Zfat Is Indispensable for the Development of Erythroid Cells in the Fetal Liver.

Background/Aim: In mice, fetal liver is the first tissue of definitive erythropoiesis for definitive erythroid expansion and maturation. ZFAT, originally identified as a candidate susceptibility gene for autoimmune thyroid disease, has been reported to be involved in primitive hematopoiesis and T cell development. The aim of this study was to examine whether or not Zfat is involved in definitive erythropoiesis in the fetal liver during mammalian development. Materials and Methods: The role of Zfat during mouse fetal erythropoiesis in the fetal liver was examined using tamoxifen-inducible CreERT2 Zfat-deficient mice. Results: Zfat-deficient mice exhibit moderate anemia with small and pale fetal liver through a decreased number of erythroblasts by E12.5. Apoptosis sensitivity in fetal liver erythroid progenitors was enhanced by Zfat-deficiency ex vivo. Moreover, Zfat knockdown partially inhibited CD71(-/low)Ter119(-) to CD71(high)Ter119(-)transition of fetal liver erythroid progenitors with impairment in the elevation of CD71 expression. Conclusion: Zfat plays a critical role for erythropoiesis in the fetal liver.