Mice were generated with targeted disruptions in the hoxb-1 gene. Two
separate mutations were created: the first disrupts only the homeodoma
in and the second inactivates the first exon as well as the homeodomai
n. The phenotypes associated with these two mutant alleles are indisti
nguishable in surviving adult mice. The predominant defect in these mu
tant mice is a failure to form the somatic motor component of the VIIt
h (facial) nerve, possibly through a failure to specify these neurons.
The phenotype of hoxb-1 mutant homozygotes closely resembles features
of the clinical profile associated with humans suffering from Bell's
Palsy or Moebius Syndrome. These animals should therefore provide a us
eful animal model for these human diseases.