One of the most common skeletal affections in humans is achondroplasia, a s
hort-limbed dwarfism that is, in most cases, caused by mutations in the tra
nsmembrane domain of the fibroblast growth factor receptor-3 (FGFR-8) gene.
Due to the lack of sufficient radiological, genetic, and molecular studies
, most types of skeletal anomalies in dogs are classified as achondroplasia
. To initiate the molecular characterization of some osteochondrodysplastic
dog breeds, we obtained the DNA sequence of the transmembrane domain of th
e FGFR-3 gene from the dachshund, basset hound, bulldog, and German shepher
d dogs. All 4 breeds showed no mutation in the evaluated region. This indic
ates that the mutation responsible for the osteoehondrodysplastic phenotype
in the tested dog breeds lies either elsewhere in the FGFR3 gene or in oth
er ones involved in the formation and development of endochondral bone.