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Transformation of axial skeleton due to overexpression of bmi-1 in transgenic mice

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Abstract

THE oncogene bmi-l, which was originally found to be involved in B- and T-cell lymphoma formation1–3 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 Poly comb-group gene family, which is required to maintain the repression of homeotic genes that regulate the identities of Drosophila segments6. The possibility that bmi-l may play a similar role in vertebrates was suggested by our previous finding7 that mice lacking the bmi-l gene show posterior transformations of the axial skeleton. Here we report that transgenic mice overexpressing Bmi-l 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-l is involved in the repression Hox genes. We propose that Bmi-l is a member of a vertebrate Polycomb complex that regulates segmental identity by repressing Hox genes throughout development.

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Author notes

  1. Maarten van Lohuizen

    Present address: Department of Biochemistry and Biophysics, UCSF School of Medicine, San Francisco, California, 94143-0448, USA

Authors and Affiliations

  1. Division of Molecular Genetics, The Netherlands Cancer Institute, and Department of Biochemistry, the University of Amsterdam, Plesmanlaan 121, 1066 CX, Amsterdam, The Netherlands

    Mark J. Alkema, Nathalie M. T. van der Lugt, René C. Bobeldijk, Anton Berns & Maarten van Lohuizen

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  1. Mark J. Alkema
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  2. Nathalie M. T. van der Lugt
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  3. René C. Bobeldijk
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  4. Anton Berns
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  5. Maarten van Lohuizen
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Alkema, M., van der Lugt, N., Bobeldijk, R. et al. Transformation of axial skeleton due to overexpression of bmi-1 in transgenic mice. Nature 374, 724–727 (1995). https://doi.org/10.1038/374724a0

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