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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 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 Citation Map 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 Hematopoiesis and Stem Cells Hemostasis, Thrombosis, and Vascular Biology Free Research Articles Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS 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 From the Department of Gene and Cell Medicine, Mount Sinai School of Medicine, New York, NY; and Monash Institute for Research of Reproduction and Development, Clayton, Victoria, Australia. 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 embryonic stem (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/lacZ- 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 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-1+ 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 3-dimensional aggregates indicating that specific cellular interactions are required for maintenance of the Scl-/- endothelial lineage in vitro. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: A tale of two lineages: the origins of blood and endothelium Anthony R. Green Blood 2005 105: 3758. [Full Text] [PDF] This article has been cited by other articles: M. T. Kassouf, H. Chagraoui, P. Vyas, and C. Porcher Differential use of SCL/TAL-1 DNA-binding domain in developmental hematopoiesis Blood, August 15, 2008; 112(4): 1056 - 1067. [Abstract] [Full Text] [PDF] J. Sausville, A. A. Molinolo, X. Cheng, J. Frampton, N. Takebe, J. S. Gutkind, and R. A. Feldman RCAS/SCL-TVA Animal Model Allows Targeted Delivery of Polyoma Middle T Oncogene to Vascular Endothelial Progenitors In vivo and Results in Hemangioma Development Clin. Cancer Res., June 15, 2008; 14(12): 3948 - 3955. [Abstract] [Full Text] [PDF] S. Pearson, P. Sroczynska, G. Lacaud, and V. 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