Trait Descriptions
Admin-only. These descriptions appear on horse profiles when the trait or subtag is assigned.
Modifiers
Palomino results from a single copy of the cream dilution gene acting on a chestnut base coat. Palomino is a horse coat color characterized by a golden body with a white or cream mane and tail. The shade of the body coat can vary widely, ranging from light cream to rich, dark gold. Unless influenced by other unrelated genes, palomino horses typically have dark skin and typical eye color is brown, although some individuals may have lighter brown or amber eyes. The cream gene is inherited in an incompletely dominant manner. A palomino carries one copy of the cream gene and can pass it to about 50% of its offspring on average. When two single cream carriers are bred together, about 25% of foals inherit no copy of the gene, 50% inherit one copy, and 25% inherit two copies. Horses that inherit two copies of the cream gene are known as double cream dilutes—cremello, perlino, or smoky cream—which have very pale coats and typically blue eyes.
Buckskin results from a single copy of the cream dilution gene acting on a bay or brown base coat. Buckskin is a horse coat color characterized by a tan or golden body with black points, including the mane, tail, and lower legs. The shade of the body coat can vary from light sandy tan to a deeper golden color. Buckskins should not be confused with dun horses, as the dun gene does not occur in the Thoroughbred breed. The cream gene is inherited in an incompletely dominant manner. A buckskin carries one copy of the cream gene and can pass it to about 50% of its offspring on average. When two single cream carriers are bred together, about 25% of foals inherit no copy of the gene, 50% inherit one copy, and 25% inherit two copies. Horses that inherit two copies of the cream gene are known as double cream dilutes—cremello, perlino, or smoky cream—which have very pale coats and typically blue eyes.
Smoky black results from a single copy of the cream dilution gene acting on a black base coat. In most cases, a smoky black horse appears nearly identical to a black horse, as the dilution effect is often minimal or not visibly apparent. The coat may, however, be slightly more prone to fading to a brownish shade when exposed to sunlight or weathering. Smoky black should not be confused with other dark coat colors such as dark brown, grullo or even liver chestnut. In particular, grullo results from the dun dilution acting on a black base coat, and the dun gene is not present in the Thoroughbred breed. The cream gene is inherited in an incompletely dominant manner. A buckskin carries one copy of the cream gene and can pass it to about 50% of its offspring on average. When two single cream carriers are bred together, about 25% of foals inherit no copy of the gene, 50% inherit one copy, and 25% inherit two copies. Horses that inherit two copies of the cream gene are known as double cream dilutes—cremello, perlino, or smoky cream—which have very pale coats and typically blue eyes.
Cremello results from two copies of the cream dilution gene acting on a chestnut base coat. Cremellos have very pale cream or nearly white body with a white or cream mane and tail. Unlike single-cream dilutes, cremellos have pink skin and blue eyes, but some variation from light blue to a greenish blue or amber can occur. A cremello carries two copies of the cream gene and passes one copy to 100% of its offspring. When bred to a horse without the cream gene, all foals inherit a single copy of the cream gene and will therefore be single-cream dilutes. When bred to a single-cream horse, about 50% of the foals inherit one copy of the gene and about 50% inherit two copies.
Perlino results from two copies of the cream dilution gene acting on a bay or brown base coat. Perlinos have very pale cream or nearly white body with a white or cream mane and tail. Unlike single-cream dilutes, perlinos have pink skin and blue eyes, but some variation from light blue to a greenish blue or amber can occur. A perlino carries two copies of the cream gene and passes one copy to 100% of its offspring. When bred to a horse without the cream gene, all foals inherit a single copy of the cream gene and will therefore be single-cream dilutes. When bred to a single-cream horse, about 50% of the foals inherit one copy of the gene and about 50% inherit two copies.
Smoky cream results from two copies of the cream dilution gene acting on a black base coat. Smoky creams have very pale cream or nearly white body with a white or cream mane and tail. Unlike single-cream dilutes, smoky creams have pink skin and blue eyes, but some variation from light blue to a greenish blue or amber can occur. A smoky cream carries two copies of the cream gene and passes one copy to 100% of its offspring. When bred to a horse without the cream gene, all foals inherit a single copy of the cream gene and will therefore be single-cream dilutes. When bred to a single-cream horse, about 50% of the foals inherit one copy of the gene and about 50% inherit two copies.
Rabicano is an uncommon pattern featuring interspersed white hairs over the base coat. In its most minimal form, rabicano may appear only as a concentration of white hairs at the top of the tail, sometimes referred to as a “coon tail” or “skunk tail.” In more pronounced cases, the pattern begins with white hairs at the flanks and may spread outward to other parts of the body. Rabicano may occur on any base coat color and in combination with other white patterns or modifiers, including gray. Rabicanos have often been misregistered as roans, although the two traits are genetically distinct and can usually be distinguished by their visual characteristics. True roan is characterized by an even mixture of white and colored hairs across most of the body while the head, mane, tail, and lower legs remain darker. True roan is extremely rare in the Thoroughbred breed, with only a small number of documented individuals worldwide, most (if not all) tracing their ancestry to the stallion Catch A Bird. The inheritance of rabicano is not well understood and has not yet been formally studied.
Flaxen is a coat trait that causes the mane and tail of chestnut horses to be noticeably lighter than the body coat color, often appearing golden, cream, or blonde. The degree of expression varies considerably: some chestnut horses show only slightly lighter mane and tail, while in others the contrast can be very pronounced. Flaxen should not be confused with the silver dilution caused by the Silver (PMEL) gene. Silver gene is not present in the Thoroughbred breed and while both can produce lighter manes and tails, the silver gene affects black pigment and therefore alters black and bay coats, whereas flaxen appears only on chestnut horses and does not dilute the body coat itself. The inheritance of flaxen is not fully understood. Earlier studies suggested that it might be caused by a recessive allele, sometimes described as "Ff". More recent observations, however, indicate that the trait may be polygenic and influenced by multiple genes. There are documented cases of flaxen chestnut foals born to parents that are black or bay, suggesting that the genetic factors responsible for flaxen can be carried without being expressed and may be masked in darker-colored horses while still being passed on to their offspring.
Gulastra plume, sometimes called “silver tail,” is a trait in which a horse’s tail—and occasionally the mane—appears noticeably lighter, often flaxen or silvery, despite the absence of known dilution genes that would normally lighten these areas. The trait is relatively rare and is usually most visible in younger horses, with the pale hair often darkening as the horse ages. Expression varies widely, ranging from a strongly pale or silvery tail to only a subtle lightening compared with the body coat. Gulastra plume should not be confused with the silver dilution caused by the Silver (PMEL) gene. The silver gene affects black pigment and produces characteristic coat color changes in black and bay horses, and it is not present in the Thoroughbred breed. In contrast, Gulastra plume affects only the tail and/or mane and does not produce the broader coat color dilution associated with the silver gene. The trait is named after the Arabian stallion Gulastra, who sired several offspring displaying the pale-tail characteristic, although he himself was chestnut and did not visibly display the trait. The genetic cause of Gulastra plume has not yet been identified, and its mode of inheritance remains unclear.
White ticking refers to scattered white hair appearing randomly throughout an otherwise normally pigmented coat. The hair may occur individually or in small, irregular concentrations, with the amount varying considerably between horses. White ticking does not follow a consistent body pattern and may occur on any base coat color. White ticking should not be confused with roan, rabicano, or sabino. Roan and sabino can be identified through genetic testing - roan (Rn) is extremely rare in the Thoroughbred and is confined to a very narrow family line tracing to the stallion Catch A Bird, while sabino (Sb1) is not present in the breed at all. Rabicano, unlike the regular white ticking, has to be always complemented by a “skunk tail”. It is generally considered an individual coat characteristic rather than a distinct, established white-spotting pattern, and no specific genetic cause has been identified to date.
Gray is a coat color modifier that causes a horse’s coat to progressively lose pigment over time. Horses carrying the gray gene are born with a normal base color—such as black, bay, or chestnut—but gradually develop increasing amounts of white hair as they age. This process can produce many different appearances throughout the horse’s life, including steel gray, dapple gray, flea-bitten gray, and nearly white. Gray horses have dark skin and dark eyes. This is an important visual distinction from many white spotting mutations, which often produce areas of pink skin and sometimes lighter eyes. In the records of The Jockey Club, gray horses are often registered as “gray/roan,” particularly when they are young and show intermixed white hairs that resemble roan. This designation is inaccurate as true roan is genetically different and extremely rare in the Thoroughbred breed. Gray is caused by a mutation affecting pigment regulation associated with the STX17 gene and is inherited as a dominant trait. A horse carrying one copy of the gray gene has approximately a 50% chance of passing it to each offspring, while a horse with two copies will pass the gene to all of its offspring.
Mutations
White spotting (previously known as dominant white) is one of several known depigmentation phenotypes in horses. It is the result of a spontaneous mutation of the KIT-gene which is why white foals tend to be a surprise when born to solid parents. White spotting patterns are highly variable in expression. They can range from minimal markings—sometimes described as sabino-like spotting—to horses that appear almost entirely white. White spotting mutations themselves do not affect eye color. As a result, horses with white spotting patterns usually have brown eyes unless another gene influencing eye color is also present. For many years, the sabino-like patterning seen in some heavily marked Thoroughbred horses was believed to be caused by the sabino allele Sb1. However, genetic testing has shown that Sb1 has not been identified in Thoroughbreds, and the white patterning observed in the breed is instead associated with other mutations (W) of the KIT gene. White spotting should not be confused with Lethal White Syndrome, which is caused by a different gene and occurs in frame overo horses. Likewise, white horses are not albinos, as true albinism has not been documented in horses. White spotting mutations are generally inherited as autosomal dominant or incomplete/semi-dominant traits. They require only one copy of the gene for expression, though homozygous horses often display more white (incomplete dominance) or, in some cases, the mutation is lethal.
This specific white spotting mutation has not been isolated yet.
🪄 Founder: White Beauty (born 1963) 🔬 Genomic coordinate / type: chr3:79549540C>T / missense 🧬 Inheritance: autosomal dominant W2 usually produces a fully white individual though slight sabino-like patterning is also common. As homozygotes have not been observed, W2/W2 is thought to be embryonic lethal.
🪄 Founder: Puchilingui (born 1984) 🔬 Genomic coordinate / type: chr3:79545900delC / small deletion 🧬 Inheritance: autosomal dominant W5 usually produces a sabino-like pattern. When combined with another W mutation, it often results in a fully white individual. As homozygotes have not been observed, W5/W5 is thought to be embryonic lethal.
🪄 Founder: Marumatsu Live (born 2004) 🔬 Genomic coordinate / type: chr3:79573754C>T / missense 🧬 Inheritance: autosomal dominant Since Marumatsu Live, the only known carrier of W6, left no progeny, the full phenotype is unknown. The mare displayed a loud sabino-like pattern.
🪄 Founder: Turf Club (born 2005) 🔬 Genomic coordinate / type: chr3:79580000C>G / splice site 🧬 Inheritance: autosomal dominant W7 usually produces a sabino-like pattern. When combined with another W mutation, it often results in a fully white individual. As homozygotes have not been observed, W7/W7 is thought to be embryonic lethal.
🪄 Founder: Shirayukihime (born 1996) 🔬 Genomic coordinate / type: chr3:79544151_79544204del / gross deletion 🧬 Inheritance: autosomal dominant W14 usually produces a fully white individual, though some pigmentation may occasionally remain. As homozygotes have not been observed, W14/W14 is thought to be embryonic lethal.
🪄 Founder: none - present in multiple breeds 🔬 Genomic coordinate / type: chr3:7948220T>C / missense 🧬 Inheritance: autosomal dominant W20 often produces little or no white on its own. However, it can increase the amount of white when combined with other white spotting mutations and acts as a "white booster". Homozygous W20/W20 horses are viable.
🪄 Founder: Not Quite White (born 1989) 🔬 Genomic coordinate / type: chr3:79548925_79550822del1898 / gross deletion 🧬 Inheritance: autosomal dominant W22 usually produces a sabino-like pattern. When combined with another W mutation, it often results in a fully white individual. As homozygotes have not been observed, W22/W22 is thought to be embryonic lethal.
🪄 Founder: Laughyoumay (born 2001) 🔬 Genomic coordinate / type: chr3:77769878T>C / missense 🧬 Inheritance: autosomal dominant W25 usually produces a sabino-like pattern. When combined with another W mutation, it often results in a fully white individual. As homozygotes have not been observed, W25/W25 is thought to be embryonic lethal.
🪄 Founder: Marbrowell (born 1997) 🔬 Genomic coordinate / type: chr3:79544150del / small deletion 🧬 Inheritance: autosomal dominant W26 usually produces a sabino-like pattern. When combined with another W mutation, it often results in a fully white individual. As homozygotes have not been observed, W26/W26 is thought to be embryonic lethal.
🪄 Founder: Milady Fair (born 1960) 🔬 Genomic coordinate / type: chr3:79552028A>C / missense 🧬 Inheritance: autosomal dominant W27 usually produces a sabino-like pattern. When combined with another W mutation, it often results in a fully white individual. As homozygotes have not been observed, W27/W27 is thought to be embryonic lethal.
Roan in horses is considered to be caused by mutations or variants in the KIT gene region on chromosome 3 (ECA3). Roan is characterized by an even mixture of colored and white hairs across the body, while the head, mane, tail, and lower legs remain mostly solid-colored. Roans are sometimes mistaken for gray horses; however, gray horses progressively lighten with age, whereas roan coats remain relatively stable throughout life. Other coat patterns that may resemble roan include sabino, rabicano, and certain other mutations associated with the KIT gene, which can also produce intermixed white hairs. The roan pattern is typically inherited as a dominant trait, meaning a horse only needs one copy of the gene to display the pattern. A roan horse with one copy of the gene passes it to approximately 50% of its offspring, while a horse with two copies will pass the gene to all of its offspring. In the Thoroughbred breed, however, true roan is extremely rare and is known from only a single family descending from the stallion Catch A Bird. The mutation responsible for roan in this line has not yet been isolated or formally named and appears to be unrelated to the roan mutations identified in other breeds, commonly referred to as “Rn.”
Non-KIT white spotting refers to depigmentation patterns in horses caused by mutations in genes other than KIT, most commonly MITF or EDNRB. These mutations affect the development and migration of melanocytes during embryonic development, preventing them from reaching certain areas of the skin and resulting in distinctive white markings. Non-KIT white spotting patterns are often associated with characteristic phenotypes that can vary widely in expression, ranging from minimal white markings to large white areas covering significant portions of the body. Some non-KIT white spotting patterns may also influence eye color. Non-KIT white spotting mutations are typically inherited as autosomal dominant traits, meaning only one copy of the mutation is required for expression. However, expression can vary significantly between individuals, and some mutations may be lethal in the homozygous state.
Frame overo is caused by a mutation in the EDNRB gene. Frame overos have sharply defined, irregular, horizontally oriented white patches. Expression of the frame overo pattern can vary widely. The head is often white or bald-faced, and blue eyes are not uncommon. There are a few frame overo lines in the Thoroughbred breed. Frame overo is autosomal dominant. All adult frame overo horses are heterozygous, carrying only one copy of the gene, and have a 50% chance of passing it down to their offspring. Homozygotes develop Lethal White Syndrome and die within few days after birth as their intestines don’t develop the nerves needed to move food. Lethal White Syndrome can be completely eliminated by testing all mares and stallions and is 100% preventable through education and responsible breeding. Frame overo gene can be carried without obvious large markings, so carriers cannot always be identified visually. Therefore, genetic testing is essential.
This specific splashed white mutation has not been isolated yet.
🪄 Founder: Southern Phantom (born 2016) 🔬 Genomic coordinate / type: chr16:21555811_21558139del / gross deletion 🧬 Inheritance: autosomal dominant SW8 is caused by a mutation of the MITF-gene. The mutation usually produces a bald face, blue eyes, tall stockings, and belly white markings similar to other splashed white patterns.
Somatic mutations often appear as irregular patches of color in unexpected areas. Their appearance can sometimes resemble chimerism, and without genetic testing it may be difficult to determine which condition is responsible. However, somatic mutations typically produce asymmetrical or uneven patches rather than evenly distributed patterns. These markings arise when a genetic change occurs in a group of cells during development, causing that localized area to express pigment differently from the rest of the coat. As a result, the mutation may appear as a small white spot where pigment cells failed to develop normally, or as a larger patch of a different color. Somatic mutations are usually not heritable, as they affect only a portion of the body’s cells rather than the horse’s entire genetic makeup. They are often present from birth, although they may become more noticeable as the horse ages.
Somatic mutation patches are usually not heritable, as they affect only a portion of the body’s cells rather than the horse’s entire genetic makeup.
Birdcatcher spots are small, random white spots, usually no larger than an inch across. They pop up spontaneously on the body of horses of practically any solid color and usually appear later in life. Sometimes the markings seem to move around a bit, vanishing and reappearing elsewhere on the body. They may also disappear entirely over time. Mainly because of this, many believe they are not tied to a permanent genetic marker but perhaps influenced by environment, age, or hormonal changes. The name comes from a Thoroughbred horse named Birdcatcher. Interestingly, Birdcatcher was actually a rabicano, but his white ticking was so prominent that the name "Birdcatcher spots" was later linked to larger white spots, completely unrelated to rabicano. Birdcatcher spots are not heritable.
Bend-Or spots are random dark spots, ranging from tiny and inconspicuous to large and obvious, most commonly found on chestnut horses. Bend-Or spots are not heritable.
Bloodmarks are darker patches that appear within the coat of gray horses. They can range from small spots to much larger areas, sometimes covering significant parts of the body, such as the shoulder (often called a “bloody shoulder”). As gray horses age, most pigment cells gradually lose their ability to produce color, causing the coat to turn white. In areas where a somatic mutation occurs, pigment cells continue producing color, creating darker patches that stand out against the lighter coat. Bloodmarks are not heritable, as they affect only a portion of the body’s cells rather than the horse’s entire genetic makeup.
Tetrarch (chubari) spots are white spots that can appear in the coat of horses with the Gray modifier. The spots are usually larger than Birdcatcher spots and are typically egg-shaped and about egg-sized. The name "Tetrarch spots" comes from the famous spotted gray racehorse The Tetrarch, who displayed an unusually large number of them. Tetrarch spots are not hereditary. Even if The Tetrarch does appear in the horse’s lineage, it has no connection to the occurrence of these spots.
Other
Vitiligo in horses is a relatively rare, non-painful skin condition characterized by the gradual loss of pigment, leading to white or depigmented patches on the skin. It most commonly appears around the face—especially the muzzle, eyes, and lips—but can occur elsewhere on the body. The condition is believed to be autoimmune, meaning the horse’s immune system mistakenly attacks the pigment-producing cells (melanocytes). Vitiligo does not affect a horse’s overall health, performance, or lifespan, and it is not contagious. The exact cause is unknown, though genetics, stress, and environmental factors may play a role. There is no definitive cure, but since the condition is cosmetic, treatment is usually unnecessary.
Acquired markings in horses are permanent changes in coat color that develop after skin damage, such as from injections (“jabs”), wounds, or infections like ringworm. When the skin heals, the hair that grows back may lack pigment, creating small white spots or patches.