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Agouti

Agouti controls the restriction of true black pigment (eumelanin) in the coat. Horses with the normal agouti gene have the genotype A/A or A/a. Horses without a normal agouti gene have the genotype a/a, and if they are capable of producing black pigment, it is uniformly distributed throughout the coat.^[1] A third option, A^t, restricts black pigment to a black-and-tan pattern called seal brown.^[2] This allele is recessive to A and dominant to a, such that horses with the genotype A/A^t appear bay, while A^t/A^t and A^t/a horses are seal brown in the presence of a dominant Extension allele E.

The Agouti locus is occupied by the Agouti signalling peptide (Asip) gene, which encodes the eponymous protein (ASIP). Agouti signalling peptide is a paracrine signaling molecule that competes with alpha-melanocyte stimulating hormone (α-MSH) for melanocortin 1 receptor proteins (MC1R). MC1R relies on α-MSH to halt production of red-yellow pheomelanin, and initiate production of black-brown eumelanin in its place.^[3]

In many species, successive pulses of ASIP block contact between α-MSH and MC1R, resulting in alternating production of eumelanin and pheomelanin; hairs are banded light and dark as a result. In other species, Asip is regulated such that it only occurs in certain parts of the body. The light undersides of most mammals are due to the carefully controlled action of ASIP. In mice, two mutations on Agouti are responsible for yellow coats and marked obesity, with other health defects. Additionally, the Agouti locus is the site of mutations in several species that result in black-and-tan pigmentations.^[4]^[5] In normal horses, ASIP restricts the production of eumelanin to the "points": the legs, mane, tail, ear edges, etc. In 2001, researchers discovered a recessive mutation on Asip that, when homozygous, left the horse without any ASIP. As a result, horses capable of producing true black pigment had uniformly black coats.^[6] One genetics testing lab began offering a test for A^t,^[2] but it was later found to be inaccurate and is no longer offered.

Agouti phenotypes

A/A wildtype, homozygous. Visually, the horse may be bay, buckskin, bay dun, amber champagne, and so on, or gray, or any member of the red family. However, such a horse will never be black, grullo, and so on, nor will a homozygous A horse ever produce uniform-black offspring or seal brown offspring.
A/A^t Heterozygous Agouti. Visually Indistinguishable from the homozygous A Bay colored horse. Such horses are unable to produce Black colored foal.
A/a wildtype, Heterozygous Agouti. Visually Indistinguishable from homozygous A. With the right partner, such horses have the ability to produce Black colored foals.
A^t/A^t Theorized mutation of Agouti known as Brown or Seal Brown. In the absence of a dominant E allele. The presence of the theorized Agouti mutation A^t A Theorized mutation of the Agouti gene which is responsible in modifying the coat by restricting eumelanin in the coat to the points of the horse (Legs, ears, mane and tail). In the presence of at least 1 dominant E allele, the theorized mutation results in what is a [Brown/Seal Brown (horse)|brown] coat color. The Color is that of a Brown to almost black color body with light brown to tan hairs on the muzzle, around the eyes and on the withers of the horse. Variations of the theorized brown/seal brown coat color include: Dark Buckskin (also referred to as Smokey Brown) - A brown based horse with 1 cream gene; Perlino - a brown horse with 2 cream genes; Brown Dun - A brown based horse with at least 1 dun gene; and Sable Champagne - A brown based coat with at least 1 Champagne gene.
A^t/a Indistinguishable from the homozygous Brown. Such horses have the ability to produce Black and black based colored horses.
a/a homozygous recessive. Visually, in the presence of a dominant E allele, the horse's coat will be black. With the presence of a single cream gene, the coat will be smoky black, and with the presence of 2 cream genes the coat will be smoky cream. The Presence of at least 1 Dun gene will result in a grullo colored coat (Black Dun). The presence of at least 1 Champagne gene will result in classic champagne coat, and the presence of the at least 1 Silver gene will turn the black coat into a silver black coat, and so on.

References

^ "Gene A: Distribution of Black Pigmented Hair". UC Davis Veterinary Genetics Laboratory. Retrieved 2009-05-26.
^ ^a ^b "Equine Testing Services". Pet DNA Services of AZ. Archived from the original on 2009-05-22. Retrieved 2009-05-26. {{cite web}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help)
^ [1] Online Mendelian Inheritance in Man, OMIM (TM). Johns Hopkins University, Baltimore, MD. MIM Number: {600201}: {9/4/2008}:. World Wide Web URL: https://www.ncbi.nlm.nih.gov/omim/
^ Drogemuller, C; Giese, A.; Martins-Wess, F.; Wiedemann, S.; Andersson, L.; Brenig, B.; Fries, R.; Leeb, T (2006). "The mutation causing the black-and-tan pigmentation phenotype of Mangalitza pigs maps to the porcine ASIP locus but does not affect its coding sequence". Mammalian Genome. 17 (1): 58–66. doi:10.1007/s00335-005-0104-1. PMID 16416091.
^ "a^t Spontaneous Allele Detail". The Jackson Laboratory. 2009-05-23. Retrieved 2009-05-26.
^ Rieder, S et al 2001. "The 11-bp deletion in ASIP exon 2 (ADEx2) alters the amino acid sequence and is believed to extend the regular termination signal by 210 bp to 612 bp. The frameshift initiated by the deletion results in a novel modified agouti-signaling-protein. ADEx2 was completely associated with horse recessive black coat color (A^a/A^a) in all horses typed so far."

[VGLintro-A-1] "Gene A: Distribution of Black Pigmented Hair". UC Davis Veterinary Genetics Laboratory. Retrieved 2009-05-26.

[PETDNAAZ-2] "Equine Testing Services". Pet DNA Services of AZ. Archived from the original on 2009-05-22. Retrieved 2009-05-26. {{cite web}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help)

[OMIM-ASIP-3] [1] Online Mendelian Inheritance in Man, OMIM (TM). Johns Hopkins University, Baltimore, MD. MIM Number: {600201}: {9/4/2008}:. World Wide Web URL: https://www.ncbi.nlm.nih.gov/omim/

[drogemuller2006-4] Drogemuller, C; Giese, A.; Martins-Wess, F.; Wiedemann, S.; Andersson, L.; Brenig, B.; Fries, R.; Leeb, T (2006). "The mutation causing the black-and-tan pigmentation phenotype of Mangalitza pigs maps to the porcine ASIP locus but does not affect its coding sequence". Mammalian Genome. 17 (1): 58–66. doi:10.1007/s00335-005-0104-1. PMID 16416091.

[AtJAX-5] "a^t Spontaneous Allele Detail". The Jackson Laboratory. 2009-05-23. Retrieved 2009-05-26.

[rieder2001-3-6] Rieder, S et al 2001. "The 11-bp deletion in ASIP exon 2 (ADEx2) alters the amino acid sequence and is believed to extend the regular termination signal by 210 bp to 612 bp. The frameshift initiated by the deletion results in a novel modified agouti-signaling-protein. ADEx2 was completely associated with horse recessive black coat color (A^a/A^a) in all horses typed so far."

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