| First Author | Alkema MJ | Year | 1995 |
| Journal | Nature | Volume | 374 |
| Issue | 6524 | Pages | 724-7 |
| PubMed ID | 7715727 | Mgi Jnum | J:24505 |
| Mgi Id | MGI:72244 | Doi | 10.1038/374724a0 |
| Citation | Alkema MJ, et al. (1995) Transformation of axial skeleton due to overexpression of bmi-1 in transgenic mice. Nature 374(6524):724-7 |
| abstractText | The oncogene bmi-1, which was originally found to be involved in B- and T-cell lymphoma formation encodes a protein with a domain of homology to the Drosophila protein Posterior sex combs (Psc) and its relative Suppressor 2 of Zeste (Su(z)2) (refs 4 and 5). Psc is a member of the Polycomb-group gene family, which is required to maintain the repression of homeotic genes that regulate the identities of Drosophila segments. The possibility that bmi-1 may play a similar role in vertebrates was suggested by our previous finding that mice lacking the bmi-1 gene show posterior transformations of the axial skeleton. Here we report that transgenic mice overexpressing Bmi-1 protein show the opposite phenotype, namely a dose-dependent anterior transformation of vertebral identity. The anterior expression boundary of the Hoxc-5 gene is shifted in the posterior direction, indicating that Bmi-1 is involved in the repression of Hox genes. We propose that Bmi-1 is a member of a vertebrate Polycomb complex that regulates segmental identity by repressing Hox genes throughout development. |
