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Specific Signals Generated by the Cytoplasmic Domain of the Granulocyte
Colony-Stimulating Factor (G-CSF) Receptor Are Not Required for
G-CSF-Dependent Granulocytic Differentiation
Jason Jacob,
Jeffery S. Haug,
Sofia Raptis, and
Daniel C. Link
From the Division of Bone Marrow Transplantation and Stem Cell
Biology, Department of Medicine and Pathology, Washington University
Medical School, St Louis, MO.
Granulocyte colony-stimulating factor (G-CSF) is the principal
growth factor regulating the production of neutrophils, yet its role in
lineage commitment and terminal differentiation of hematopoietic
progenitor cells is controversial. In this study, we describe a system
to study the role of G-CSF receptor (G-CSFR) signals in granulocytic
differentiation using retroviral transduction of G-CSFR-deficient,
primary hematopoietic progenitor cells. We show that ectopic expression
of wild-type G-CSFR in hematopoietic progenitor cells supports
G-CSF-dependent differentiation of these cells into mature
granulocytes, macrophages, megakaryocytes, and erythroid cells.
Furthermore, we show that two mutant G-CSFR proteins, a truncation
mutant that deletes the carboxy-terminal 96 amino acids and a chimeric
receptor containing the extracellular and transmembrane domains of the
G-CSFR fused to the cytoplasmic domain of the erythropoietin receptor,
are able to support the production of morphologically mature,
chloroacetate esterase-positive, Gr-1/Mac-1-positive neutrophils in
response to G-CSF. These results demonstrate that ectopic expression of
the G-CSFR in hematopoietic progenitor cells allows for multilineage
differentiation and suggest that unique signals generated by the
cytoplasmic domain of the G-CSFR are not required for G-CSF-dependent
granulocytic differentiation.
Blood, Vol. 92 No. 2 (July 15), 1998:
pp. 353-361
© 1998 by the American Society of Hematology.
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