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Development, Vol 122, Issue 10 3217-3228, Copyright © 1996 by Company of Biologists
JOURNAL ARTICLES |
JM Goddard, M Rossel, NR Manley and MR Capecchi
Howard Hughes Medical Institute, Department of Human Genetics, University of Utah, School of Medicine, Salt Lake City 84112, USA.
Mice were generated with targeted disruptions in the hoxb-1 gene. Two separate mutations were created: the first disrupts only the homeodomain and the second inactivates the first exon as well as the homeodomain. The phenotypes associated with these two mutant alleles are indistinguishable in surviving adult mice. The predominant defect in these mutant mice is a failure to form the somatic motor component of the VIIth (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 useful animal model for these human diseases.
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M Studer, A Gavalas, H Marshall, L Ariza-McNaughton, F. Rijli, P Chambon, and R Krumlauf Genetic interactions between Hoxa1 and Hoxb1 reveal new roles in regulation of early hindbrain patterning Development, January 3, 1998; 125(6): 1025 - 1036. [Abstract] [PDF]
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A Gavalas, M Studer, A Lumsden, F. Rijli, R Krumlauf, and P Chambon Hoxa1 and Hoxb1 synergize in patterning the hindbrain, cranial nerves and second pharyngeal arch Development, January 3, 1998; 125(6): 1123 - 1136. [Abstract] [PDF]
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