Lethal acrodermatitis (LAD) is a rare, autosomal recessive mutation affecting Bull Terriers. The clinical manifestations of the disease are similar to the human disease, acrodermatitis enteropathica. The difference, however, between the disease in Bull Terriers and that in humans is that the symptoms of LAD cannot be ameliorated with zinc supplementation. Recently the genetic defect in the human disease was found to be mutations in the SLC39A gene (ZIP4), which enclodes a zinc uptake transporter located within the brush border membrane of the small intestine, resutling in the reduced zinc absorption observed in these patients. The biochemical lesion associated with LAD is unknown, but is thought to be systemic since neither oral nor parenteral supplementation is effective in treating the clinical signs of zinc deficiency observed in affected dogs. It is the goal of this current proposal to identify proteins that will be useful in diagnosing LAD in affected Bull Terriers as well as identifying the heterozygous condition.