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Proliferative but not nonproliferative responses to granulocyte colony-
stimulating factor are associated with rapid activation of the p21ras/MAP
kinase signalling pathway
A Bashey, L Healy and CJ Marshall
Section of Cell and Molecular Biology, Chester Beatty Laboratories,
Institute of Cancer Research, London, UK.
Granulocyte colony-stimulating factor (G-CSF) can elicit responses that
include proliferation, granulocytic differentiation, and activation of
cellular functions in target cells. The biochemical pathways responsible
for transduction of these signals from the G-CSF receptor (G-CSFR) have not
been defined. In this report, we show that, in murine (NFS-60) and human
(OCI-AML 1) myeloid leukemia cell lines and in murine pro-B-lymphocytic
cells, BAF/B03, transfected with the murine G- CSFR, proliferative
responses to G-CSF are associated with rapid activation of p42 and p44 MAP
kinases and p21ras. Truncation of the cytoplasmic portion of the murine
G-CSFR at residue 646 but not at residue 739 abolished G-CSF-induced
stimulation of cellular proliferation as well as activation of MAP kinase
and p21ras in transfected BAF/B03 cells. G-CSF-induced granulocytic
differentiation of the murine leukemic cell line 32DC13(G) occurred in the
absence of detectable activation of p42 MAP kinase. Nonproliferative
responses to G-CSF in the human promyelocytic cell line HL-60 and in human
neutrophils were similarly associated with no MAP kinase activation. These
results imply that differing cellular effects of G-CSF may be involve the
recruitment of differing signal transduction pathways with the p21ras/MAP
kinase pathway being limited to proliferative responses.
Volume 83,
Issue 4,
pp. 949-957,
02/15/1994
Copyright © 1994 by The American Society of Hematology
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