Background

Canine hip dysplasia is a developmental orthopedic disease. Because hip dysplasia is passed on genetically, there is perhaps an even graver consequence of the disease remaining undiscovered. To reduce the prevalence of hip dysplasia, genetic aetiology should be unveiled.

Aims

To isolate, characterize and screen canine SLC26A2 in dogs with hip dysplasia.

Methods

The canine SLC26A2, a good candidate for unraveling canine dystrophic bone diseases such as hip dysplasia was isolated and characterized using molecular biological methods. The coding exons of canine SLC26A2 was then screened using direct sequencing method in German Shepherd dog family with hip dysplasia.

Results

We firstly isolated and characterized the canine SLC26A2 (known as diastrophic dysplasia sulfate transporter; DTDST) gene. This canine homologue has high homology in genomic structure and functional domains to other SLC26A2 across a number of different species. In genetic screening of the coding exons of SLC26A2, we could not identify any mutations in affected German Shepherd dog family.

Conclusion

Given the critical role of SLC26A2 in sulfation of proteoglycans in cartilage matrix as seen in human dystrophic bone diseases, the availability of the canine SLC26A2 provides a good starting point for identifying mutations that may be responsible for certain forms of dystrophic bone diseases in dogs. However, in this screen, we could not find any mutations and polymorphisms associated with phenotypic consequence.