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Papers In Press, published online ahead of print December 13, 2001
Department of Biochemistry, Vanderbilt University School of Medicine, Nashville, TN 37232-0146
Corresponding Author: graham.carpenter{at}mcmail.vanderbilt.edu
Mice nullizygous for Plcg1 cease growing at early to mid-gestation. 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. 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 PECAM-1. In addition, Plcg1 nullizygous embryos express a greatly reduced level of VEGFR-2/flk-1, consistent with significantly impaired vasculogenesis and erythropoiesis. Interestingly, these early embryos do express PLC-
J. Biol. Chem, 10.1074/jbc.M109955200
Submitted on October 15, 2001
Revised on November 16, 2001
Accepted on December 13, 2001
Absence of erythrogenesis and vasculogenesis in Plcg1-deficient mice
2; however, it is unable to substitute for the absence of PLC-1, which can be detected in its tyrosine phosphorylated state.
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