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Science 21 October 1994:
Vol. 266. no. 5184, pp. 443 - 448
DOI: 10.1126/science.7939685
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Articles

Science, Vol 266, Issue 5184, 443-448
Copyright © 1994 by American Association for the Advancement of Science

articles

c-Fos: a key regulator of osteoclast-macrophage lineage determination and bone remodeling

AE Grigoriadis, ZQ Wang, MG Cecchini, W Hofstetter, R Felix, HA Fleisch, and EF Wagner

Research Institute of Molecular Pathology (IMP), Vienna, Austria.

Mice lacking the proto-oncogene c-fos develop the bone disease osteopetrosis. Fos mutant mice were found to have a block in the differentiation of bone-resorbing osteoclasts that was intrinsic to hematopoietic cells. Bone marrow transplantation rescued the osteopetrosis, and ectopic c-fos expression overcame this differentiation block. The lack of Fos also caused a lineage shift between osteoclasts and macrophages that resulted in increased numbers of bone marrow macrophages. These results identify Fos as a key regulator of osteoclast-macrophage lineage determination in vivo and provide insights into the molecular mechanisms underlying metabolic bone diseases.


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J. Li, I. Sarosi, X.-Q. Yan, S. Morony, C. Capparelli, H.-L. Tan, S. McCabe, R. Elliott, S. Scully, G. Van, et al. (2000)
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Placental vascularisation requires the AP-1 component fra1.
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Targeted disruption of the murine junD gene results in multiple defects in male reproductive function.
D Thepot, J. Weitzman, J Barra, D Segretain, M. Stinnakre, C Babinet, and M Yaniv (2000)
Development 127, 143-153
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Commitment and Differentiation of Osteoclast Precursor Cells by the Sequential Expression of c-Fms and Receptor Activator of Nuclear Factor {kappa}B (RANK) Receptors.
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   Abstract »    Full Text »    PDF »
Functions of c-Jun in Liver and Heart Development.
R. Eferl, M. Sibilia, F. Hilberg, A. Fuchsbichler, I. Kufferath, B. Guertl, R. Zenz, E. F. Wagner, and K. Zatloukal (1999)
J. Cell Biol. 145, 1049-1061
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Signaling in Human Osteoblasts by Extracellular Nucleotides. THEIR WEAK INDUCTION OF THE c-fos PROTO-ONCOGENE VIA Ca2+ MOBILIZATION IS STRONGLY POTENTIATED BY A PARATHYROID HORMONE/cAMP-DEPENDENT PROTEIN KINASE PATHWAY INDEPENDENTLY OF MITOGEN-ACTIVATED PROTEIN KINASE.
W. B. Bowler, C. J. Dixon, C. Halleux, R. Maier, G. Bilbe, W. D. Fraser, J. A. Gallagher, and R. A. Hipskind (1999)
J. Biol. Chem. 274, 14315-14324
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TRAF6 deficiency results in osteopetrosis and defective interleukin-1, CD40, and LPS signaling.
M. A. Lomaga, W.-C. Yeh, I. Sarosi, G. S. Duncan, C. Furlonger, A. Ho, S. Morony, C. Capparelli, G. Van, S. Kaufman, et al. (1999)
Genes & Dev. 13, 1015-1024
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Tumor necrosis factor receptor family member RANK mediates osteoclast differentiation and activation induced by osteoprotegerin ligand.
H. Hsu, D. L. Lacey, C. R. Dunstan, I. Solovyev, A. Colombero, E. Timms, H.-L. Tan, G. Elliott, M. J. Kelley, I. Sarosi, et al. (1999)
PNAS 96, 3540-3545
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Platelet-derived Growth Factor Induces Interleukin-6 Transcription in Osteoblasts through the Activator Protein-1 Complex and Activating Transcription Factor-2.
N. Franchimont, D. Durant, S. Rydziel, and E. Canalis (1999)
J. Biol. Chem. 274, 6783-6789
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Mechanically induced c-fos expression is mediated by cAMP in MC3T3-E1 osteoblasts.
J. FITZGERALD and M. HUGHES-FULFORD (1999)
FASEB J 13, 553-557