In mice, little is known about the surface markers that characterize embryonic hematopoietic stem cells (HSCs). During my PhD, I have studied in the placenta (Pl) and the yolk sac (YS) three populations (CD34+c-kithi, CD144+CD45+ and Sca-1+AA4.1+) that have already been described as enriched in HSCs in other contexts. The whole project shows that enrichment in HSCs do not involve the same markers according to the tissue concerned: in sites of emergence (AGM) and emergence/amplification of HSCs (YS), the most enriched population in HSCs is the CD144+CD45+ one; in the Pl, an amplification organ of HSCs, the best one is the CD34+c-kithiSca-1+ population, whereas in the fetal liver (FL), an amplification/differentiation organ of HSCs, it is the CD34+c-kithiSca-1+AA4.1+ one. Molecular analysis of these populations will reveal specific regulatory molecules concerning the emergence and amplification of HSCs. In addition, we have used VECR transgenic mice to study the origin of CD34+c-kithi HSCs from Pl at E11.5, and it seems that all cells of this population are not derived from the endothelium. Preliminary results performed on Mpl-/- mice, which show a defect in HSCs content in the Pl and the FL, indicate that at E11.5, the hematopoietic potential of CD34+c-kithi population in Mpl-/- Pl is lower than the CD34+c-kithi population in wild type Pl, and this difference is no more visible at E12.5. Thus, the Pl appears to be a transient niche of HSCs amplification/maturation, but it also remains possible that it can be able to directly produce HSCs
