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  • Author or Editor: Keith E. Murphy x
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Abstract

Objective—To elucidate the pathogenesis of Greyhound meningoencephalitis by evaluating gene expression in diseased brain tissue.

Animals—Cadavers of 3 diseased (8- to 15-month-old) and 3 (10-month-old) control Greyhounds.

Procedures—Samples of RNA were extracted from brain tissue of all dogs and evaluated by use of a canine-specific microarray.

Results—A unique profile involving significant alterations in expression of 21 genes was evident in diseased dogs, compared with expression in control dogs. Most genes with up-regulated expression were related to immune function, with the remaining genes involved in ligand binding, signal transduction, transcriptional regulation, and formation and transportation of proteins including enzymes. Of notable involvement were genes encoding for major histocompatibility complexes, small inducible cytokine A5 precursor, myxovirus-resistant proteins, and components of the classical complement pathway, which are all genes common to pathways of viral infections and autoimmunity.

Conclusions and Clinical Relevance—Although results of microarray analysis did not clearly define a potential etiology of Greyhound meningoencephalitis, they did highlight a consistent gene alteration signature that would suggest a common etiology and pathogenesis for this condition.

Full access
in American Journal of Veterinary Research

Abstract

Objective—To develop a set of microsatellite markers, composed of a minimal number of these markers, suitable for use in forensic genetic investigations in dogs.

Sample Population—Blood, tissue, or buccal epithelial cells from 364 dogs of 85 breeds and mixed breeds and 19 animals from related species in the family Canidae.

Procedure—61 tetranucleotide microsatellite markers were characterized on the basis of number and size of alleles, ease of genotyping, chromosomal location, and ability to be coamplified. The range in allele size, number of alleles, total heterozygosity, and fixation index for each marker were determined by use of genotype data from 383 dogs and related species. Polymorphism information content was calculated for several breeds of dogs.

Results—7 microsatellite markers could be coamplified. These markers were labeled with fluorescent dyes, multiplexed into a single reaction, and optimized for resolution in a commercial genetic analyzer. The multiplex set was used to identify sires for 2 mixed litters. The test was not species specific; genotype information collected for wolves, coyotes, jackals, New Guinea singing dogs, and an African wild dog could not distinguish between these species.

Conclusions and Clinical Relevance—This set of 7 microsatellite markers is useful in forensic applications (ie, identification of dogs and determination of parentage) in closely related animals and is applicable to a wide range of species belonging to the family Canidae. (Am J Vet Res 2004;65:1446–1450)

Full access
in American Journal of Veterinary Research

Abstract

Objective—To identify the quantitative trait loci (QTL) that contribute to hip dysplasia in dogs.

Animals—192 Labrador Retrievers.

Procedures—Hip dysplasia was measured by use of the Norberg angle (NA), dorsolateral subluxation (DLS) score, and distraction index (DI). Genome-wide screening was conducted by use of 276 unique microsatellites. Linkage analysis was performed with a variance-based linear model. Logarithm of the odds (LOD) scores were reported when values were > 2.0.

ResultsCanis familiaris autosomes (CFAs) 01, 02, 10, 20, 22, and 32 harbored significant QTL at LOD scores > 2.0. Among the 6 QTL, the QTL on CFA02 had not been reported to harbor QTL for hip dysplasia. The highest LOD score of 3.32 on CFA20 contributed to the second principal component of the DLS score and NA of the right hip joint. The QTL that was mapped on CFA01 (LOD score of 3.13 at 55 centimorgans) was located on the same chromosome reported to harbor a QTL for hip dysplasia in Portuguese Water Dogs and German Shepherd Dogs. In this study, CFAs 10, 20, 22, and 32 harbored QTL for hip dysplasia that have been identified in a Labrador Retriever–Greyhound pedigree and in German Shepherd Dogs.

Conclusions and Clinical Relevance—Multiple QTL were clearly involved with hip dysplasia. Identification of these QTL will enable fine-resolution mapping and subsequent assessment of candidate genes within the refined intervals to enable researchers to develop genetic screening tests and preventative and novel therapeutic regimens.

Full access
in American Journal of Veterinary Research

Abstract

Objective—To identify microsatellite markers linked to progressive retinal atrophy (PRA) in American Eskimo Dogs.

Sample Population—Blood samples or buccal epithelial cells from 66 American Eskimo Dogs, including 53 PRA-unaffected and 13 PRA-affected dogs.

Procedure—The genotypes of unaffected and affected dogs were determined by use of microsatellite markers spanning canine chromosome 9 (CFA09). Homozygosity mapping was used to detect linkage between markers and the gene locus for PRA.

Results—Significant allelic association between marker alleles and the gene locus for PRA was detected for GALK1 and TK1, indicating linkage between these markers and the causative gene locus for PRA.

Conclusions and Clinical Relevance—These data indicate that PRA in American Eskimo Dogs is located on CFA09 and allow for the development of a microsatellite-based test to identify carrier (unaffected) and affected dogs before clinical signs appear. (Am J Vet Res 2005;66:1900–1902)

Full access
in American Journal of Veterinary Research

Abstract

Objective—To identify quantitative trait loci (QTL) associated with osteoarthritis (OA) of hip joints of dogs by use of a whole-genome microsatellite scan.

Animals—116 founder, backcross, F1, and F2 dogs from a crossbred pedigree.

Procedures—Necropsy scores and an optimized set of 342 microsatellite markers were used for interval mapping by means of a combined backcross and F2 design module from an online statistical program. Breed and sex were included in the model as fixed effects. Age of dog at necropsy and body weight at 8 months of age were also included in the model as covariates. The chromosomal location at which the highest F score was obtained was considered the best estimate of a QTL position. Chromosome-wide significance thresholds were determined empirically from 10,000 permutations of marker genotypes.

Results—4 chromosomes contained putative QTL for OA of hip joints in dogs at the 5% chromosome-wide significance threshold: chromosomes 5, 18, 23, and 31.

Conclusions and Clinical Relevance—Osteoarthritis of canine hip joints is a complex disease to which many genes and environmental factors contribute. Identification of contributing QTL is a strategy to elucidate the genetic mechanisms that underlie this disease. Refinement of the putative QTL and subsequent candidate gene studies are needed to identify the genes involved in the disease process.

Full access
in American Journal of Veterinary Research

Abstract

Objective—To assess the heritability of pancreatic acinar atrophy (PAA) in German Shepherd Dogs (GSDs) in the United States.

Animals—135 GSDs belonging to 2 multigenerational pedigrees.

Procedure—Two multigenerational pedigrees of GSDs with family members with PAA were identified. The clinical history of each GSD enrolled in the study was recorded, and serum samples for canine trypsinlike immunoreactivity (cTLI) analysis were collected from 102 dogs. Dogs with a serum cTLI concentration ≤ 2.0 µg/L were considered to have exocrine pancreatic insufficiency (EPI) and were assumed to have PAA.

Results—Pedigree I consisted of 59 dogs and pedigree II of 76 dogs. Serum cTLI concentrations were measured in 48 dogs from pedigree I and 54 dogs from pedigree II. A total of 19 dogs (14.1%) were determined to have EPI, 9 in pedigree I (15.3%) and 10 in pedigree II (13.6%). Of the 19 dogs with EPI, 8 were male and 11 were female.

Conclusion and Clinical Relevance—Evaluation of data by complex segregation analysis is strongly suggestive of an autosomal recessive mode of inheritance for EPI in GSDs in the United States. (Am J Vet Res 2002;63:1429–1434)

Full access
in American Journal of Veterinary Research

Abstract

In collaboration with the American College of Veterinary Pathologists

Open access
in Journal of the American Veterinary Medical Association