The anemic Friend virus gp55 envelope protein induces erythroid differentiation in fetal liver colony-forming units-erythroid

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 mechan...

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Bibliographic Details
Published in:Blood 1998-02, Vol.91 (4), p.1163-1172
Main Authors: CONSTANTINESCU, S. N, HONG WU, XUEDONG LIU, BEYER, W, FALLON, A, LODISH, H. F
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Cell differentiation, maturation, development, hematopoiesis
Cell physiology
Erythropoiesis - physiology
Female
Friend murine leukemia virus - genetics
Fundamental and applied biological sciences. Psychology
Gene Expression Regulation, Viral
Liver - cytology
Liver - embryology
Liver - physiology
Mice
Molecular and cellular biology
Pregnancy
Recombinant Fusion Proteins - physiology
Transfection
Viral Envelope Proteins - physiology
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Summary: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.
ISSN:0006-4971
1528-0020
DOI:10.1182/blood.v91.4.1163