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Blood, 15 May 2005, Vol. 105, No. 10, pp. 3862-3870. Prepublished online as a Blood First Edition Paper on January 27, 2005; DOI 10.1182/blood-2004-09-3611. This Article Full Text (PDF) All Versions of this Article: 2004-09-3611v1 105/10/3862    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by D'Souza, S. L Articles by Keller, G. Search for Related Content PubMed PubMed Citation Articles by D'Souza, S. L Articles by Keller, G. Related Collections Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted September 22, 2004 Accepted January 12, 2005 SCL/Tal-1 is essential for hematopoietic commitment of the hemangioblast, but not for its development Sunita L D'Souza, Andrew G Elefanty, and Gordon Keller* Department of Gene and Cell Medicine, Mount Sinai School of Medicine, New York, NY, USA Monash Institute for Research of Reproduction and Development, Clayton, Victoria, Australia * Corresponding author; email: Gordon.Keller{at}mssm.edu. In this report, we have defined the stage at which SCL functions in the establishment of the hematopoietic system and provide evidence that its primary role is in the generation of the hematopoietic lineages from a progenitor called the blast colony forming cell (BL-CFC), a cell considered to be the in vitro equivalent of the hemangioblast. Using an ES cell line in which lacZ cDNA has been targeted to the Scl locus, we show that most of the BL-CFCs are detected in the SCL/lacZneg population, indicating that this progenitor does not express Scl. In the blast colony assay, Scl -/- cells initiate colony growth but are unable to generate endothelial and hematopoietic progeny and thus form colonies consisting of vascular smooth muscle (VSM) cells only. The capacity to give rise to blast colonies can be rescued by retroviral transduction of a wild type Scl gene into Scl-/-FLK-1pos cells, suggesting that the BL-CFC is generated in this population. Finally, we show that Scl-/- endothelial cells display a growth deficiency in monolayer cultures that can be partially overcome by maintaining this population as three-dimensional aggregates indicating that specific cellular interactions are required for maintenance of the Scl-/- endothelial lineage in vitro. 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