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Bone and haematopoietic defects in mice lacking c-fos
Z Q Wang1, C Ovitt, A E Grigoriadis
1Research Institute of Molecular Pathology (IMP), Vienna, Austria.
Nature
|December 24, 1992
Summary
Mice lacking the c-Fos gene exhibit growth retardation, bone defects, and altered blood cell development. These findings highlight the essential role of c-Fos protein in cellular development.
Area of Science:
- Molecular Biology
- Genetics
- Developmental Biology
Background:
- The proto-oncogene c-fos encodes the Fos protein, a key component of the AP-1 transcription factor.
- c-Fos expression is observed in various tissues, including bone, teeth, hematopoietic cells, and the central nervous system.
- Previous studies suggested c-Fos involvement in signal transduction, cell proliferation, and differentiation.
Purpose of the Study:
- To elucidate the in vivo function of c-Fos using gene targeting.
- To characterize the developmental consequences of c-Fos deficiency.
Main Methods:
- Gene targeting in embryonic stem cells to generate c-fos knockout mice.
- Phenotypic analysis of heterozygous (fos +/-) and homozygous (fos -/-) mice.
Main Results:
- Homozygous fos -/- mice display growth retardation, osteopetrosis, impaired bone remodeling, and delayed tooth eruption.
- Altered hematopoietic cell development was observed in fos -/- mice.
- Heterozygous fos +/- mice generally appear normal, with some exhibiting skewed transmission frequencies in females.
Conclusions:
- The c-Fos protein is essential for normal development of bone, cartilage, and hematopoietic cells.
- Loss of c-Fos function leads to significant developmental defects, underscoring its critical role in specific cellular compartments.
