Summary
The study of colony stimulating factor 1 (CSF-1), a homodimeric serum growth factor that
regulates mononuclear phagocytes and is involved in maternal-fetal interactions during
pregnancy, was dramatically enhanced by the observation that the recessive mutation
osteopetrosis, op, is an inactivating mutation in the CSF-1-encoding gene. Homozygous
mutant (op/op) mice completely lack CSF-1, are osteopetrotic consequent to a deficiency in
osteoclasts, have severely reduced numbers of macrophages, and have reduced fertility
evident at the pre- and postimplantation stages of pregnancy. We show here that op/op
females have a lactational defect, and consequently, although some are able to produce
offspring, few nurture any pups and none feeds a full litter. This lactational defect is
due to incomplete mammary gland ductal growth during pregnancy, a precocious development
of the lobulo-alveolar system, and despite expression of milk proteins, a failure to
switch to a lactational state. These data show that CSF-1 has a role in the development of
the mammary gland during pregnancy.
Citation
Pollard JW and Hennighausen, L. (1994) Colony stimulating factor 1 is required for mammary
gland development during pregnancy. Proc Natl Acad Sci U S A 1994 Sep 27;91(20):9312-6
contributed March 1996
last update: December 1998