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[7] [13] [14] Without genetic testing, some carriers are misidentified as having white markings due to another gene, while some are even classified as solids. [3] The presence of this gene in a variety of horse populations in North America suggests that the mutation occurred in early American history, perhaps in a Spanish-type horse. [5] [6] [7]
[16] [17] In horses, both known mutations break the protein and therefore result in red coats. Various mutations in the human MC1R gene result in red hair, blond hair, fair skin, and susceptibility to sunburnt skin and melanoma. [8] Polymorphisms of MC1R also lead to light or red coats in mice, [18] cattle, [19] and dogs, [20] among others.
In 1994, researchers at the University of Pittsburgh, with a grant from horse organizations, [1] isolated the genetic mutation responsible for the problem and developed a blood test for it. Using this test, horses may be identified as: H/H, meaning they have the mutation and it is homozygous. These horses always pass on the disease.
This Thoroughbred stallion (W2/+) has one form of dominant white.His skin, hooves, and coat lack pigment cells, giving him a pink-skinned white coat. Dominant white (W) [1] [2] is a group of genetically related coat color alleles on the KIT gene of the horse, best known for producing an all-white coat, but also able to produce various forms of white spotting, as well as bold white markings.
Champagne is a dominant trait, based on a mutation in the SLC36A1 gene. [1] A horse with either one or two champagne genes will show the effects of the gene equally. However, if a horse is homozygous for a dominant gene, it will always pass the gene on to all of its offspring, while if the horse is heterozygous for the gene, the offspring will not always inherit the color.
The word "points" is given to the mane, tail, lower legs, and ear rims with respect to horse coloration. The overall name given to a horse coat color depends on the color of both the points and the body. For example, bay horses have a reddish-brown body with black points. [3] Point coloration is most often produced by the action of the agouti gene.
A full accounting of this work, detailing the mapping and identification of a mutation in the gene coding for peptidylprolyl isomerase B, was published on May 11, 2007. [11] Concurrent with publication of these results, the Veterinary Genetics Laboratory at UC Davis began offering a genetic test to identify carriers of the disease allele.
The Belgian Draft Horse is one breed in which JEB occurs. Junctional epidermolysis bullosa (JEB) is an inherited disorder that is also known as red foot disease or hairless foal syndrome. [1] JEB is the result of a genetic mutation that inhibits protein production that is essential for skin adhesion. [2]