Horse Coat Colors, Dilutions & Patterns – Genetics Guide

Horse coat colors are highly diverse and carry historical, cultural, and even functional significance within many horse breeds. The colors and patterns that mark these breeds result from a complex interaction of several genes that geneticists have studied for centuries.

Genetically, equine coat colors are primarily determined by three base colors: chestnut, black, or bay. All other coat colors and patterns are derived form these base colors through various genetic modifications.

Understanding the genetic inheritance of coat colors helps breeders predict the color of their foals, allowing them to make breeding decisions to select for particularly desirable colors or those that meet their breed’s standard. Additionally, applied genetic theory can even help mitigate color-associated diseases such as lethal white overo syndrome.

Read on to learn more about the genetic basis of equine coat colors, how each coat color develops, the possible interactions between different colors and patterns, and health impacts related to color genes.

Horse Coat Color Genetics

Coat colors are governed by a complex interplay of genes located on different chromosomes. These genes determine the base color of a horse’s coat and influence various modifiers that create the wide range of colors and patterns observed on horse coats.

Horses have 64 chromosomes, organized into 32 pairs, that carry the genetic material (DNA) that determines all inherited traits, including coat color. ^[1] One chromosome in each pair comes from the horse’s dam and one comes from their sire.

Each chromosome has identical gene sites, called loci, consisting of segments of DNA that code for specific proteins or perform different functions. At each gene site, the form of the gene expressed can differ between the two paired chromosomes. ^[1] These different gene forms are called alleles. ^[1]

Gene sites that control color in horses are found throughout the horse’s DNA, on many different chromosomes. ^[1] The horse’s final color depends on the alleles expressed at these different gene sites, and how those different genes interact. ^[1]

For example, all horses have a base color of chestnut, black, or bay. ^[1] Some color genes may dilute these colors, resulting in a paler coat color. ^[1] Other color genes add white, making loud patterns on the horse’s body. ^[1]

Most horse colors follow a Mendelian inheritance pattern, which means that only one gene site controls production of that color. ^[1] There are four key concepts in Mendelian inheritance:

• Dominant alleles
• Recessive alleles
• Homozygosity
• Heterozygosity

Dominant Alleles

Every horse has two gene sites for each color pattern, which means that there are two possible alleles. Some alleles are dominant to the opposing allele, meaning if a dominant allele is present, it will always produce the color that allele is associated with. ^[1]

For example, the allele that produces Dun coloring is dominant, so any horse expressing a Dun allele will have a Dun coat color. ^[1]

Researchers use capital letters to designate dominant alleles. For example, a horse with a Dun allele on both chromosomes can be written as D/D. ^[1]

Recessive Alleles

The alleles that dominant alleles override are recessive alleles. The color associated with these alleles only develops if there are no dominant alleles present. In other words, these colors only occur if both chromosomes have the recessive allele.

For example, the Extension gene, which controls chestnut coloring, only produces chestnut if both alleles are recessive. ^[1]

Lower case letters designate recessive alleles. A chestnut horse would be written as e/e for Extension, since both genes are recessive. ^[1]

Homozygosity and Heterozygosity

Homozygosity describes having the same allele on both chromosomes for any gene site. Therefore, there are two options for homozygosity: homozygous dominant (two dominant alleles) or homozygous recessive (two recessive alleles). ^[1]

Horses that have one dominant and one recessive allele are heterozygous. A heterozygous horse expresses the color associated with the dominant gene, even though a recessive allele is present. ^[1] For example, a horse with heterozygous Dun genes (i.e. D/d) would still be dun, as the dominant D allele would cause dun coloring. ^[1]

Mendelian Inheritance

Only one of the two chromosomes in each pair passes to developing sperm and eggs. ^[1] This means that the resulting foal has a 50% chance of receiving each one of their parent’s chromosomes.

Depending on which alleles are present on these chromosomes, the resulting combinations of dominant and recessive alleles can produce new coat colors, including colors that neither parent has themselves. ^[1]

Geneticists use Punnett squares, a type of table, to calculate the odds of each possible genetic outcome. ^[1] Each table shows the four possibilities for resulting chromosome pairs, and the probability of that outcome can be determined by adding up the number of instances of that outcome in the table and dividing it by 4. ^[1]

Examples of four common interactions for genes with Mendelian inheritance are shown below. ^[1]

Two Homozygous Dominant Horses

In this scenario, there is a 100% chance that the foal will be homozygous dominant like its parents.

Table 1. Punnet square: crossing homozygous dominant parents

Two Homozygous Recessive Horses

In this scenario, there is a 100% chance that the foal will be homozygous recessive like its parents.

Table 2. Punnet square: crossing homozygous recessive parents

Two Heterozygous Horses

In this scenario, there are three possible outcomes. There is a 25% chance that the foal will receive both dominant alleles, making them homozygous dominant. There is also a 25% chance that the foal receives both recessive alleles. There is a 50% chance that the foal receives one dominant and one recessive allele, making them heterozygous like their parents.

Table 3. Punnet square: crossing heterozygous parents

Homozygous Recessive and Homozygous Dominant

In this scenario, there is a 100% chance that the foal will be heterozygous, even though neither of its parents are heterozygous. This is because no matter what scenario occurs, the foal receives one dominant allele from its dam and one from its sire.

Table 4. Punnet square: crossing homozygous parents where one is dominant and the other is recessive

Base Colors

All horses have a base coat color of chestnut, bay, or black. ^[1] When present, other color genes modify these base colors, producing different coat colors. ^[1] Most horses have a bay or chestnut base color. ^[1]

Genetic Control

There are two main genes that control base coloring: Extension and Agouti. ^[1] These genes interact with each other to produce bay, chestnut, and black coloring. ^[1]

The Extension gene controls the production of eumelanin, the pigment that produces black hair coloring. ^[1] Horses that do not have a dominant Extension gene (E) cannot produce black hair. ^[1]

The Agouti gene controls the distribution of black hairs. ^[1] Horses that have a dominant Agouti gene (A) have a restricted distribution of black hairs, resulting in black points. ^[1]

Black points include black legs, a black muzzle, black mane and tail, and often black ear tips. ^[1] Horses that are homozygous recessive for Agouti can produce black hairs anywhere on their body. ^[1]

Bay

Bay horses have a red-brown body color with black points. Bay is currently the most frequent horse color occurring worldwide. ^[1] They are found in virtually every breed, however some breeds select against bay by preventing registration of bay horses. ^[1] One breed, the Cleveland Bay, only allows registration of bay horses. ^[1]

Genetic Control

Genetically, bay horses must have a dominant Extension gene, to allow them to produce black hairs, and a dominant Agouti gene, to restrict the black hairs to their black points. ^[1] Therefore, any combination of E/E or E/e and A/A or A/a will produce a bay horse. ^[1]

Chestnut

Chestnut, also called sorrel, refers to horses with a red-brown body color and a red-brown or flaxen (light yellow) mane and tail. ^[1] They do not have black points, which distinguishes them from bays. ^[1]

Chestnut is the second most common horse color in many breeds worldwide. ^[1] Some breeds, such as the Haflinger and Suffolk Punch, are all chestnut due to genetic selection. ^[1]

Genetic Control

Chestnuts are all homozygous recessive (e/e) for Extension, which causes their body to produce no black hairs. ^[1] Since Agouti only acts on black hair, the interaction of Agouti gene with Extension is irrelevant in a chestnut horse. ^[1] Therefore, any combination of e/e with Agouti will result in a chestnut. ^[1]

Black

Black horses have an entirely black body color. ^[1] Some black horses may have a reddish tinge, particularly during the summer, due to sun bleaching. ^[1]

Black is the least common base color. ^[1] Some breeds select exclusively for black, such as Friesians. ^[1] Other breeds that commonly have black horses include Shires and Percherons. ^[1]

Genetic Control

Black horses are a rare base color because there are only two genetic combinations that can produce black: E/e a/a and E/E a/a. ^[1] The dominant Extension gene allows the horse to produce black hair, while the homozygous recessive Agouti gene prevents restriction of the black hair to the black points. ^[1]

Grey

Grey is often included as a base color for horses, due to how common it is. However, it is technically a pattern of white hairs that affects the entire body. ^[1] Newborn grey foals have a colored coat, and as the horse ages their coat color shifts to white. ^[1]

Greys are very common worldwide, and most breeds have grey as part of their registerable colors. ^[1] Some breeds who select for a specific base color, such as chestnut or bay, do not allow registration of greys. ^[1] Some breeds are almost exclusively grey, such as Andalusians and Lipizzaners. ^[1]

Genetic Control

The Grey gene (G) is a dominant gene, meaning that any horse with a G allele will turn grey. ^[1] The process of greying occurs due to genetic mutation of melanocytes, the skin cells that produce skin pigment. ^[1] As the horse ages, the melanocytes produce less pigment, resulting in white hairs rather than colored hairs. ^[1]

The genetic mutation causing grey may also increase the number of melanocytes present in skin tissue, which could explain why grey horses have a higher risk of developing melanomas. ^[1] Horses who are homozygous for grey (G/G) are more likely to develop melanomas. ^[1]

Dilutions

Dilution genes act on the horse’s base color, causing lightening of the normal base coat. ^[1] The most common dilution genes are dun and cream. ^[1]

Dun

Dun horses have both a pale body color and primitive marks as their notable features. ^[1] Primitive marks are areas of black or dark coloring on the body. ^[1] Dun horses also have dark manes and tails, often with lighter tips. ^[1]

Types of primitive marks include: ^[1]

• Dorsal stripe: A black line down the back, following the spine
• Zebra or tiger stripes: Striping on the sides of the hocks and knees
• Withers stripe: A dark line extending over the withers
• Cobwebbing: Dark rings or strips on the forehead or front of the face

Dun is very common in primitive horse breeds, such as the Tarpan, Przewalski’s horse, and Sorraia. ^[1] Modern breeds that are commonly dun include the Fjord and American Quarter Horse. ^[1]

Since dun modifies the existing coat color, dun can have a different appearance based on the underlying coat. ^[1] Common categories of dun include: ^[1]

• Bay or zebra: Dun modifying a bay base coat. These horses have a yellow-brown body color with black points and dark primitive markings.
• Grullo/grulla or blue: Dun modifying a black base coat. These horses have a bluish-grey body color, black points, black primitive markings, and often a black head.
• Red: Dun modifying a chestnut base coat. These horses are pale red-brown and do not have black points. Their primitive markings are a darker shade of red than their body color.

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Genetic Control

The Dun gene (D) is a dominant gene that controls the production of both dun features: a lighter coat color and primitive markings. ^[1] Any horse with one or two D alleles has both of these features to some extent. ^[1]

Dun also has two variant alleles besides the dominant Dun allele. ^[1] These are non-dun 1 (nd1) and non-dun 2 (nd2).

Non-dun 1 produces primitive marks without dilution of the body color. ^[1] Horses with at least one copy of nd1 produce varying levels of primitive marks on top of their typical, non-diluted base coat color. ^[1]

Non-dun 2 is the default allele that all horses without dun coloring have. ^[1] These horses show up as nd2/nd2 on a color genetics panel. ^[1]

Table 5. Summary of the genetic control of Dun ^[2]

Cream & Pearl

Cream is a common dilution gene in many breeds, producing a yellowish body color. ^[1] Cream has the most drastic effects on red hairs, however it can also cause color changes in black base colors. ^[1] Cream horses also tend to have pale amber or light brown eyes. ^[1]

Cream has a stronger dilution effect in horses that are homozygous for the cream (Cr) gene. ^[1] Homozygous dominant horses have extremely pale coats that may be near white in some cases. ^[1]

Some breeds specifically select for horses with the cream gene, such as the Palomino breed or American Creme Horse. ^[1] The cream gene is also common in British pony breeds and American Quarter Horses. ^[1]

Horse colors associated with cream include: ^[1]

• Buckskin: One cream allele on a bay base coat. These horses have a yellowish body color with black points and a black mane and tail.
• Palomino: One cream allele on a chestnut base coat. These horses have a yellowish body color with a flaxen mane and tail.
• Smoky black: One cream on a black base coat. Although cream does not affect black hairs, smoky black horses may be more reddish-brown than a traditional black horse.
• Perlino: Two cream alleles on a bay base coat. Perlinos have a very pale, off-white body color with somewhat darker body points. Perlinos have blue eyes.
• Cremello: Two cream alleles on a chestnut base coat. These horses have a very pale, off-white body color. Cremellos have blue eyes.
• Smoky Cream: Two cream alleles on a black base coat. These horses are usually a pale brown color on the body and points. Smoky cream horses have blue eyes.

Pearl is a variant of cream that is very rare. ^[1] Pearl horses are usually gold or light tan, with light or pale colored eyes. ^[1] Their mane and tails are typically a similar golden shade, or slightly darker, than their body color. ^[1]

Pearl colors include: ^[1]

• Sable or classic: Two pearl alleles on a black base coat, or one pearl allele on a smoky black base coat. These horses are typically light tan with amber-colored eyes.
• Amber: Two pearl alleles on a bay base coat, or one pearl allele on a buckskin base coat. These horses are typically tan to cold with a darker mane and tail.
• Gold: Two pearl alleles on a chestnut base coat, or one pearl allele on a palomino base coat. These horses are typically a gold color with a gold mane and tail.

Genetic Control

Cream (Cr) is a dominant gene that dilutes the base color. This produces a yellowish body color in heterozygous horses, and an off-white color in homozygous horses. ^[1]

Pearl (prl), a variant allele of cream, also dilutes the base color. ^[1] This allele is recessive to other alleles that can occur at the Cream gene site, including the “non-Cream” allele. ^[1] This means that a horse with a single copy of prl and a non-Cream allele does not show any color changes. However, a horse with two copies of prl (homozygous recessive) does have a dilute coat. ^[1]

Pearl has an interaction effect with Cream, causing increased dilution in horses with a single Cream allele. ^[1] For example, a horse with one copy of prl and one copy of Cream typically has a lighter or more golden coat color than a similar horse with no Pearl allele. ^[1]

Table 6. Summary of the genetic control of Cream ^[2]

Champagne

Champagne causes coat dilution, similar to cream, with pinkish or light brown skin and amber-colored eyes. ^[1] Champagne can appear very similar to pearl, however it is more common than pearl in most breeds. ^[1] Other notable features of champagne include a very shiny coat and reverse dapples, or dapples with a darker center and a paler outer ring. ^[1]

Champagne is a rare color across all horse breeds, however selection for the coloring has increased its frequency in some breeds. ^[1] Common breeds carrying champagne include Spanish Mustangs, Tennessee Walking Horses, and American Quarter Horses. ^[1]

Champagne colors include: ^[1]

• Classic: Champagne dilution on a black base coat. These horses are pinkish or beige with light brown body points.
• Amber: Champagne dilution on a bay base coat. These horses have a light tan or yellow body color with chocolate brown points. They are commonly mistaken for buckskins.
• Gold: Champagne dilution on a chestnut base coat. These horses have a bright gold body color, and typically have a white mane and tail. They are commonly mistaken for palominos.

Genetic Control

Champagne is a dominant allele (Ch) affecting pigmentation, resulting in a dilute body color. ^[1] The effect of the champagne gene dilutes black hairs to brown and red hairs to a yellowish color. ^[1] In general, homozygotes for champagne tend to have paler body colors than heterozygotes. ^[1]

Silver Dapple

Silver dapple, also called taffy or chocolate, refers to a gene that can lighten the base body color, however not all horses with this gene have pale coats. ^[1] The colors produced by silver dapple range from pale dilute colors to heavily pigmented, dark, nondilute colors. ^[1]

Common breeds carrying the silver dapple gene include: ^[1]

• Rocky Mountain Horses
• Icelandic Horses
• Kentucky Mountain Saddle Horses

The most characteristic feature of silver is the heavy dappling of the coat, however dappling typically only occurs on black-base horses. ^[1] This color is called black silver or chocolate silver. Horses typically have a brown body color with manes, tails, and lower legs that range from black to nearly white. ^[1]

Bay silvers have a silver gene on top of a bay base color, resulting in a brown body color with flaxen points that may have variable areas of black hairs. ^[1] These horses may be confused for flaxen chestnut when they have very pale black points. ^[1] They can also appear as a plain bay if their silvering is subtle. ^[1]

Silver dapple does not affect red hairs, so chestnuts with the silver gene have a typical chestnut appearance. ^[1]

The silver dapple color is closely linked to eye abnormalities at birth. ^[1] Heterozygotes for the silver gene develop ocular cysts, large fluid-filled sacs within the eye that can impact the horse’s vision. ^[1]

Homozygotes develop multiple congenital ocular abnormalities (MCOA), which can result in improper formation of the horse’s iris, cornea, and retina. ^[1] Depending on the severity of the defects, the horse’s vision can be severely compromised. ^[1]

Genetic Control

Silver dapple is a dominant allele (Z) affecting the black pigmentation of hair. ^[1] Only black pigmented hairs become pale with this allele, leaving red pigmented hairs completely unaffected. ^[1] Therefore, chestnut horses do not show any evidence of having the silver gene, however any of their black or bay-base foals may show signs of silvering. ^[1]

Currently, horse breeders aim to avoid breeding silvers together, as homozygous silver foals are very likely to have severe ocular abnormalities that affect their vision. ^[1] Genetic testing is recommended prior to breeding two horses who may have the silver gene, to avoid producing a homozygous foal. ^[1]

White Patterns

The white patterns that occur in horses superimpose themselves over top of the horse’s base coat color. ^[1] This means that any coat color can have the addition of a white pattern on top if the horse’s genetics allow. White patterns range from flecks of white hair, such as roan, to large patches of white, such as tobiano. ^[1]

Frame Overo

Frame overo, or lethal white overo, refers to horses with extensive white patterning, but who have dark hooves and legs and usually faces extensively marked with white. ^[1] The name “frame” comes from the patches of white generally being confined to the middle of the horse, producing a dark border consisting of the horse’s legs, spine, and lower abdomen. ^[1]

Some horses show minimal white patterning even though they carry the frame overo gene. ^[3] One study showed that 18% of breeding stock in a particular population were solid-colored, despite carrying the frame gene. ^[3]

Breeds that commonly have frame overo include: ^[1]

• Paints
• Pintos
• Miniature horses

Genetic Control

The frame gene is a dominant allele (LWO) that controls the production of endothelin receptor B. This protein is responsible for development of melanocytes and nerves in the intestinal tract. ^[3]

Foals homozygous for lethal white overo are non-viable, as they do not develop nerves within their intestinal tract. ^[1] They quickly develop colic and megacolon after birth, requiring euthanasia. ^[1] Affected foals are usually entirely or mostly white, hence the name “lethal white“. ^[1]

Since horses may not express frame overo visibly, genetic testing is important in any breeding program where horses may carry the gene. ^[3]

Splashed White

Splashed white refers to horses who look like they have been dipped in or “splashed” from below by white paint. ^[3] These horses typically have white markers on all four legs that may extend up to the abdomen and face. ^[3] Horses that have white on the face often have blue eyes, and may be deaf if the white extends around their ears. ^[3]

Breeds with splashed white include: ^[1]

• Welsh ponies
• Icelandic horses
• Paint horses

There are also rare individuals in traditionally solid-colored breeds, such as Thoroughbreds and Morgans, who carry splashed white. ^[1]

Genetic Control

Two separate loci control splashed white coloration: PAX3 and MITF. ^[3] Currently there are at least 10 alleles at these locations associated with splashed white. ^[3] These alleles are named SW plus a number identifying a specific mutation (e.g. SW1). ^[3] Horses may carry a splashed white allele on both PAX3 and MITF at the same time. ^[3]

Most splashed white alleles are dominant. ^[3] Many of the alleles are presumed to be lethal to embryos in the homozygous state, as living homozygous horses have not been reported. ^[3] However, horses with two different splashed white alleles at the same locus (e.g. SW1/SW7) can be viable, and typically show extensive white and deafness. ^[3]

Leopard Complex

The leopard complex controls the Appaloosa patterning characteristic of Appaloosa horses, Knabstruppers, and Ponies of the Americas. ^[1]

There are three main components of Appaloosa patterning: ^[1]

• White patterning that is symmetrical
• Roaning that increases over time
• Leopard spotting within the white pattern that reveals the underlying base color

The degree of expression of each of these components depends on the Appaloosa pattern. ^[1] There are many Appaloosa patterns described, however some horses may show multiple patterns at the same time. ^[1]

Common patterns include: ^[1][4]

• Mottled: Horses with a standard body color that show only the depigmentation of the muzzle and striping of the hooves characteristic of Appaloosas.
• Varnish roan: Horses with a standard body color that progressively roan as they age.
• Blanket: Horses with white over their rump and hips that may or may not contain leopard spots.
• Leopard: Primarily white horses with several large leopard spots in their coat.

The genetic basis of Appaloosa patterning predisposes them to two health conditions: congenital stationary night blindness and equine recurrent uveitis (ERU). Both conditions are associated with having LP alleles.

In congenital stationary night blindness, horses homozygous for LP do not produce the necessary signals for night vision. These horses have difficulty maneuvering at night and may be more prone to injury unless housed in lighted areas. ^[3]

Equine recurrent uveitis is associated with cataracts, glaucoma, and blindness in affected horses. ^[3] This condition progressively worsens with age and may require affected eyes to be removed for the welfare of the horse. ^[3] Homozygotes are more likely to develop ERU, however heterozygotes can also be affected. ^[3]

Genetic Control

The leopard complex consists of two loci: LP and PATN1. ^[3] The LP gene controls whether the Appaloosa pattern is present and its presentation, while the PATN1 gene controls the extent of the patterning. ^[1]

Horses that are heterozygous for LP tend to have leopard spotting, while homozygotes have very few leopard spots. ^[1] Both heterozygotes and homozygotes have the mottled skin and striped hooves characteristic of Appaloosas. ^[1]

PATN1 determines the extent of white patterning. ^[1] Most horses with a dominant PATN1 allele have body colors that are more than 60% white. ^[1] They also typically have fewer leopard spots. ^[1]

Appaloosas that do not have a PATN1 allele are usually maximum 40% white. ^[1] Horses that inherit PATN1 but do not have the LP gene do not show any white patterning. ^[1]

Table 7. Summary of leopard complex genetic control. For clarity, the “normal”, non-Appaloosa alleles are shown as n. ^[1][3]

KIT Region White Patterns

Many of the white pattern alleles occur at or near the KIT locus, a genetic location that plays a critical role in pigmentation of the horse’s coat. ^[5] This means that the interaction of different white pattern alleles at this particular genetic location can produce highly variable white patterning. ^[3]

White patterns controlled by the KIT region include: ^[1][5]

• Dominant white
• Sabino
• Roan
• Tobiano

Most horses carry only one or two pattern alleles at the KIT locus, as expected with traditional Mendelian inheritance. ^[6] However, recent genetic analysis shows that horses may carry up to 6 different KIT variants at a time. ^[6] This suggests that inheritance of white patterns on the KIT locus is much more complex than simple Mendelian inheritance. ^[6]

Dominant White

Dominant white horses are almost entirely white, and typically have pink skin and dark eyes. ^[1]

Currently, there are 35 allele variants associated with dominant white described in the literature. ^[3] Researchers use the W symbol to represent dominant white, followed by a number identifying the specific mutation causing the pattern. ^[1]

Most of these variants are restricted to a single breed, except for W20 which has been identified in many breeds. ^[1]

Breeds carrying dominant white genes include: ^[3]

• American Quarter Horses
• Thoroughbreds
• Shetland ponies

Homozygosity for a single dominant white allele may cause fetal loss during early gestation. ^[3] So far, W variants W1-W14, W16-18, W21-28, W30 and W31 are presumed to be lethal to homozygous embryos, as no living homozygous horses have been found for these variants. ^[3]

Horses may have multiple dominant white alleles at the same time. ^[3] For example, horses with W22/W20 and W19/W34 have been described. ^[3]

Sabino

Sabino results in white patches on the legs and face with roan or speckled edges. ^[1] Minimally marked sabinos often have roan flecking on the flanks, with high white socks and large facial markings. ^[1] Maximally marked sabinos may be entirely white with only a few flecks of color on their ears. ^[1]

Sabino is common in many horse breeds, particularly: ^[1]

• Clydesdales
• American Quarter Horses
• Welsh Ponies
• Warmbloods

Unlike many other horse colors, sabino is not caused by a single allele. ^[1] Multiple alleles present at the KIT locus, which encodes for several white patterns, can produce sabino. ^[1] There are currently at least 8 alleles that can produce sabino patterning when expressed at the KIT locus. ^[1]

The most common allele causing sabino, sabino-1 (Sb1), is a dominant allele present at the KIT locus. ^[1] Heterozygotes typically have white body patches with sabino speckling, while homozygotes are nearly white with only a few colored areas. ^[1]

Roan

Roan refers to a white pattern that produces a mixture of white and colored hairs throughout the horse’s body. ^[1]

The degree of white flecking varies seasonally and with the horse’s age. ^[1] In general, roans are lightest in the spring when they shed their winter coat, then progressively darken throughout the year. ^[1] They can also become darker with age. ^[1]

Roan occurs in a variety of breeds, however it is most common in breeds such as the Brabant and Ardennes horses who select for this coloration. ^[1]

Experts name the roan colors based on the base coat the roan flecking applies to. ^[1]

Roan colors include: ^[1]

• Blue: Roan flecking on a black base coat, producing a blueish body color.
• Red or bay: Roan flecking on a bay base coat. Some refer to roan on a chestnut as “red roan”, so bay roan is a clearer name for this coat color.
• Strawberry: Roan flecking on a chestnut base coat, producing a pinkish body color.

Roan is a dominant allele (Rn) presumed to be at the KIT locus. ^[3] Since it is a dominant gene, any horse carrying the allele will have roan flecking. ^[1]

The specific protein affected by roan helps control the number of melanocytes during development, and the maintenance of melanocyte numbers during life. ^[1] Therefore, the roan mutation likely causes depletion of melanocytes, producing white hairs. ^[1]

Tobiano

Tobiano is a form of pinto patterning, producing large white patches on the horse’s body. ^[1] In general, tobiano horses have white hooves and lower legs, and the white on the body crosses the topline at some point between the horse’s ears and their tail. ^[1] The head is rarely marked by white patches. ^[1]

Breeds commonly expressing tobiano include: ^[1]

• Cobs
• European pony breeds
• Paint and Pinto breeds

Tobiano is a dominant allele (To), so all horses carrying the allele have some form of tobiano spotting. ^[1] However, they can be very minimally marked and may appear similar to a non-patterned horse. Whether the horse is heterozygous or homozygous does not appear to affect the degree of white patterning. ^[1]

The tobiano gene occurs upstream of KIT and is thought to have a regulatory effect on KIT expression. ^[3] This regulation produces the white patches characteristic of tobiano. ^[3] Since tobiano is on a separate locus from KIT, horses can have both tobiano patterning and dominant white or sabino. ^[3]

Summary

Not only does horse color genetics impact the color palette of our equine companions, it can also impact their health. Careful genetic selection when making breeding pairs is critical to preserving the health of our horses and ensuring that these interesting and diverse colors are available for generations to come.

• Generally, horse coloring is a result of the genetic interplay between the horse’s base color genes and its diluting genes
• Breeders select for different colors and in avoidance of potential diseases using genetic testing and Mendelian selection principles
• Some colors have a strong association with specific genetic health conditions, some of which are fatal