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J. Biol. Chem., Vol. 277, Issue 11, 9335-9341, March 15, 2002
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,
,
**
From the Departments of Mice nullizygous for Plcg1
cease growing at early to mid-gestation. An examination of carefully
preserved wild-type embryos shows clear evidence of erythropoiesis, but
erythropoiesis is not evident in Plcg1 nullizygous embryos
at the same stage. The analyses of embryonic materials demonstrate that
in the absence of Plcg1, erythroid progenitors cannot be
detected in the yolk sac or embryo body by three different assays,
burst-forming units, colony-forming units, and analysis for the
developmental marker Ter119. However, non-erythroid
granulocyte/macrophage colonies are produced by Plcg1 null
embryos. Further analysis of these embryos demonstrates significantly
diminished vasculogenesis in Plcg1 nullizygous embryos
based on the lack of expression of the endothelial marker platelet
endothelial cell adhesion molecule-1. In addition,
Plcg1 nullizygous embryos express a greatly reduced level
of vascular endothelial growth factor receptor-2/Flk-1, consistent with significantly impaired vasculogenesis and
erythropoiesis. Interestingly, these early embryos do express
phospholipase C-
Biochemistry,
§ Cell Biology, and ** Medicine, Vanderbilt
University School of Medicine, Nashville, Tennessee 37232 and the
¶ Department of Biochemistry, St. Jude Children's Research
Hospital, Memphis, Tennessee 38105
2, however, it is unable to substitute for the
absence of phospholipase C-
1, which can be detected in its
tyrosine-phosphorylated state.
Present address: PPS International Communications Ltd.,
Worthing, UK.

To whom correspondence should be addressed: Dept. of
Biochemistry, Vanderbilt University School of Medicine, Nashville,
TN 37232-0146. Tel.: 615-322-6678; Fax: 615-322-2931; E-mail:
graham.carpenter@mcmail.vanderbilt.edu.
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