Endothelial precursors and primitive hematopoietic cells are closely associated during development. They are thought to originate from a common progenitor, the hemangioblast, but the molecular mechanisms that control the fate of hemangioblasts have been unclear. In the February 1 Genes & Development, Masatsugu Ema and colleagues at the Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Canada show that Flk1 and Tal1 act to regulate cell fate choice of hemangioblast development into hematopoietic, endothelial, and smooth muscle lineages (Genes & Development, 17: 380-393, February 1, 2003).

Ema et al. used Flk1-/- murine embryos which fail to form both endothelial and hematopoietic cells. They observed that expression of Tal1 under the Flk1 promoter partially rescued the loss of endothelial and hematopoietic cells in Flk1 mutants. Ectopic expression of Tal1 under the Flk1 promoter in Flk1+/- cells increased the number of blast colonies (BL-CFCs) and enhanced...

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