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Blood, Vol. 94 No. 11 (December 1), 1999:
pp. 3754-3763
SCL Expression in the Mouse Embryo Detected With a Targeted
lacZ Reporter Gene Demonstrates Its Localization to
Hematopoietic, Vascular, and Neural Tissues
Andrew G. Elefanty,
C. Glenn Begley,
Lynne Hartley,
Bette Papaevangeliou, and
Lorraine Robb
From The Walter and Eliza Hall Institute of Medical Research, the
Cooperative Research Centre for Cellular Growth Factors and the Rotary
Bone Marrow Research Laboratories, Victoria, Australia.
The 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 vasculogenesis 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 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.

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