| First Author | Wang ZQ | Year | 1992 |
| Journal | Nature | Volume | 360 |
| Issue | 6406 | Pages | 741-5 |
| PubMed ID | 1465144 | Mgi Jnum | J:3493 |
| Mgi Id | MGI:52006 | Doi | 10.1038/360741a0 |
| Citation | Wang ZQ, et al. (1992) Bone and haematopoietic defects in mice lacking c-fos. Nature 360(6406):741-5 |
| abstractText | The proto-oncogene c-fos is the cellular homologue of v-fos originally isolated from murine osteosarcoma. Fos protein is a major component of the AP-1 transcription factor complex, which includes members of the jun family. Stable expression of c-fos in mice has been demonstrated in developing bones and teeth, haematopoietic cells, germ cells and in the central nervous system. It has been proposed that c-fos has an important role in signal transduction, cell proliferation and differentiation. We have previously demonstrated that overexpression of c-fos in transgenic and chimaeric mice specifically affects bone, cartilage and haematopoietic cell development. To understand better the function of c-fos in vivo, we used gene targeting in embryonic stem cells to generate cells and mice lacking c-fos. Here we report that heterozygous fos +/- mice appear normal, although females exhibit a distorted transmission frequency. All homozygous fos -/- mice are growth-retarded, develop osteopetrosis with deficiencies in bone remodelling and tooth eruption, and have altered haematopoiesis. These data define the c-Fos protein as an essential molecule for the development of specific cellular compartments. |
