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 frame with the first exon of Hoxb8. These mice express a fusion protein with a functional beta-galactosidase activity instead of Hoxb8. Mutant embryos were analyzed for anatomical changes. The results indicate that Hoxb8 is not an indispensable regulator of A-P patterning in the forelimb, unlike suggested by our Hoxb8 gain of function experiments (Charité J, DeGraaff W, Shen S, Deschamps J. Cell 1994;78:589-601). The null mutant phenotypic traits include degeneration of the second spinal ganglion (C2), an abnormality opposite to the alteration in the gain of function transgenic mice. Subtle changes in the thoracic part of the vertebral column were observed as well. Adult homozygous mutants exhibit an abnormal clasping reflex of the limbs.
van den Akker
E
E
Hubrecht Laboratory, The Netherlands Institute for Developmental Biology, Uppsalalaan 8, 3584 CT, Utrecht, Netherlands.
Reijnen
M
M
Korving
J
J
Brouwer
A
A
Meijlink
F
F
Deschamps
J
J
D000818:Animals; D019521:Body Patterning / Q000235:genetics; D005091:Exons; D005121:Extremities / Q000503:physiopathology*; D005260:Female; D005727:Ganglia, Spinal / Q000002:abnormalities / Q000196:embryology*; D018507:Gene Expression Regulation, Developmental; D020868:Gene Silencing; D018398:Homeodomain Proteins / Q000235:genetics* / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008815:Mice, Inbred Strains; D008817:Mice, Mutant Strains; D009069:Movement Disorders / Q000235:genetics; D011993:Recombinant Fusion Proteins / Q000235:genetics / Q000378:metabolism; D012021:Reflex, Abnormal / Q000235:genetics*; D013131:Spine / Q000002:abnormalities; D001616:beta-Galactosidase / Q000235:genetics
D018398:Homeodomain Proteins; C095822:Hoxb8 protein, mouse; D011993:Recombinant Fusion Proteins; D001616:beta-Galactosidase