SCL expression in the mouse embryo detected with a targeted lacZ reporter gene demonstrates its localization to hematopoietic, vascular, and neural tissues
- Author(s)
- Elefanty, AG; Begley, CG; Hartley, L; Papaevangeliou, B; Robb, L;
- Details
- Publication Year 1999-12-01,Volume 94,Issue #11,Page 3754-3763
- Journal Title
- BLOOD
- Publication Type
- Journal Article
- Abstract
- dThe helix-loop-helix transcription factor SCL (TAL1) is indispensable for blood cell formation in the mouse embryo, We have explored the localization and developmental potential of cells fated to express SCL during murine development using SCL-lacZ mutant mice in which the Escherichia coli lacZ reporter gene was knocked in' to the SCL locus. In addition to the hematopoietic defect associated with SCL deficiency, the yolk sac blood vessels in SCLlacZ/lacZ embryos formed an abnormal primary vascular plexus, which failed to undergo subsequent remodeling and formation of large branching vessels. Intraembryonic vascurogenesis in precirculation SCLlacZ/lacZ embryos appeared normal but; in embryos older than embryonic day (E) 8.5 to E9, absolute anemia leading to severe hypoxia precluded an accurate assessment of further vascular development. In heterozygous SCLlacZ/w embryos, lacZ was expressed in the central nervous system, vascular endothelia, and primitive and definitive hematopoietic cells in the blood, aortic wall, and fetal liver. Culture of fetal liver cells sorted for high and low levels of beta galactosidase activity from SCLlacZ/w heterozygous embryos indicated that there was a correlation between the level of SCL expression and the frequency of hematopoietic progenitor cells. (C) 1999 by The American Society of Hematology.
- Publisher
- AMER SOC HEMATOLOGY
- Keywords
- RECEPTOR TYROSINE KINASE; TRANSCRIPTION FACTOR SCL; YOLK-SAC HEMATOPOIESIS; BLOOD-VESSEL FORMATION; MICE LACKING; ERYTHROID DEVELOPMENT; ENFORCED EXPRESSION; PROGENITOR CELLS; PROTEIN LMO2; ADULT-MOUSE
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Creation Date: 1999-12-01 12:00:00