Wang X, Miller A B, Lepine A J, Scott J D, Murphy K E
Department of Microbiology and Molecular Cell Sciences, University of Memphis, TN 38152-6041, USA.
J Hered. 1999 Jan-Feb;90(1):99-103. doi: 10.1093/jhered/90.1.99.
Canine hip dysplasia is a heritable developmental disease resulting, in part, from increased laxity in hip joints and is a precursor to degenerative joint disease. Identification of genetic markers linked to joint laxity would foster development of more accurate diagnostic methods, facilitate identification of the disease gene(s), and supplement efforts to establish physical/genetic maps of the canine genome. Work presented here describes analysis of randomly amplified polymorphic DNA in the search for markers which cosegregate with increased joint laxity in Canis familiaris, the domestic dog. The Boykin spaniel, a highly inbred breed afflicted with an extremely high incidence of hip dysplasia, served as a model for study of canine hip dysplasia. Only 5% of 200 random primers revealed significant polymorphisms within this breed. However polymorphisms were detected in seemingly nonpolymorphic amplification products when digested with restriction enzymes. Restriction digestion revealed polymorphisms in 15% of the monomorphic amplification products. Among the primers that revealed polymorphisms, one primer correctly identified 9 of 12 dogs with regard to joint laxity. However, extensive evaluation is required before any assertion can be made regarding linkage of this marker to joint laxity. Of interest, another primer amplified a genomic segment unique to the canine Y chromosome.
