%A Fantin,Alessandro %A Tacconi,Carlotta %A Villa,Emanuela %A Ceccacci,Elena %A Denti,Laura %A Ruhrberg,Christiana %D 2021 %J Frontiers in Cell and Developmental Biology %C %F %G English %K KIT,hemogenic endothelium,erythromyeloid progenitors,yolk sac (YS),Fetal liver %Q %R 10.3389/fcell.2021.648630 %W %L %M %P %7 %8 2021-July-29 %9 Brief Research Report %# %! KIT regulates fetal liver erythropoiesis %* %< %T KIT Is Required for Fetal Liver Hematopoiesis %U https://www.frontiersin.org/articles/10.3389/fcell.2021.648630 %V 9 %0 JOURNAL ARTICLE %@ 2296-634X %X In the mouse embryo, endothelial cell (EC) progenitors almost concomitantly give rise to the first blood vessels in the yolk sac and the large vessels of the embryo proper. Although the first blood cells form in the yolk sac before blood vessels have assembled, consecutive waves of hematopoietic progenitors subsequently bud from hemogenic endothelium located within the wall of yolk sac and large intraembryonic vessels in a process termed endothelial-to-hematopoietic transition (endoHT). The receptor tyrosine kinase KIT is required for late embryonic erythropoiesis, but KIT is also expressed in hematopoietic progenitors that arise via endoHT from yolk sac hemogenic endothelium to generate early, transient hematopoietic waves. However, it remains unclear whether KIT has essential roles in early hematopoiesis. Here, we have combined single-cell expression studies with the analysis of knockout mice to show that KIT is dispensable for yolk sac endoHT but required for transient definitive hematopoiesis in the fetal liver.