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Background  Development of the hematopoietic and endothelial lineages derives from a common mesodermal precursor, the Flk1 +  hemangioblast. However, the signaling pathways that regulate the development of hematopoietic and endothelial cells from this common progenitor cell remains incompletely understood. Using mouse models with a conditional  Spry1  transgene, and a  Spry1  knockout mouse, we investigated the role of Spry1 in the development of the endothelial and hematopoietic lineages during development.    Methodology/Principal Findings  Quantitative RT-PCR analysis demonstrates that Spry1, Spry2, and Spry4 are expressed in Flk1 +  hemangioblasts  in vivo , and decline significantly in c-Kit +  and CD41 +  hematopoietic progenitors, while expression is maintained in developing endothelial cells. Tie2-Cre-mediated over-expression of Spry1 results in embryonic lethality. At E9.5  Spry1;Tie2-Cre  embryos show near normal endothelial cell development and vessel patterning but have reduced hematopoiesis. FACS analysis shows a reduction of primitive hematopoietic progenitors and erythroblastic cells in  Spry1;Tie2-Cre  embryos compared to controls. Colony forming assays confirm the hematopoietic defects in  Spry1;Tie2-Cre  transgenic embryos. Immunostaining shows a significant reduction of CD41 or CD71 and dpERK co-stained cells in  Spry1;Tie2-Cre  embryos compared to controls, whereas the number of VEC +  and dpERK co-stained cells is comparable. Compared to controls,  Spry1;Tie2-Cre  embryos also show a decrease in proliferation and an increase in apoptosis. Furthermore, loss of Spry1 results in an increase of CD41 +  and CD71 +  cells at E9.5 compared with controls.    Conclusions/Significance  These data indicate that primitive hematopoietic cells derive from Tie2-expressing hemangioblasts and that Spry1 over expression inhibits primitive hematopoietic progenitor and erythroblastic cell development and expansion while having no obvious effect on endothelial cell development.

Spry1 Is Expressed in Hemangioblasts and Negatively Regulates Primitive Hematopoiesis and Endothelial Cell Function