The silver, silver dapple, chocolate flax or Taffy gene
silver, silver dapple, chocolate flax and Taffy are all caused by the same gene
Silver, or silver dapple is the common term used for horses with a dilution gene that works to dilute black pigment. The gene usually causes a partial lightening of black pigment in the body coat and a more extreme lightening (or “silvering”) of the mane and tail. The dilution effect is often, but not necessarily, accompanied by dappling.
The name silver dapple should probably be reserved for horses that have both dapples and a silver mane and tail. Not all horses with the dilution gene look like that. Similarly the term "chocolate" is often used in the Rocky Mountain Horse breed, but doesn’t describe the color of all horses with the dilution gene. Taffy is a more general term that’s sometimes used and is probably a better one since the dilution gene can occur in horses of any color of base coat, giving different visual affects accordingly, but it isn't generally accepted, and the term silver is now more usual. The silver gene is denoted by the symbol “Z” and the dilution allele is dominant over non-dilution.
The silver gene occurs in several breeds, including Connemaras, Saddlebreds and Mustangs. In the United States it's found most commonly in the gaited Mountain Horse breeds, including the Rocky Mountain Horse, the Kentucky Mountain horse and the Missouri Fox Trotter. It also occurs in Icelandic Ponies, Shetland Ponies, the Welsh Pony and some miniature horse breeds.
The silver gene is said not to affect chestnut horses so that from time to time a chestnut horse carrying silver can have an unexpected color of foal. However I know of some miniature horses breeders who believe it does have a subtle affect, and that they can tell which of their chestnut horses carries silver on the basis of what they look like.
Silver changes black body coat pigment to a color that ranges from a creamy chocolate to a deep bluish gray to a deep orangey red. Manes and tails are often, but not always, turned to white or very nearly white, often said to be “silvery”. Such manes and tails are often mistaken for flaxen, but unlike with flaxen the roots are dark. Silver horses may often have a dark mask on the face, similar to that which occurs in dun horses. They may also have striped hooves, and often have light blonde or white eyelashes, especially as foals.
Bay horses with the silver gene are turned to a bright reddish orange with rich chocolate or tan points. The mane and tail are blonde, sometimes streaked with silvery black hairs. They may look like flaxen chestnut but their manes and tails have dark rather than flxen roots.
Brown horses with silver are unusual and quite stunning. Their coats are a dark bluish gray, like slate, but with an orangish highlights. The mane and tail contains an admixture of black and blonde hairs, making them appear silvery.
Black horses with silver can either be silver dapple itself or chocolate (called chocolate flax in some breeds). Both are most attractive colors. Silver dapple horses have a sepia brown colored body with cream or flaxen dapples, which are especially striking on horses with a darker coats. Their manes and tails are flaxen or ivory. Dark silvers without dapples are called chocolate or choclate flax, and are especially common among the Rocky Mountain breed of gaited horses. Their manes and tails may be flaxen or silver, but can also be somewhat darker chocolatey color.
The silver gene has been identified
The gene responsible for the Silver dilution is in the PMEL17 gene on horse chromosome 6 (Brunberg et al, 2006, Reissmann et al, 2007).
A few mutations of the PMEL17 gene have been found, and some are entirely associated with silver. Most are situated within a non-coding regions (introns)and either have no affect on the structure of the PMEL17 protein, or are otherwise thought to be non-causative.
Both Brunberg et al (2006) and Reissmann et al (2007) seem to have independently found mutations in exon 11 and intron 9, completely associated with silver (an exon is a coding region of the gene). A silver dilution test assays for mutation sites in both places.
Pmel17 is a membrane protein in melanosomes that is active from quite early in embryonic development. It is active in mature melanosomes also, and is involved with the production of the black pigment eumelanin. Pmel17 mutations are known to be related to pigmentation in other animals, including premature silvering in mice, diluted and white plumage in chickens, and the merle dilution in dogs. The merle coat in dogs is associated with deafness and eye disorders. Pmel17 mutations in zebrafish are also associated with vision defects.
Anterior segment dysgenesis in silver dapple horses
Anterior segment dysgenesis is a genetic eye defect of the horse. Affected horses may have a variety of abnormalities of the eyes, including lesions and cysts, with defects in the iris, cornea, lens, and eyelids (Ramsey et al, 1999, Ewart et al, 2000). They do not respond normally to light, but affected horses don’t usually seem to have significantly impaired vision. Vets had noticed that anterior segment dysgenesis is more common in horses with the silver dapple gene than it is in other horses.
Ewart et al (2000) performed a study to determine wether anterior segment dysgenesis was inherited (Ewart et al., 2000). They studied the eye phenotypes and pedigree information from 516 horses in an extended Rocky Mountain Horse family. They found that anterior segment dysgenesis was inherited in a codominant manner in these horses. They concluded that it was being caused by a single gene, with cysts expressed in heterozygous horses and complex lesions expressed in the homozygous horses. Only in homozoygous horses was the disorder potentially a problem. Such horses should be bred to non Taffys to avoid passing the condition on to their foals. Nonpenetrance of the cyst phenotype appeared to occur in a small number of heterozygotes, and was associated with a particular lineage (i.e. not all heterozygotes showed eye abnormalities).
It would appear that either the silver gene can cause eye abnormalities (i.e. it has pleiotropic affects), or that (in some Rocky Mountain Horses) it is tightly linked to another gene that causes them. Horses with the palest manes and tails were most affected, possibly indicating that homozygous horses are also more diluted in color than heterozygous ones. Anterior segment dysgenesis does occassionally occur in horses of other colors. This might well mean that the gene for it is separate from the silver dapple gene (but closely linked to it). However it is also possible that another gene is involved in these cases.
We now know that there are probably two or more causative silver mutations in the Pmel17 gene. It is possible that one or other of these, or another mutation in the same gene, is associated with ASD.
References
Brunberg E, Andersson L, Cothran G, Sandberg K, Mikko S and Lindgren G. 2006. A missense mutation in PMEL17 is associated with the Silver coat color in the horse. BMC Genetics 7:46.
Ramsey DT, Ewart SL, Render JA, Cook CS, and Latimer CA. 1999. Anterior megalopthalmos and megalocornea of Rocky Mountain Horses. Vet Opthalmol 2, 47-59.
Reissmann, M. Bierwolf, J. and Brockmann, G. A. 2007. Two SNPs
in the SILV gene are associated with silver coat colour in ponies. Animal Genetics 38: 1-6.
Ewart SL, Ramsey DT, Xu J-F, and Meyers DA. 2000. The horse homologue of congenital aniridia conforms to semidominant inheritance. Journal of Heredity 91, 93-98.
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