Gray (Complete)



Gray

Turnaround: 3-5 business daysTurnaround: 7-10 business days

Price: $35.00Price: £35.00

Breeds: All

Description

Gray is the dominant gene responsible for the gradual and progressive de-pigmentation (fading) of the carrying horse. Gray is not considered a base-color or a dilution, but rather a gene which slowly removes pigment from the coat. Gray is considered to be the 'strongest' of all coat modifiers. Gray acts upon any base color regardless of the carrying horse's phenotype. The fading process itself may last for years, but once hair is de-pigmented, the horse's original coloring will never return.

Because gray is a dominant gene, it is always expressed if present. However, the final phenotype of the carrier will vary from horse to horse. Some gray horses fade to full de-pigmentation (almost pure white) whereas others may be ‘flea-bitten.’ The term flea-bitten refers to gray horses with tiny non-faded spots, which are known as ‘flea-bites.’ The gray carrying horse may also experience a de-pigmentation of the skin itself. Before skin is fully faded, it may display ‘mottling.’

Melanomas:

Equine melanomas occur most often in gray horses, and it is expected that at least 80% of gray horses will develop melanoma. When a gray horse develops melanomas, two pigment-producing genes are overexpressed. This means that they produce more melanocytes (a skin cell) than needed, which then spirals into out-of-control growth, or cancerous growth.

Most melanomas found in horses are benign – once present, these benign types of melanoma are not aggressive in their growth and may progress over several years. These typically require little treatment. A melanoma is one of the most common skin tumors seen in a horse or pony.

Malignant melanomas in horses can cause severe problems and can be life-threatening. Problems develop when melanomas are present internally or if they become so large that they ulcerate, bleed, and become infected. Equine melanomas sometimes grow so large that they can cause severe weight loss and/or colic. If a melanoma is situated in an area where a bridle, saddle, head collar or rug might rub, it will be highly uncomfortable for the horse, potentially causing behavioral problems. Infections can also occur.

Genetic Testing of the Gray Gene May Be Beneficial for a Number of Reasons:

For those interested in specifically breeding gray foals, homozygous gray specimens are ideal. This means that the horse has two copies of the gray mutation (G/G). They will always transmit the gray gene when bred, thus guaranteeing eventual gray progeny. In contrast, a heterozygous horse only has one copy (G/g) and there is a 50% chance per foal that the gray gene will be passed to the offspring instead of 100%.

Those looking to 'breed out' the gray modifier to gain non-fading foals (or normal foals) may hope for heterozygous gray horses. Some breed-types have a large percentage of gray stock, which, through historical lineage, may harbor colors and dilutions that are 'hidden' by the masking effect of the gray.

Because gray may cause slow de-pigmentation, it may not be visually apparent whether or not a newborn foal will eventually fade to grey. The de-pigmentation process may take many years. DNA testing is useful in these cases. If a foal is born to one or more gray parents, it can be useful to test whether or not the foal will eventually turn gray without waiting several years for the gray to appear.

Possible Results

Genotype Description
G/G Horse has two copies of the Gray gene and will always produce offspring that will gray.
G/g Horse has one copy of the Gray gene mutation, and will likely gray out over time.
g/g Negative for the Gray gene mutation.

Reference

Nat Genet. 2008 Aug;40(8):1004-9. doi: 10.1038/ng.185. Epub 2008 Jul 20. A cis-acting regulatory mutation causes premature hair graying and susceptibility to melanoma in the horse. Rosengren Pielberg G1, Golovko A, Sundström E, Curik I, Lennartsson J, Seltenhammer MH, Druml T, Binns M, Fitzsimmons C, Lindgren G, Sandberg K, Baumung R, Vetterlein M, Strömberg S, Grabherr M, Wade C, Lindblad-Toh K, Pontén F, Heldin CH, Sölkner J, Andersson L.