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Vol. 11, Issue 11, 3835-3848, November 2000
#
Colony-stimulating factor-1 (CSF-1) induces expression of immediate
early gene, such as c-myc and c-fos and delayed early genes such as
D-type cyclins (D1 and D2), whose products play essential roles in the
G1 to S phase transition of the cell cycle. Little is known, however,
about the cytoplasmic signal transduction pathways that connect the
surface CSF-1 receptor to these genes in the nucleus. We have
investigated the signaling mechanism of CSF-1-induced D2 expression.
Analyses of CSF-1 receptor autophosphorylation mutants show that,
although certain individual mutation has a partial inhibitory effect,
only multiple combined mutations completely block induction of D2 in
response to CSF-1. We report that at least three parallel pathways, the
Src pathway, the MAPK/ERK kinase (MEK)/extracellular
signal-regulated kinase (ERK) pathway, and the c-myc pathway,
are involved. Induction of D2 is partially inhibited in
SrcDepartment of Medicine, Division of Dermatology,
University of Southern California Keck School of Medicine, Los Angeles,
California 90033; *The Ben May Institute for Cancer Research, and
§Center for Molecular Oncology, University of Chicago,
Chicago, Illinois 60637; Fred Hutchinson Cancer Research
Center, Seattle, Washington 98104; and ¶H. Lee Moffitt
Cancer Center and Research Institute, University of South Florida,
Tampa, Florida 33612
/ bone marrow-derived macrophages and by Src
inhibitor PP1 and is enhanced in v-Src-overexpressing cells. Activation
of myc's transactivating activity selectively induces D2 but not D1.
Blockade of c-myc expression partially blocks CSF-1-induced D2
expression. Complete inhibition of the MEK/ERK pathway causes 50%
decrease of D2 expression. Finally, simultaneous inhibition of Src, MEK activation, and c-myc expression additively blocks CSF-1-induced D2
expression. This study indicates that multiple signaling pathways are
involved in full induction of a single gene, and this finding may also
apply broadly to other growth factor-inducible genes.
These authors contributed equally to this work.
#
Corresponding author. E-mail address:
wli{at}hsc.usc.edu.
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