Breed Distribution and Allele Frequencies of Base Coat Color, Dilution, and White Patterning Variants across 28 Horse Breeds.

Since domestication, horses have been selectively bred for various coat colors and white spotting patterns. To investigate breed distribution, allele frequencies, and potential lethal variants for recommendations on genetic testing, 29 variants within 14 genes were investigated in 11,281 horses from 28 breeds. The recessive chestnut ea allele in melanocortin 1 receptor (MC1R) (p.

Prevalence of clinical signs and factors impacting expression of myosin heavy chain myopathy in Quarter Horse-related breeds with the MYH1 mutation.

Background: The prevalence of clinical signs and factors triggering muscle atrophy and rhabdomyolysis associated with an MYH1 mutation in Quarter Horses and related breeds (QH) remain poorly understood.

Hypothesis/objectives: Determine the prevalence and potential triggers of atrophy and stiffness in horses homozygous reference (N/N), heterozygous (My/N), and homozygous (My/My) for the MYH1 mutation.

Animals: Two-hundred seventy-five N/N, 100 My/N, and 10 My/My QH.

Genetic heterogeneity and diversity of North American golden retrievers using a low density STR marker panel.

Thirty-three autosomal short tandem repeat (STR) markers were used to evaluate genetic heterogeneity and diversity in 525 golden retrievers (GRs). This breed was selected because of its popularity and artificial selection for conformation vs. performance phenotypes.

The effect of genetic bottlenecks and inbreeding on the incidence of two major autoimmune diseases in standard poodles, sebaceous adenitis and Addison's disease.

Background: Sebaceous adenitis (SA) and Addison's disease (AD) increased rapidly in incidence among Standard Poodles after the mid-twentieth century. Previous attempts to identify specific genetic causes using genome wide association studies and interrogation of the dog leukocyte antigen (DLA) region have been non-productive. However, such studies led us to hypothesize that positive selection for desired phenotypic traits that arose in the mid-twentieth century led to intense inbreeding and the inadvertent amplification of AD and SA associated traits.