Targeted inactivation of Hoxb8 affects survival of a spinal ganglion and causes aberrant limb reflexes

Hoxb8 mutant mice were generated by inserting the lacZ coding sequence in F rame with the first exon of Hoxb8. These mice express a fusion protein with a functional P-galactosidase activity instead of Hoxb8, Mutant embryos wer e analyzed for anatomical changes. The results indicate that Hoxb8 is not a n indispensable regulator of A-P patterning in the forelimb, unlike suggest ed by our Hoxb8 gain of function experiments (Charite J, DeGraaff W, Shen S , Deschamps J. Cell 1994;78:589-601). The null mutant phenotypic traits inc lude degeneration of the second spinal ganglion (C2), an abnormality opposi te to the alteration in the gain of function transgenic mice. Subtle change s in the thoracic part of the vertebral column were observed as well. Adult homozygous mutants exhibit an abnormal clasping reflex of the limbs. (C) 1 999 Elsevier Science Ireland Ltd. All rights reserved.