Sealing a cell's fate( These Tal1-expressing Flk1-deficient m...)

These Tal1-expressing, Flk1-deficient mouse embryos still died in utero, but the development of endothelial and hematopoietic cells was improved. More marked, though, was the ability of Tal1-expressing, Flk1-deficient ES cells to differentiate into hematopoietic cells at levels comparable to that of ES cells missing only one copy of Flk1 (Flk1-heterozygous ES cells). The researchers also expressed additional Tal1 in Flk1-heterozygous ES cells, and found that this enhanced expression of Tal1 both augmented the cells' hematopoietic potential and enabled the cells to differentiate into smooth muscle cells.

Taken together, these findings provide further support for the existence of a common hemangioblast progenitor cell, in which the dual expression of Flk1 and Tal1 steer cells into a path of either endothelial, hematopoietic, or smooth muscle cell fate.

"Using mouse embryonic stem cells we have been able to manipulate the proportions of the three different cell types arising from the hemangioblast by altering expression of a signaling pathway and one of its downstream effector molecules. These kinds of studies will help us understand how to manipulate human stem cells for therapeutic uses in vascular damage and disease," states Dr. Rossant.

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Contact: Heather Cosel
coselpie@cshl.org
Cold Spring Harbor Laboratory
31-Jan-2003

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