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The Anemic Friend Virus gp55 Envelope Protein Induces Erythroid
Differentiation in Fetal Liver Colony-Forming
Units-Erythroid
Stefan N. Constantinescu,
Hong Wu,
Xuedong Liu,
Wendy Beyer,
Amy Fallon, and
Harvey F. Lodish
From the Whitehead Institute for Biomedical Research, Cambridge, MA;
and the Department of Biology, Massachusetts Institute of Technology,
Cambridge, MA.
The gp55 envelope proteins of the spleen focus-forming virus
initiate erythroleukemia in adult mice. Because the gp55 from the
polycythemic strain (gp55-P), but not from the anemic strain (gp55-A),
activates the erythropoietin receptor (EpoR) for proliferation of
hematopoietic cell lines, the mechanism by which gp55-A initiates erythroleukemia has remained a mystery. We show here that gp55-A activates the EpoR in fetal liver cells. In contrast to previous studies using bone marrow cells from phenylhydrazine-treated, anemic
mice, we find that both gp55-A and gp55-P induce erythroid differentiation from colony-forming unit-erythroid (CFU-E)
progenitors in fetal liver cells. The effects on CFU-Es of both gp55-A
and -P are mediated by the EpoR, because no colonies are seen upon expression of either gp55 in EpoR / fetal liver cells.
However, only gp55-P induces erythroid bursts from burst-forming
unit-erythroid progenitors and only gp55-P induces Epo
independence in Epo-dependent cell lines. Using chimeric gp55 P/A
proteins, we extend earlier work showing that the transmembrane sequence determines the capacity of gp55 proteins to differentially activate EpoR signaling. We discuss the possibilities for different signaling capacities of gp55-A and -P in fetal liver and bone marrow-derived erythroid progenitor cells.
Blood, Vol. 91 No. 4 (February 15), 1998:
pp. 1163-1172
© 1998 by The American Society of Hematology.
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