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Originally published In Press as doi:10.1074/jbc.M109955200 on December 13, 2001
J. Biol. Chem., Vol. 277, Issue 11, 9335-9341, March 15, 2002
Absence of Erythrogenesis and Vasculogenesis in
Plcg1-deficient Mice*
Hong-Jun
Liao ,
Tsutomu
Kume§,
Catriona
McKay¶ ,
Ming-Jiang
Xu**,
James N.
Ihle¶, and
Graham
Carpenter **
From the Departments of 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
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- 2, however, it is unable to substitute for the
absence of phospholipase C- 1, which can be detected in its
tyrosine-phosphorylated state.
*
This work was supported by National Institutes of Health
Grant CA75195.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
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.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.

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Copyright © 2002 by the American Society for Biochemistry and Molecular Biology.
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