N-terminal domain of GATA1 and the downregulation of ERG expression are essential for normal fetal erythropoiesis.
Key Points
Vegfc is essential for mobilization, maturation, and enucleation of primitive erythroblasts. Vegfc deletion compromises liver colonization by erythro-myeloid progenitors and subsequent macrophage/erythroid expansion.
Key Points
Rcor1 knockout mice show a block in fetal erythropoiesis at the proerythroblast stage. Rcor1 represses expression of HSCs and myeloid genes during erythropoiesis, including Csf2rb, which is important in myeloid function.
Fetal erythropoiesis in steel mutant mice. III. Defect in differentiation from BFU-E to CFU-E during early development
