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Journal Article

Craniofacial abnormalities induced by ectopic expression of the homeobox gene Hox-1.1 in transgenic mice.

MPS-Authors
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Balling,  R.
Department of Molecular Cell Biology, MPI for biophysical chemistry, Max Planck Society;

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Gruss,  P.
Department of Molecular Cell Biology, MPI for biophysical chemistry, Max Planck Society;

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Kessel,  M.
Department of Molecular Cell Biology, MPI for biophysical chemistry, Max Planck Society;

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Citation

Balling, R., Mutter, G., Gruss, P., & Kessel, M. (1989). Craniofacial abnormalities induced by ectopic expression of the homeobox gene Hox-1.1 in transgenic mice. Cell, 58(2), 337-347. doi:10.1016/0092-8674(89)90848-9.


Cite as: http://hdl.handle.net/11858/00-001M-0000-002C-3E33-1
Abstract
Hox-1.1 is a murine homeobox-containing gene expressed in a time- and cell-specific manner during embryogenesis. We have generated transgenic mice that ectopically express Hox-1.1 from the chicken β-actin promoter. In these mice Hox-1.1 expression was changed to an almost ubiquitous pattern. Ectopic expression of Hox-1.1 leads to death of the transgenic animals shortly after birth and is associated with multiple craniofacial anomalies, such as cleft palate, open eyes at birth, and nonfused pinnae. This phenotype is similar to the effects seen after systemic administration of retinoic acid during gestation. This suggests that retinoic acid embryopathy and the specific developmental defects caused by ectopic expression of a potential developmental control gene share a common pathogenic mechanism.