reddish-brown color uniform over entire body other thanmarkings
Phenotype
Body
reddish-brown
Head and Legs
same as body, occasionally lighter
Mane and tail
flaxen to brown
Skin
Usually black, may be lighter at birth in some breeds
Eyes
Brown, eyes may be lighter at birth
Chestnut is ahair coat color ofhorses consisting of a reddish-to-brown coat with amane and tail the same or lighter in color than the coat. Chestnut is characterized by the absolute absence of trueblack hairs. It is one of the most commonhorse coat colors, seen in almost every breed of horse.
Chestnut is a very common coat color but the wide range of shades can cause confusion. The lightest chestnuts may be mistaken forpalominos, while the darkest shades can be so dark they appearblack. Chestnuts have dark brown eyes and black skin, and typically are some shade of red or reddish brown. The mane, tail, and legs may be lighter or darker than the body coat, but unlike thebay they are never truly black. Like any other color of horse, chestnuts may have pink skin with white hair where there arewhite markings, and if such white markings include one or both eyes, the eyes may be blue. Chestnut foals may be born with pinkish skin, which darkens shortly afterwards.[1][better source needed]
Chestnut is produced by arecessive gene. Unlike many coat colors, chestnut can be true-breeding; that is, assuming they carry no recessive modifiers likepearl ormushroom, the mating between two chestnuts will produce chestnut offspring every time. This can be seen in breeds such as theSuffolk Punch andHaflinger, which are exclusively chestnut. Other breeds including theAmerican Belgian Draft andBudyonny are predominantly chestnut. However, a chestnut horse need not have two chestnut parents. This is especially apparent in breeds like theFriesian horse andAriegeois pony which have been selected for many years to be uniformlyblack, but on rare occasions still produce chestnut foals.
Chestnuts can vary widely in shade and different terms are sometimes used to describe these shades, even though they are genetically indistinguishable. Collectively, these coat colors are usually called "red" by geneticists.
A basic chestnut or "red" horse has a solid copper-reddish coat, with a mane and tail that is close to the same shade as the body coat.
Sorrel is a term used by Americanstock horse registries to describe red horses with manes and tails the same shade or lighter than the body coat color. In these registries, chestnut describes the darker shades of red-based coats.[2]
A liver chestnut
Liver chestnut ordark chestnut are not a separate genetic color, but a descriptive term. The genetic controls for the depth of shade are not presently understood. Liver chestnuts are a very dark-reddish brown. Liver chestnuts are included in the term "dark chestnut." The darkest chestnuts, particularly common in theMorgan horse, may be indistinguishable from trueblack without very careful inspection. Often confusingly called "black chestnuts", they may be identified by small amounts of reddish hair on the lower legs, mane and tail, or byDNA or pedigree testing. Recently, it has been suggested that the trait or traits that produce certain darker shades of chestnut andbay, referred to as"sooty" coloration follow arecessive mode of inheritance.[3]
This light, flaxen, mealy chestnut Haflinger might be mistaken for a palomino
Flaxen chestnut andblond chestnut are terms that describe manes and/or tails that areflaxen, or significantly lighter than the body color. Sometimes this difference is only a shade or two, but other flaxen chestnuts have near-white or silverish manes and tails.Haflingers are exclusively of this shade. It is considered desirable in other breeds, though the genetic mechanism is not fully understood. Some flaxen chestnuts can be mistaken forpalominos and have been registered in palomino color registries.
Pangaré ormealy is thought to be controlled by a single gene, unrelated to chestnut color, and produces distinct characteristics common towild equids: pale hairs around the eyes and muzzle and a pale underside.Haflingers andBelgians are examples of mealy chestnuts. The flaxen characteristic is sometimes associated withpangaré.
Chestnut is considered a "base color" in the discussion of equine coat color genetics. Additional coat colors based on chestnut are often described in terms of their relationship to chestnut:
Palominos have a chestnut base coat color that is genetically modified to a golden shade by a single copy of theincomplete dominantcream gene. Palominos can be distinguished from chestnuts by the lack of true red tones in the coat; even the palest chestnuts have slight red tints to their hair rather than gold. The eyes of chestnuts are usually dark brown, while those of a palomino are sometimes a slightly lighter amber.[4] Somecolor breed registries that promote palomino coloring have accepted flaxen chestnuts because registration is based on a physical description rather than a genetic identity.
Cremellos have a chestnut base coat and homozygous (two copies) for thecream gene. They have a cream-colored coat, blue eyes and lightly pigmented pink skin.
Red duns have a chestnut base coat with thedun gene (one or two copies). Their body color is pale, dusty tan shade that resembles the light undercoat color of a body-clipped chestnut but with a bold, dark dorsal stripe in dark red, a red mane, tail and legs. They may have additionalprimitive markings, which distinguish a red dun from a light or body-clipped chestnut.
Gold champagnes have a chestnut base coat with thechampagne gene (one or two copies). They resemble a palomino, or they may be an all-over apricot shade, but can be distinguished from other colors by amber or green eyes and lightened skin color with freckling.
Red or"strawberry" roans have a chestnut base coat with theclassic roan gene (one or two copies).
Combinations of multipledilution genes do not always have consistent names. For example, "dunalinos" are chestnuts with both thedun gene and one copy of thecream gene.
Bay horses also have reddish coats, but they have a black mane, tail, legs and otherpoint coloration. The presence of true black points, even if obscured bywhite markings, means that a horse is not chestnut.
Seal brown ordarkbay horses are not chestnut but may be confused with a liver chestnut. Those unfamiliar with horse coat color terminology often call most horses "brown". including chestnuts. Brown, which may be difficult to distinguish visually from darkbay, is always accompanied by black points. Liver chestnuts, in particular, are mistakenly called brown or "seal brown".
Silver bay horses typically have chocolate- to red-brown bodies with silvered mane, tail, and legs. The flat reddish-brown color and lack of easily identified black points can confuse even knowledgeable horse persons. Silver dapple horses usually hint at black or dark gray pigment at the roots of the mane and tail, and where their silver points end on the legs. Silvers look a bit "off"-chestnut. To further confuse matters, some flaxen chestnuts have silverish streaks in their manes and tails. However,genetic testing can clarify matters.
A young chestnut foal, showing slight lightening of skin, possibly related to thepheomelaninistic characteristics of chestnut genetics. The skin will darken as the foal becomes older. Skin depigmentation is not always seen in chestnut foals.A chestnut foal with body-clipped head and neck, showing two-toned hair shaft, lighter at the roots
The chestnut or sorrel color, genetically considered "red", is caused by one of tworecessivealleles at theextensionlocus (genetics).Extension has three known alleles: thewildtype "E", necessary for thebay andblack coat colors, plus twomutations "e" and "ea", both of which are capable of causing the chestnut color. Each individual horse has two copies of theextension gene. If either copy is "E", then the horse will be bay- or black-based. But if the two copies are any combination of "e" and "ea" (e/e, e/ea, or ea/ea), then the horse will be red-based. Alternate extension "ea" is rare and there is no known difference in appearance between it and the more common "e".[5][6]
Because the red color is recessive, two bay or black parents can produce a chestnut foal if both carry "e" or "ea". However, two chestnut parents cannot produce a bay or black foal.
Theextensionlocus (genetics) is found onchromosome 3 (ECA3) and is part of the gene that codes for the equinemelanocortin 1 receptor (MC1R). This receptor is part of a signalling pathway which when activated causesmelanocytes to produceeumelanin, or black pigment, instead ofpheomelanin, or red pigment.[7] The two mutant alleles "e" and "ea" code for dysfunctional receptors unable to activate this pathway, so absent "E", only red pigment can be produced. At least one copy of the functional "E" allele is required to activate the signal and produce black pigment. In general, alleles that create fully functional MC1R proteins are inheriteddominantly and result in a black-based coat color ("E"), while mutated alleles that create "dysfunctional" MC1R are recessive and result in a lighter coat color ("e").
Normally MC1R would bind to theMelanocyte-stimulating hormone (MSH) which is released by thepituitary gland[7] and stimulates the production and release of melanin in skin and hair. Red hair color in horses ("e") is created by amissense mutation in the code for MC1R,[8] which results in a protein that cannot bind to MSH. When only mutant copies ("e) of the gene are available, non-functional MC1R proteins are produced. As a result, no black pigment is deposited into the hair and the entire coat is red-based. However, the skin of chestnut horses is still generally black, unless affected by other genes. Some chestnut foals are also born with lighter eyes and lightened skin, which darken not long after birth. This is not the same as the blue eyes and pink skin seen at birth in foals carrying thechampagne gene. It is a genetic mechanism not fully understood, but may be related to the pheomelanistic characteristics of "e".
Though "E" allows the production of black pigment, it can also allow for red pigment in some parts of the animal as seen inbay horses. This happens when it is locallyantagonized by theagouti signalling peptide (ASIP), oragouti gene, which "suppresses" black color and allows some red pigment to be formed.
^"General Glossary". American Quarter Horse Association. Archived fromthe original on July 7, 2011. RetrievedDecember 25, 2010.
^Henner, J; PA Poncet; L Aebi; C Hagger; G Stranzinger; S Rieder (August 2002). "Horse breeding: genetic tests for the coat colors chestnut, bay and black. Results from a preliminary study in the Swiss Freiberger horse breed".Schweizer Archiv für Tierheilkunde.144 (8):405–412.doi:10.1024/0036-7281.144.8.405.The statistical analysis of 1369 offspring from five stallions indicate, that darker shades of basic color phenotypes (dark chestnut, dark bay) follow a recessive mode of inheritance in the Franches-Montagnes horse breed.
^Locke, MM; LS Ruth; LV Millon; MCT Penedo; JC Murray; AT Bowling (2001). "The cream dilution gene, responsible for the palomino and buckskin coat colors, mapes to horse chromosome 21".Animal Genetics.32 (6):340–343.doi:10.1046/j.1365-2052.2001.00806.x.PMID11736803.The eyes and skin of palominos and buckskins are often slightly lighter than their non-dilute equivalents.
^"Red Factor". UC Davis Veterinary Genetics Laboratory. RetrievedOctober 5, 2023.
^Wagner, H-J; Reissmann, M. (2000). "New polymorphism detected in the horse MC1R gene".Animal Genetics.31 (4):289–290.doi:10.1046/j.1365-2052.2000.00655.x.PMID11086549.Within the tested chestnut coloured horse population, no association between both allelese respectivelyea and one of the variable chestnut phenotypes could be observed. Different individuals regarding to the shade of their chestnut coat colour were found in every group of the genotypes (e/e), (e/ea) and (ea/ea).
^Marklund, L.; M. Johansson Moller; K. Sandberg; L. Andersson (1996). "A missense mutation in the gene for melanocyte-stimulating hormone receptor (MC1R) is associated with the chestnut coat color in horses".Mammalian Genome.7 (12):895–899.doi:10.1007/s003359900264.PMID8995760.S2CID29095360.
