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This page has basic information regarding Equine Genetic Diseases and Equine Genetic Color Testing. We have also provided links to UC Davis and Animal Genetics at the bottom of the page for those interested in testing or more information.
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EQUINE GENETIC DISEASES
We have provided a basic description of the five genetic disorders found in stock horses (Quarter Horses, Paints, Morgans, etc.). These disorders are now testable by submitting a hair sample, with root bulbs attached. We are including this information for those horse enthusiasts or breeders who are unfamiliar or unaware with these disorders.
GBED ~ Glycogen Branching Enzyme Deficiency
Glycogen Branching Enzyme Deficiency (GBED) is a fatal condition caused by the bodies inability to properly store sugar. In a normal horse, the body stores sugar as energy by converting glucose to glycogen. This inherited disorder prevents the body from producing the enzyme needed to branch the glycogen structure, preventing the horse from being able to adequately store the sugars. This means that the horse will not be able to store enough energy to fuel important organs, such as the muscles and brain. Foals born affected by GBED suffer from a range of symptoms associated with this lack of fuel, such as low energy, weakness, and difficulty rising. Other symptoms include low body temperature, contracted muscles, seizures, and sudden death. Unfortunately, GBED is always fatal; most affected foals will die before the age of 8 weeks. GBED often causes fetuses to be aborted in utero. Research suggests that as many as 3% of aborted Quarter Horse foals were homozygous for the GBED mutation. Studies show that the mutation responsible for GBED is carried by as many as 10% of Quarter Horse, Paint Horse breeds and related breeds. GBED is an autosomal recessive trait, meaning a foal can only by affected if the foal inherits the disease from both parents. Horses that are carriers of the GBED have 1 copy of the mutation, but do not have any symptoms associated with the disorder. This makes DNA testing important to screen for carriers and prevent this fatal condition. The mutation, which causes this disease, has been identified by Dr. Stephanie Valberg and Dr. James Mickelson of the University of Minnesota.
Glycogen Branching Enzyme Deficiency (GBED) is a fatal condition caused by the bodies inability to properly store sugar. In a normal horse, the body stores sugar as energy by converting glucose to glycogen. This inherited disorder prevents the body from producing the enzyme needed to branch the glycogen structure, preventing the horse from being able to adequately store the sugars. This means that the horse will not be able to store enough energy to fuel important organs, such as the muscles and brain. Foals born affected by GBED suffer from a range of symptoms associated with this lack of fuel, such as low energy, weakness, and difficulty rising. Other symptoms include low body temperature, contracted muscles, seizures, and sudden death. Unfortunately, GBED is always fatal; most affected foals will die before the age of 8 weeks. GBED often causes fetuses to be aborted in utero. Research suggests that as many as 3% of aborted Quarter Horse foals were homozygous for the GBED mutation. Studies show that the mutation responsible for GBED is carried by as many as 10% of Quarter Horse, Paint Horse breeds and related breeds. GBED is an autosomal recessive trait, meaning a foal can only by affected if the foal inherits the disease from both parents. Horses that are carriers of the GBED have 1 copy of the mutation, but do not have any symptoms associated with the disorder. This makes DNA testing important to screen for carriers and prevent this fatal condition. The mutation, which causes this disease, has been identified by Dr. Stephanie Valberg and Dr. James Mickelson of the University of Minnesota.
HERDA / HC ~ Test patented by University of California-Davis
Hereditary Equine Regional Dermal Asthenia (HERDA) also known as Hyperelastosis Cutis (HC) is a genetic skin disease predominately found in the American Quarter Horse. Researchers at Mississippi State University and Cornell University believe that the origin of this genetic disorder may be the Poco Bueno's sire line. Symptoms of this disorder is a lack of adhesion within the layers of skin due to a genetic defect in the collagen that holds the skin in place. This defect causes the outer layer of skin to split or separate from the deeper layers sometimes tearing off completely. Areas under saddle seem to be most prone to these lesions often leaving permanent scares, preventing the horse from being ridden. The disorder is recessive, which means that a horse must be homozygous positive or have two copies of the defective gene to suffer from the disease. Consequently both the sire and the dam must possess at least one copy of the mutated gene in order for the offspring to be afflicted. Offspring born with one copy of the defective gene and one non-defective copy are considered a carrier and have a 50% chance of passing the defective gene on.
Hereditary Equine Regional Dermal Asthenia (HERDA) also known as Hyperelastosis Cutis (HC) is a genetic skin disease predominately found in the American Quarter Horse. Researchers at Mississippi State University and Cornell University believe that the origin of this genetic disorder may be the Poco Bueno's sire line. Symptoms of this disorder is a lack of adhesion within the layers of skin due to a genetic defect in the collagen that holds the skin in place. This defect causes the outer layer of skin to split or separate from the deeper layers sometimes tearing off completely. Areas under saddle seem to be most prone to these lesions often leaving permanent scares, preventing the horse from being ridden. The disorder is recessive, which means that a horse must be homozygous positive or have two copies of the defective gene to suffer from the disease. Consequently both the sire and the dam must possess at least one copy of the mutated gene in order for the offspring to be afflicted. Offspring born with one copy of the defective gene and one non-defective copy are considered a carrier and have a 50% chance of passing the defective gene on.
HYPP ~ Hyperkalemic Periodic Paralysis Disease
Hyperkalemic Periodic Paralysis Disease (HYPP) is a muscular disease that affects both horses and humans. In horses, HYPP has been traced back to one horse named Impressive and has the alternative name, Impressive Syndrome, named after this horse. Symptoms of HYPP may include muscle twitching, unpredictable paralysis attacks which can lead to sudden death, and respiratory noises. Severity of attacks varies from unnoticeable to collapse or sudden death. The cause of death is usually respiratory failure and/or cardiac arrest. The HYPP gene is dominant so both homozygous positive (HH) and heterozygous (nH) will cause this muscular disorder. Only homozygous negative (nn) has no HYPP effect. Since HYPP is dominant, the effects of it can also be transposed to other species of horses when intermixing occurs. This makes the recognition and elimination of this disorder very important in preserving the inherited health of all horses.
Hyperkalemic Periodic Paralysis Disease (HYPP) is a muscular disease that affects both horses and humans. In horses, HYPP has been traced back to one horse named Impressive and has the alternative name, Impressive Syndrome, named after this horse. Symptoms of HYPP may include muscle twitching, unpredictable paralysis attacks which can lead to sudden death, and respiratory noises. Severity of attacks varies from unnoticeable to collapse or sudden death. The cause of death is usually respiratory failure and/or cardiac arrest. The HYPP gene is dominant so both homozygous positive (HH) and heterozygous (nH) will cause this muscular disorder. Only homozygous negative (nn) has no HYPP effect. Since HYPP is dominant, the effects of it can also be transposed to other species of horses when intermixing occurs. This makes the recognition and elimination of this disorder very important in preserving the inherited health of all horses.
PSSM / EPSM ~ Polysaccharide Storage Myopathy / Equine Polysaccharide Storage Myopathy
Polysaccharide storage myopathy (PSSM) or Equine Polysaccaride Storage Myopathy (EPSM) is a glycogen storage disorder that results in the excess storage of sugar in skeletal musclesin the excess storage of sugar in skeletal muscles. It is often the cause of the common form of tying-up in horses. Affected individuals can have such minor symptoms to go unnoticed or multiple episodes of tying up, to severe colic and recumbency. Two types of PSSM have been identified. Yet, a simple DNA test currently only exists for Type 1. Horses with a single dominant gene WILL EXPRESS the disorder (at some point) AND can pass it to their offspring 50% of the time. Horses with two dominant genes will always produce afflicted offspring.
Horses on forage based, low carb diets (little to no grain) may NOT exhibit symptoms since the condition is related to sugar storage. For that reason AND the bloodline source(s) is still unknown, this is a "best to test" genetic disease.
Polysaccharide storage myopathy (PSSM) or Equine Polysaccaride Storage Myopathy (EPSM) is a glycogen storage disorder that results in the excess storage of sugar in skeletal musclesin the excess storage of sugar in skeletal muscles. It is often the cause of the common form of tying-up in horses. Affected individuals can have such minor symptoms to go unnoticed or multiple episodes of tying up, to severe colic and recumbency. Two types of PSSM have been identified. Yet, a simple DNA test currently only exists for Type 1. Horses with a single dominant gene WILL EXPRESS the disorder (at some point) AND can pass it to their offspring 50% of the time. Horses with two dominant genes will always produce afflicted offspring.
Horses on forage based, low carb diets (little to no grain) may NOT exhibit symptoms since the condition is related to sugar storage. For that reason AND the bloodline source(s) is still unknown, this is a "best to test" genetic disease.
MH / EMH ~ Malignant Hyperthermia
Malignant Hyperthermia is an inherited DOMINANT disease identified in Quarter Horses, Appaloosa, and Paints that can cause severe typing up and even death when horses are subjected to anesthesia. A gene mutation causes a dysfunction in skeletal muscles resulting in excessive release of calcium inside the muscle cells which results in a hypermetabolic state and/or death. Symptoms include fever, excessive sweating, elevated heart rate, irregular heart rhythm, shallow breathing, muscle rigidity, and death. Horses who also have Polysaccharide Storage Myopathy (PSSM) can exhibit more severe symptoms of tying up, even without anesthesia. Horses with a single dominant gene express the disorder (at some point) and can pass it to their offspring 50% of the time. Horses with two dominant genes will always produce afflicted offspring.
The only prevention is to not breed MH positive individuals.
Malignant Hyperthermia is an inherited DOMINANT disease identified in Quarter Horses, Appaloosa, and Paints that can cause severe typing up and even death when horses are subjected to anesthesia. A gene mutation causes a dysfunction in skeletal muscles resulting in excessive release of calcium inside the muscle cells which results in a hypermetabolic state and/or death. Symptoms include fever, excessive sweating, elevated heart rate, irregular heart rhythm, shallow breathing, muscle rigidity, and death. Horses who also have Polysaccharide Storage Myopathy (PSSM) can exhibit more severe symptoms of tying up, even without anesthesia. Horses with a single dominant gene express the disorder (at some point) and can pass it to their offspring 50% of the time. Horses with two dominant genes will always produce afflicted offspring.
The only prevention is to not breed MH positive individuals.
http://www.equinews.com/article/malignant-hyperthermia-horses
http://www.thehorse.com/ViewArticle.aspx?ID=5426
http://www.thehorse.com/ViewArticle.aspx?ID=5426
IMM/MYH1 ~ Immune-Mediated Myositis
Quarter Horse and related breeds are susceptible to developing rapid onset of muscle atrophy and severe muscle damage at rest (nonexertional rhabdomyolysis). An autoimmune muscle disease called immune-mediated myositis (IMM) can cause this severe atrophy, which can result in the loss of 40% of muscle mass within 72 hours in Quarter Horse and related breeds.
IMM is characterized by infiltration of inflammatory cells, particularly lymphocytes, into muscle fibers and surrounding blood vessels, with preferential targeting of the gluteal (rump) and epaxial (along the vertebral column) muscles. IMM is characterized by stiffness, weakness, and nonspecific malaise. Affected horses are usually 8 years and younger or 17 years and older, with no sex predilection. Environmental factors combined with genetic susceptibility are important triggers for the development of muscle atrophy or severe rhabdomyolysis. About 39% of IMM horses have a history of exposure to a triggering factor such as Streptococcus equi subsp. equi infection, respiratory virus, or vaccination with influenza, Equine Herpes Virus 4, or Streptococcus equi subsp. equi.
Researchers at Michigan State University and University of California, Davis identified a mutation in the Myosin Heavy Chain 1 (MYH1) gene (Chr11:52,993,878T>C) that causes an amino acid change (denoted as p.E321G) detrimental to normal function of the myosin protein in muscle cells. In other words, a missense mutation in the DNA causes a change from a glutamic acid (E) to glycine (G) at position 321 of the protein.
This mutation is associated with increased susceptibility to develop IMM in Quarter Horses and related breeds characterized by significant muscle atrophy. Another clinical presentation of the MYH1 mutation in young Quarter Horses is severe, sudden muscle damage not associated with exercise (nonexertional rhabdomyolysis). Horses with nonexertional rhabdomyolysis do not necessarily have muscle atrophy.
IMM and nonexertional rhabdomyolysis belong to the group of muscle diseases known as MYH1 myopathy (MYHM). The mode of inheritance for MYHM is autosomal dominant with variable penetrance, which means that both males and females are affected and not all horses that have 1 (N/My) or 2 copies (My/My) of the mutation will develop IMM or nonexertional rhabdomyolysis. Horses with two copies (My/My) may be more severely affected. The frequency of the MYH1 mutation in the general Quarter Horse population is estimated at about 4%. About 7.5% of Quarter Horses have 1 copy of the mutation. The mutation frequency is higher in the reining (13.5%), working cow (8.5%) and halter (8%) categories, and not observed in barrel and racing categories.
Testing for IMM/MYHM can benefit clinicians by assisting with the diagnosis of IMM or nonexertional rhabdomyolysis cases suspected to be MYHM. The test assists breeders wanting to identify breeding stock that have 1 or 2 copies of the mutation in order to design appropriate breeding strategies that avoid producing at-risk offspring and help reduce the incidence of the disease in the breed.
Testing is recommended for Quarter Horses, Quarter Horse crosses, and related breeds with Quarter Horse influence.
Quarter Horse and related breeds are susceptible to developing rapid onset of muscle atrophy and severe muscle damage at rest (nonexertional rhabdomyolysis). An autoimmune muscle disease called immune-mediated myositis (IMM) can cause this severe atrophy, which can result in the loss of 40% of muscle mass within 72 hours in Quarter Horse and related breeds.
IMM is characterized by infiltration of inflammatory cells, particularly lymphocytes, into muscle fibers and surrounding blood vessels, with preferential targeting of the gluteal (rump) and epaxial (along the vertebral column) muscles. IMM is characterized by stiffness, weakness, and nonspecific malaise. Affected horses are usually 8 years and younger or 17 years and older, with no sex predilection. Environmental factors combined with genetic susceptibility are important triggers for the development of muscle atrophy or severe rhabdomyolysis. About 39% of IMM horses have a history of exposure to a triggering factor such as Streptococcus equi subsp. equi infection, respiratory virus, or vaccination with influenza, Equine Herpes Virus 4, or Streptococcus equi subsp. equi.
Researchers at Michigan State University and University of California, Davis identified a mutation in the Myosin Heavy Chain 1 (MYH1) gene (Chr11:52,993,878T>C) that causes an amino acid change (denoted as p.E321G) detrimental to normal function of the myosin protein in muscle cells. In other words, a missense mutation in the DNA causes a change from a glutamic acid (E) to glycine (G) at position 321 of the protein.
This mutation is associated with increased susceptibility to develop IMM in Quarter Horses and related breeds characterized by significant muscle atrophy. Another clinical presentation of the MYH1 mutation in young Quarter Horses is severe, sudden muscle damage not associated with exercise (nonexertional rhabdomyolysis). Horses with nonexertional rhabdomyolysis do not necessarily have muscle atrophy.
IMM and nonexertional rhabdomyolysis belong to the group of muscle diseases known as MYH1 myopathy (MYHM). The mode of inheritance for MYHM is autosomal dominant with variable penetrance, which means that both males and females are affected and not all horses that have 1 (N/My) or 2 copies (My/My) of the mutation will develop IMM or nonexertional rhabdomyolysis. Horses with two copies (My/My) may be more severely affected. The frequency of the MYH1 mutation in the general Quarter Horse population is estimated at about 4%. About 7.5% of Quarter Horses have 1 copy of the mutation. The mutation frequency is higher in the reining (13.5%), working cow (8.5%) and halter (8%) categories, and not observed in barrel and racing categories.
Testing for IMM/MYHM can benefit clinicians by assisting with the diagnosis of IMM or nonexertional rhabdomyolysis cases suspected to be MYHM. The test assists breeders wanting to identify breeding stock that have 1 or 2 copies of the mutation in order to design appropriate breeding strategies that avoid producing at-risk offspring and help reduce the incidence of the disease in the breed.
Testing is recommended for Quarter Horses, Quarter Horse crosses, and related breeds with Quarter Horse influence.
EQUINE COLOR TESTING
The basic coat colors of chestnut, bay, brown and black horses are controlled by the interaction between two genes: Extension (gene symbol E) and Agouti (gene symbol A). The Extension gene (red factor) controls the production of red and black pigment. Agouti controls the distribution of black pigment either to a points pattern (mane, tail, lower legs, ear rims) or uniformly over the body.
We have provided basic information regarding the genetic color testing for the blue roan, red roan, bay roan or brown roan. In order to have a true blue roan the genetic test results must have at least one black Gene (E), one roan gene (Rn) and NO AGOUTI (aa).
Possible blue roan color genetics can be EE/aa/RnRn ~ homozygous black, homozygous roan, EE/aa/RnN ~ homozygous black, heterozygous roan, Ee/aa/RnRn ~ heterozygous black, homozygous roan, or Ee/aa/RnN ~ heterozygous black, heterozygous roan. A true blue roan will NEVER have an agouti gene. We use the following tests to ensure the color of our horses are correctly identified: Red/Black Factor, Agouti, and Roan Zygosity.
RED FACTOR/BLACK FACTOR (Extension)
The coat color of all horses is built on one of two possible base pigments: red or black. The Extension gene controls the production of this base pigment (red or black). All of the coat colors we see today, from white to black, sorrel to gray, every single one of them begins with one of these two possible base pigments (red or black). All horses will have the genetics for black or red pigment, regardless of their physical appearance. There are a number of dilutions, patterns, and modifiers which a horse can carry that affect the base pigment of a horse.
Horses that are bay, black, grullo, buckskin, black/blue roan, etc. are black pigmented horses that carry at least one copy of the Black Factor (E) allele. The black (E) allele of the Extension gene is dominant and causes a black pigmented base both in the heterozygous (Ee) and homozygous (EE) state. A horse that is heterozygous for Red/Black Factor means that it carries one copy of the black allele (E) and one copy of the red allele (e). A horse that is heterozygous for red/black factor can pass on either red or black pigment to its foals. A homozygous black (EE) horse means that it carries two copies of the black allele (EE). A homozygous black horse will always produce black based foals regardless of it’s mate.
Horses that are chestnut or sorrel, palomino, red dun, red roan, etc. are red pigmented horses and must carry two copies of the Red Factor (e) allele The red (e) allele of the Extension gene is recessive and will only cause red pigmentation when the horse carries two copies of this allele; this is referred to as Homozygous red (ee). Therefore, a red based foal results when both parent have passed on a copy of the red (e) allele.
Why test for Red/Black Factor?
Often breeders of black horses will want to test for Red Factor to determine if the horse is homozygous for black (EE). Homozygous black horses will always throw black as a base pigment. Thus, the resulting offspring will always be black based and could never be red such as a chestnut or sorrel. Other reasons to test for Red Factor would be to verify that a horse has a red pigment base. Cremello and Palomino horses are homozygous for Red Factor (ee).
Results are given using the following symbolic notation:
ee ~ Only the red factor detected. The horse tested homozygous for red pigment. The basic color is chestnut or sorrel unless modified by other color modifying genes.
Ee ~ Both black and red factors detected. The horse tested heterozygous for the red factor. It can transmit either E or e to its offspring. The basic color of the horse will be black, bay or brown unless modified by other color modifying genes.
EE ~ Only the black factor detected. The horse tested homozygous for black pigment. It cannot have red foals regardless of the color of the mate. The basic color of the horse will be black, bay or brown unless modified by other color modifying genes.
AGOUTI
The Agouti gene controls the distribution of black pigment. This pigment can be either uniformly distributed or distributed to "points" of the body (ear rims, lower legs, mane, tail). Agouti has been linked to a deletion of 11 nucleotides in the agouti gene. Only when the agouti gene is homozygous for the deletion (aa) is the black pigment evenly distributed. Heterozygous (Aa) or homozygous (AA) results in point distribution of black pigment. Agouti has no effect on homozygous positive red factor (ee) horses for there has to be black pigment present for agouti to have an effect.
Why test for Agouti?
There are several reasons an individual might want to test their horse for Agouti. Agouti is not shown physically on red (ee) horses. Therefore, a breeder might want to test a chestnut base horse to see if it is an Agouti carrier. Testing bay horses might be desired to see whether the horse carries one (Aa) or two (AA) copies of the Agouti allele. A homozygous Agouti (AA) horse will always pass Agouti to its offspring whereas a heterozygous (Aa) horse will have a 50% chance of passing on the gene. Another reason to test for Agouti might be if there is some doubt whether a black horse is truly black or a very dark bay. The effects of other genes might also make it hard to tell if Agouti is present or not. This test does not determine if a horse is homozygous for black factor. To determine black homozygosity, a breeder should test for Red Factor.
Results are given using the following symbolic notation:
aa ~ Only recessive allele detected. Black pigment distributed uniformly. The basic color of the horse will be black in the absence of other color modifying genes.
Aa ~ Horse tested Heterozygous for Agouti. Black pigment distributed in point pattern. The horse can transmit either A or a to its offspring. The basic color of the horse will be bay or brown unless modified by other color modifying genes.
AA ~ Only dominant allele detected. Black pigment distributed in point pattern. The horse cannot have black foals regardless of the color of the mate. The basic color of the horse will be bay or brown in the absence of other color modifying genes.
CREAM TEST
Cream is a dilution that caused the palomino, buckskin, smoky black, cremello, perlino and a smoky cream coat colors.
Mode of Inheritance: Incomplete dominance Alleles: N = Normal or non-cream, Cr = Cream
Explanation of Results:
Horses with N/N genotype will not be cream dilute and cannot transmit this cream dilution variant to their offspring.
Horses with N/Cr genotype are cream dilute and may transmit this cream dilute variant to 50% of their offspring. Matings with N/N genotype will result in a 50% chance of producing a cream dilute foal. Horses with a chestnut base coat color and Cr/N genotype will be palomino. Horses with a bay base coat color and Cr/N genotype will be buckskin. Horses with a black base coat color and Cr/N genotype will be smoky black.
Horses with Cr/Cr genotype are double dilute and will pass this cream dilute variant on to all of their offspring. Matings with any genotype are predicted to produce all cream dilute offspring. Horses with a chestnut base coat color and Cr/Cr genotype will be cremello. Horses with a bay base coat color and Cr/Cr genotype will be perlino. Horses with a black base coat color and Cr/Cr genotype will be smoky cream.
DUN TEST
Dun is a dominant trait of equines characterized by lightening of the body color, leaving the head, lower legs, mane, and tail undiluted. Dun is also typically characterized by “primitive markings” consisting of a dark dorsal stripe and sometimes leg barring, shoulder stripes, and concentric marks on the forehead (spiderwebbing, cobwebbing). Dun with primitive markings is considered the “wild-type state” and is found in other equids such as Przewalski horses, zebras, and wild asses. The expression of the primitive markings (with or without dun) in the domestic horse is variable, with the dark dorsal stripe being the most consistent and visible feature. Dun dilutes both red and black pigment, and the resulting colors range from apricot, golden, dark gray, olive and many more subtle variations. Three alleles explain phenotypes related to Dun dilution – D (presence of dun dilution and primitive markings), nd1 (not Dun-diluted; primitive markings are present but expression is variable), nd2 (1,617 bp deletion, not Dun-diluted, primitive markings absent). With respect to variant interactions, D is dominant over nd1 and nd2; nd1 is dominant over nd2. Testing for the dun dilution allows breeders to identify homozygous animals (animals with two copies of the variant) which will always produce dun dilute offspring.
Phenotype: Dun is a coat color dilution characterized by lightening of the coat, with the head, lower legs, mane and tail undiluted. Oftentimes, dun is also characterized by "primitive markings" such as a dark dorsal stripe, barring of the legs, shoulder stripes, and "cobwebbing" on the forehead.
Mode of Inheritance: Autosomal dominant Alleles: D = Dun dilute, nd1 = Non-dun 1, nd2 = Non-dun 2
Explanation of Results:
Horses with nd2/nd2 genotype will not be dun dilute and will not have primitive markings. They cannot transmit a dun dilution variant to their offspring.
Horses with nd1/nd2 genotype will not be dun dilute, but may have primitive markings. They may transmit the non-dun 1 variant to 50% of their offspring. Horses with nd1/nd1 genotype will not be dun dilute, but may have primitive markings. They will transmit the non-dun 1 variant to all of their offspring. Horses with D/nd1 or D/nd2 genotype will be dun dilute and will display primitive markings. They may transmit the dun dilute variant to 50% of their offspring. Matings with N/N genotype will results in a 50% chance of producing a dun dilute foal.
Horses with D/D genoytpe will be dun dilute and will transmit the dun dilute variant to all of their offspring. Matings with any genotype are predicted to produce dun dilute offspring.
ROAN ZYGOSITY TEST
Roan is a white patterning coat color trait of intermixed white and colored hairs in the body while the head, lower legs, mane and tail remain colored. Roan horses are born with the pattern, though it may not be obvious until the foal coat is shed. The white and colored hairs are evenly mixed in horses that inherit the classic Roan gene, which can differentiate this from several mimic patterns called roaning. Roaning patterns tend to be uneven in the distribution of white hairs and the inheritance of roaning has not been defined. The Roan gene is found in a variety of breeds such as Quarter Horse, Paints, Peruvian Paso, Paso Fino, Welsh Pony, Miniature and Belgian, but not in Thoroughbreds or Arabians.
Although it has been suggested that Roan is a homozygous lethal, evidence from the Quarter Horse breed indicates otherwise. Production records have documented the existence of Roan Quarter Horses that produce 100% Roan foals. DNA tests have confirmed homozygosity in the genomic region that contains the Roan gene.
Below are links to testing entities that can provide genetic disease testing or color genetic testing.
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