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Blood, 1 January 2002, Vol. 99, No. 1, pp. 111-120
HEMATOPOIESIS
Targeted disruption of the mouse colony-stimulating factor 1 receptor gene results in osteopetrosis, mononuclear phagocyte
deficiency, increased primitive progenitor cell frequencies, and
reproductive defects
Xu-Ming Dai,
Gregory R. Ryan,
Andrew J. Hapel,
Melissa G. Dominguez,
Robert G. Russell,
Sara Kapp,
Vonetta Sylvestre, and
E.
Richard Stanley
From the Department of Developmental and Molecular
Biology, Albert Einstein College of Medicine, Bronx, NY.
The effects of colony-stimulating factor 1 (CSF-1), the primary
regulator of mononuclear phagocyte production, are thought to be
mediated by the CSF-1 receptor (CSF-1R), encoded by the c-fms proto-oncogene. To investigate the in vivo
specificity of CSF-1 for the CSF-1R, the mouse Csf1r gene
was inactivated. The phenotype of
Csf1 /Csf1r mice closely
resembled the phenotype of CSF-1-nullizygous
(Csf1op/Csf1op) mice,
including the osteopetrotic, hematopoietic, tissue macrophage, and
reproductive phenotypes. Compared with their wild-type littermates, splenic erythroid burst-forming unit and high-proliferative potential colony-forming cell levels in both
Csf1op/Csf1op and
Csf1/Csf1r mice were
significantly elevated, consistent with a negative regulatory role of
CSF-1 in erythropoiesis and the maintenance of primitive hematopoietic
progenitor cells. The circulating CSF-1 concentration in
Csf1r/Csf1r mice
was elevated 20-fold, in agreement with the previously reported clearance of circulating CSF-1 by CSF-1R-mediated endocytosis and
intracellular destruction. Despite their overall similarity, several
phenotypic characteristics of the
Csf1r/Csf1r mice
were more severe than those of the
Csf1op/Csf1op mice. The
results indicate that all of the effects of CSF-1 are mediated via the
CSF-1R, but that subtle effects of the CSF-1R could result from its
CSF-1-independent activation.
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