Figure 2.

Schematic of myeloid development and maintenance in the mouse embryo and adult (see text). Circular red arrows indicate self renewal potential. Primitive progenitors do not share a common origin with endothelial cells lining the blood islands in the yolk sac (YS) and they emerge the absence of Runx1 and Myb. Within definitive hematopoiesis, HSC and EMP arise from distinct hemogenic endothelial cells through a Runx1-dependent endothelial to hematopoetic transition. Both EMP and HSC express the transcription factor Myb, and while no fetal or adult HSC-derived hematopoiesis can occur in the absence of Myb, EMPs are Myb-independent for their myeloid differentiation. EMP-derived hematopoeisis gives rises to erythrocytes and short-lived myeloid cells (monocytes, granulocytes, mast cells) that are replaced by HSC-derived cells late during gestation. EMP-derived macrophages colonise all tissues during fetal development where they specialize to their tissue of residency after birth and can persist throughout adult life by local proliferation (red arrow). Depending on the age and environmental challenges, HSC-derived cells can contribute to adult tissue resident populations.