Heterozygotes have no known health issues related to the frame allele. Cremello, Dominant white and Sabino-white are normal white or near-white coat colors for healthy horses. Can be distinguished by genetic testing.
Prevention
Avoid breeding heterozygous frame horses to each other
Treatment
None
Lethal white syndrome (LWS), also called overo lethal white syndrome (OLWS), lethal white overo (LWO), and overo lethal white foal syndrome (OLWFS), is an autosomalgenetic disorder most prevalent in the American Paint Horse. Affected foals are born after the full 11-month gestation and externally appear normal, though they have all-white or nearly all-white coats and blue eyes. However, internally, these foals have a nonfunctioning colon. Within a few hours, signs of colic appear; affected foals die within a few days. Because the death is often painful, such foals are often humanely euthanized once identified. The disease is particularly devastating because foals are born seemingly healthy after being carried to full term.[1]
The disease has a similar cause to Hirschsprung's disease in humans. A mutation in the middle of the endothelin receptor type B (EDNRB) gene causes lethal white syndrome when homozygous. Carriers, which are heterozygous—that is, have one copy of the mutated allele, but themselves are healthy—can now be reliably identified with a DNA test. Both parents must be carriers of one copy of the LWS allele for an affected foal to be born.
Horses that are heterozygous for the gene that causes lethal white syndrome often exhibit a spotted coat color pattern commonly known as "frame" or "frame overo". Coat color alone does not always indicate the presence of LWS or carrier status, however. The frame pattern may be minimally expressed or masked by other spotting patterns. Also, different genetic mechanisms produce healthy white foals and have no connection to LWS, another reason for genetic testing of potential breeding stock. Some confusion also occurs because the term overo is used to describe a number of other non tobiano spotting patterns besides the frame pattern. Though no treatment or cure for LWS foals is known, a white foal without LWS that appears ill may have a treatable condition.
Signs
Unlike the premature births and stillborn or weak foals of some coat color dilution lethals, foals born with lethal white syndrome appear to be fully formed and normal.[2][3] The coat is entirely or almost entirely white with underlying unpigmented pink skin.[2][3][4] If pigmented regions are present, they may be any color, and are most common around the muzzle, underside of the barrel, and the hindquarters or tail.[2] The eyes are blue. A few lethal white foals have been shown to be deaf.[3][5]
Healthy foals pass meconium, the first stool, soon after birth. Some healthy foals may require an enema to assist this process, but the meconium of LWS foals is impacted high in the intestine, and never appears, even with the use of enemas.[3] Signs of colic begin to appear within the first day,[2] and all foals with LWS die within the first few days of life.[4] The painful and inevitable death that follows usually prompts veterinarians and owners to euthanize foals suspected of having lethal white syndrome.[6][7]
Death is caused by an underdeveloped part of the digestive system. The large intestine of the horse is a complex system where most digestion takes place, and comprises the cecum, the colon, and the rectum.[8]Necropsies on LWS foals reveal a pale, underdeveloped colon[2] and intestinal obstruction (impaction).[4] Samples of affected tissue show a lack of nerves that allow the intestine to move material through the digestive system, a condition called intestinalagangliosis.[2][3][4]
Closer examination of the skin and hair shows both to be unpigmented, and most hair follicles are inactive and many are devoid of hair altogether.[3] All LWS foals test homozygous for a genetic abnormality.[9]
Inheritance and expression
Genetic conditions which affect more than one physical trait—in the case of lethal white syndrome, both pigment cells and entericnerve cells—are termed pleiotropic. The unusual instance of pleiotropy in LWS foals suggested early on that the syndrome was related to an important section of embryonic tissue called the neural crest.[4] As the name suggests, the stem cells of the neural crest are precursors to nerve cells. Another cell type that descends from neural crest cells are melanocytes, pigment-producing cells found in hair follicles and skin. The migration of nerve- and melanocyte-precursors from the top of the embryo to their eventual destinations is carefully controlled by regulatory genes.[10]
Such regulatory genes include endothelin receptor type B (EDNRB). A mutation in the middle of the EDNRB gene, Ile118Lys, causes lethal white syndrome.[5][11] In this mutation, a "typo" in the DNA mistakes isoleucine for lysine.[11] The resulting EDNRB protein is unable to fulfill its role in the development of the embryo, limiting the migration of the melanocyte and enteric neuron precursors.
In the case of LWS, a single copy of the EDNRB mutation, the heterozygous state, produces an identifiable trait, but with a very different outcome from the homozygous state.[12]
To produce a foal with LWS, both parents must be heterozygotes or carriers of the mutated gene.[7][13][14] Without genetic testing, some carriers are misidentified as having white markings due to another gene, while some are even classified as solids.[3]
The presence of this gene in a variety of horse populations in North America suggests that the mutation occurred in early American history, perhaps in a Spanish-type horse.[5][6][7]
This horse has irregular white markings, and would be classed by the APHA and PtHA as "overo". However, his markings are caused by a type of sabino patterning and he has been DNA-tested negative for the OLWS gene.
Horses heterozygous for the Ile118Lys mutation on the equine EDNRB gene—carriers of lethal white syndrome—usually exhibit a white-spotting pattern called "frame", or "frame overo".[5][7][9][13] Frame is characterized by jagged, sharply defined, horizontally oriented white patches that run along the horse's neck, shoulder, flank, and hindquarters. The frame pattern by itself does not produce white markings that cross the back, or affect the legs or tail. It does, however, often produce bald faces and blue eyes.[5][7][9] The term "frame" describes the effect of viewing a frame-patterned horse from the side: the white markings appear to be "framed" by a dark-colored border.[7] To date, animals which are heterozygous carriers do not exhibit health concerns associated with carrier-only status.[15]
Not all horses with the heterozygous mutation exactly fit the standard visual description. A horse with the Ile118Lys mutation on EDNRB that is not readily identified as frame-patterned is called a cryptic frame. In addition to cryptic frames, a significant proportion of horses with the frame phenotype are visually misidentified, even in clinical settings.[9] One study found from a group of visually inspected registered Paints, 18% of breeding stock solids and 35% of bald-faced horses were actually frames.[9] However, over one-quarter of Paints registered in the "overo" category were not frames, and conversely, 10% of horses registered as tobiano also carried frame genetics.[9] The difficulty in accurately identifying frames has contributed to the accidental breeding of LWS foals.
Minimally marked horses heterozygous for the Ile118Lys mutation are not uncommon: one DNA-tested Thoroughbred has white markings limited to a bottom-heavy blaze and two socks below the knee.[16] A Quarter Horse mare tested positive for the gene after she and a frame Paint stallion produced a LWS foal; the mare's markings were a thin blaze with a disconnected white spot in the right nostril, with no other white markings.[3] One major study identified two miniature horses that were completely unmarked, but were positive for the Ile118Lys gene.[9]
Multiple theories are given for this. Variability in the percentage of individuals with a specific genotype that express an associated phenotype is called penetrance, and this may simply be evidence of variable penetrance.[17][18] Several research groups have suggested that other, "suppressor" genes may limit the expression of frame-pattern white spotting.[13][19]
On the other end of the spectrum, some white-spotted horses are so extensively marked that the character of the frame pattern is masked. In particular, the tobiano pattern, a dominant gene, is epistatic to overo.[17] Other white-spotting genes include splashed white or "splash", sabino, and "calico".[9] Any combination, or all, of these white-spotting genes can act together to produce horses with so much white that the presence of frame cannot be determined without a DNA test.[20]
Ambiguous terminology has also contributed to the confusion surrounding this disease. Currently, the American Paint Horse Association categorizes horses as tobiano, solid, "overo", and tovero.[21] The association breaks down "overo" into three categories: Frame, Splash and Sabino.[21] In the past, "overo" was used even more loosely, to refer to spotted animals that were "Paint, but not tobiano".[21] However, no fewer than four—and likely many more—genetically distinct patterns are included under the term "overo".[9][19][22] To be categorized as "overo" by the APHA, a horse must fit a written description: white spotting does not cross the back, at least one solid-colored leg, solid tail, face markings, and irregular, scattered, or splashy white patches.[23] To further complicate matters, various Sabino patterns also appear in some horse breeds that do not carry genetics for frame or any other spotting pattern.[24]
Likewise, official classification of a horse as an unspotted solid is based not on genetic testing, but on a visual description. Horses carrying genetics for frame and other white-spotting patterns may be so minimally marked as to lack the registry's minimum requirements for white.[25] This helps to account for allegedly solid horses producing spotted offspring, called cropouts.[7]
The long-standing practice of categorizing Paint horses in this manner contributed to the incorporation of the word "overo" into some of the titles used to describe the disease, such as overo lethal white foal syndrome.[4] However, "overo" refers to several genetically unrelated white-spotting patterns, and only the frame pattern is indicative of the syndrome.[7][9][13] The confusion about the nature of LWS is then furthered by statements such as "there are many overos that do not carry the lethal allele",[21] which is technically correct, but only because the term "overo" also encompasses splash and sabino patterns, as well as frame.[21]
Homozygotes
Homozygotes for the Ile118Lys mutation on the equine endothelin receptor type B gene have lethal white syndrome.[5][9] In any crossing of two carrier parents, the statistical probability of producing a solid-colored, living foal is 25%; a 50% chance exists for a frame-patterned, living foal; and a 25% chance exists of a LWS foal.[14]
This Thoroughbred mare was born pure white with pink skin. Such foals are occasionally born with no apparent white ancestry. This mare does not carry the LWS gene, and her coat is termed "dominant white".
Producing frame color patterns without producing lethal white
Spotted coat colors, including frame, are popular and sought-after by breeders.[26] While many lethal white syndrome foals are accidentally produced when breeders cross two untested cryptic frames, or a known frame and a cryptic frame, some are produced by the intentional breeding of two known frames, whether out of ignorance or indifference. Producing a foal with LWS is now completely avoidable, because most major animal genetics labs now offer the DNA test for it. Whether a horse visually appears to have the frame pattern or not, testing horses of frame or "overo" lineage is highly recommended. The statistical likelihood of producing a living, frame-patterned foal by crossing two frames is 50%, the same odds of producing a living, frame-patterned foal from a frame-to-nonframe breeding which carries no risk of producing a lethal white syndrome foal.[14] Therefore, breeding two frame overos conveys no benefit to breeders hoping to produce another frame overo.
Lethal white syndrome has been described by researchers as both dominantly and recessively inherited.[27][28][29] Lethal white syndrome is described as recessive because heterozygotes (written Oo or N/O) are not affected by intestinal agangliosis. However, if the frame pattern trait is included, inheritance of the trait follows an incomplete dominant pattern. The concept of "recessive" and "dominant" antedate molecular biology and technically apply only to traits, not to genes themselves. In pleiotropic conditions, such as LWS, the application of "recessive" or "dominant" can be ambiguous.[30]
A separate issue is the nomenclature applied to the frame pattern itself. While it follows a dominant pattern of inheritance, deviations occur.[31] The majority of horses with the Ile118Lys mutation do exhibit the recognizable frame pattern, but a small percentage are too modestly marked to be classified as "spotted" by breed registries. Such "solid" horses, bred to a solid partner, can produce classically marked frames.[32] The "crop-out" phenomenon can make frame appear to follow a recessive mode of inheritance.
Prevalence
The gene for LWS is most common in the American Paint Horse, but occurs in any breed that may carry frame genetics, including American Quarter Horses, Appaloosas, Thoroughbreds, Morgan horses, miniature horses, Tennessee Walking Horses, and mustangs, as well as horses that are descended from these breeds.[citation needed] Only two Morgan horses have been identified as frame overos.[33] Breeds that do not carry genes for the frame pattern also do not carry LWS.[34]
This blue-eyed, pink-skinned, whitish filly is, in fact, a cremello, and is healthy. Her skin is a rosier shade and her coat cream-colored, as opposed to stark white.
Not all white, blue-eyed foals are affected with LWS. Other genes can produce healthy pink-skinned, blue-eyed horses with a white or very light cream-colored coat.[14] For a time, some of these completely white horses were called "living lethals", but this is a misnomer. Before reliable information and the DNA test were available to breeders, perfectly healthy, white-coated, blue-eyed foals were sometimes euthanized for fear they were lethal whites,[14] an outcome which can be avoided today with testing and a better understanding of coat color genetics or even waiting 12 hours or so for the foal to develop clinical signs. The availability of testing also allows a breeder to determine if a white-coated, blue-eyed foal that becomes ill is an LWS foal that requires euthanasia or a non-LWS foal with a simple illness that may be successfully treated.
Double-cream dilutes such as cremello, perlinos, and smoky creams, have cream-colored coats, blue eyes, and pink skin. The faint cream pigmentation of their coats can be distinguished from the unpigmented white markings and underlying unpigmented pink skin. A similar-looking "pseudo double dilute" can be produced with help from the pearl gene or "barlink factor" or the champagne gene.[citation needed]
The combination of tobiano with other white-spotting patterns can produce white or nearly white horses, which may have blue eyes.[35]
Sabino horses that are homozygous for the sabino-1 (Sb-1) gene are often called "sabino-white", and are all- or nearly all-white. Not all sabino horses carry Sb-1.[24]
Dominant white genetics are not thoroughly understood, but are characterized by all- or nearly all-white coats.
Analogous conditions
From very early in research into its genetics,[4] LWS has been compared to Hirschsprung's disease in humans, which is also caused by mutations on the EDNRB gene. Various polymorphisms on this gene result in intestinal agangliosis, in some cases attended by unusual pigmentation of the skin and eyes, and deafness. The occasionally attendant pigmentation condition in humans is called Waardenburg-Shah syndrome.[5]
The terms "piebald-lethal" and "spotting lethal" apply to similar conditions in mice and rats, respectively, both caused by mutations on the EDNRB gene.[36][37] Only lethal in the homozygous state, the mutations are associated with white-spotted coats, deafness, and megacolon caused by intestinal agangliosis.[5]
The American Paint Horse is a breed of horse that combines both the conformational characteristics of a western stock horse with a pinto spotting pattern of white and dark coat colors. Developed from a base of spotted horses with Quarter Horse and Thoroughbred bloodlines, the American Paint Horse Association (APHA) breed registry is now one of the largest in North America. The registry allows some non-spotted animals to be registered as "Solid Paint Bred" and considers the American Paint Horse to be a horse breed with distinct characteristics, not merely a color breed.
A piebald or pied animal is one that has a pattern of unpigmented spots (white) on a pigmented background of hair, feathers or scales. Thus a piebald black and white dog is a black dog with white spots. The animal's skin under the white background is not pigmented.
Skewbald is a colour pattern of horses. A skewbald horse has a coat made up of white patches on a non-black base coat, such as chestnut, bay, or any colour besides black coat. Skewbald horses which are bay and white are sometimes called tricoloured. These horses usually have pink skin under white markings and dark skin under non-white areas. Other than colour, it is similar in appearance to the piebald pattern. Some animals also exhibit colouration of the irises of the eye that match the surrounding skin. The underlying genetic cause is related to a condition known as leucism. The term is also used to describe spotting patterns in various other animals, such as goats.
Tri-coloured refers to a horse with three different coat colours in a pinto spotting pattern of large white and dark patches, usually bay and white. This colouring is also commonly called skewbald. In modern usage in British English, skewbald and piebald horses are collectively referred to as coloured, while in North American English, the term pinto is used to describe the colour pattern.
Bay is a hair coat color of horses, characterized by a reddish-brown or brown body color with a black point coloration on the mane, tail, ear edges, and lower legs. Bay is one of the most common coat colors in many horse breeds.
Equine coat color genetics determine a horse's coat color. Many colors are possible, but all variations are produced by changes in only a few genes. Bay is the most common color of horses. A change at the agouti locus is capable of turning bay to black, while a mutation at the extension locus can turn bay or black to chestnut.
A pinto horse has a coat color that consists of large patches of white and any other color. The distinction between "pinto" and "solid" can be tenuous, as so-called "solid" horses frequently have areas of white hair. Various cultures throughout history appear to have selectively bred for pinto patterns.
Tobiano is a spotted color pattern commonly seen in pinto horses, produced by a dominant gene. The tobiano gene produces white-haired, pink-skinned patches on a base coat color. The coloration is almost always present from birth and does not change throughout the horse's lifetime, unless the horse also carries the gray gene. It is a dominant gene, so any tobiano horse must have at least one parent who carries the tobiano gene.
Overo refers to several genetically unrelated pinto coloration patterns of white-over-dark body markings in horses, and is a term used by the American Paint Horse Association to classify a set of pinto patterns that are not tobiano. Overo is a Spanish word, originally meaning "like an egg". The most common usage refers to frame overo, but splashed white and sabino are also considered "overo". A horse with both tobiano and overo patterns is called tovero.
The Tovero coloration is a mix of tobiano and overo colorations in Pinto horses and American Paint Horses. The genetics of pinto coloration are not always fully understood, and some horses have a combination of patterns that does not fit cleanly in either category.
Horses exhibit a diverse array of coat colors and distinctive markings. A specialized vocabulary has evolved to describe them.
A white horse is born predominantly white and stays white throughout its life. A white horse has mostly pink skin under its hair coat, and may have brown, blue, or hazel eyes. "True white" horses, especially those that carry one of the dominant white (W) genes, are rare. Most horses that are commonly referred to as "white" are actually "gray" horses whose hair coats are completely white. Gray horses may be born of any color and their hairs gradually turn white as time goes by and take on a white appearance. Nearly all gray horses have dark skin, except under any white markings present at birth. Skin color is the most common method for an observer to distinguish between mature white and gray horses.
Sabino describes a distinct pattern of white spotting in horses. In general, Sabino patterning is visually recognized by roaning or irregular edges of white markings, belly spots, white extending past the eyes or onto the chin, white above the knees or hocks, and "splash" or "lacy" marks anywhere on the body. Some sabinos have patches of roan patterning on part of the body, especially the barrel and flanks. Some sabinos may have a dark leg or two, but many have four white legs. Sabino patterns may range from slightly bold face or leg white markings—as little as white on the chin or lower lip—to horses that are fully white.
The American Paint Horse Association (APHA) is a breed registry for the American Paint Horse. It is currently headquartered in Fort Worth, Texas. It was founded in 1965 with the merging of two different color breed registries that had been formed to register pinto-colored horses of Quarter Horse bloodlines. One of these organizations was the American Paint Quarter Horse Association and the other was the American Paint Stock Horse Association.
Endothelin receptor type B, (ET-B) is a protein that in humans is encoded by the EDNRB gene.
A cropout, crop-out or crop out is a horse with body spots, including pinto or leopard complex spotting, or "high white" horse markings, with a sire and dam who both appeared to have been solid-colored. There are several variations in the definition, depending on the breed registry involved. There are multiple genetic reasons that may cause a horse to be a cropout. Sometimes solid-colored horses throw cropouts because some spotting patterns are recessive genes that are not necessarily expressed unless the relevant allele is inherited from both parents. Other times a gene may be a dominant or incomplete dominant but so minimally expressed that the horse looks solid but can pass flashy color on to its offspring.
Splashed white or splash is a horse coat color pattern in the "overo" group of spotting patterns that produces pink-skinned, white markings. Many splashed whites have very modest markings, while others have the distinctive "dipped in white paint" pattern. Blue eyes are a hallmark of the pattern, and splash may account for otherwise "solid" blue-eyed horses. Splashed white occurs in a variety of geographically divergent breeds, from Morgans in North America to Kathiawari horses in India. The splashed white pattern is also associated with congenital deafness, though most splashed whites have normal hearing. Splashed white can be caused by multiple variants across two different genes, for which genetic testing is available.
Dominant white (W) is a group of genetically related coat color alleles on the KIT gene of the horse, best known for producing an all-white coat, but also able to produce various forms of white spotting, as well as bold white markings. Prior to the discovery of the W allelic series, many of these patterns were described by the term sabino, which is still used by some breed registries.
Roan is a horse coat color pattern characterized by an even mixture of colored and white hairs on the body, while the head and "points"—lower legs, mane, and tail—are mostly solid-colored. Horses with roan coats have white hairs evenly intermingled throughout any other color. The head, legs, mane, and tail have fewer scattered white hairs or none at all. The roan pattern is dominantly inherited, and is found in many horse breeds. While the specific mutation responsible for roan has not been exactly identified, a DNA test can determine zygosity for roan in several breeds. True roan is always present at birth, though it may be hard to see until after the foal coat sheds out. The coat may lighten or darken from winter to summer, but unlike the gray coat color, which also begins with intermixed white and colored hairs, roans do not become progressively lighter in color as they age. The silvering effect of mixed white and colored hairs can create coats that look bluish or pinkish.
Ann Trommershausen Bowling was an American scientist who was one of the world's leading geneticists in the study of horses, conducting research in the areas of molecular genetics and cytogenetics. She was a major figure in the development of testing to determine animal parentage, first with blood typing in the 1980s and then DNA testing in the 1990s. She later became known for her studies of hereditary diseases in horses and equine coat color genetics, as well as research on horse evolution and the development of horse breeds. She studied the population genetics of feral horses, did considerable work to help preserve the Przewalski's horse, and was one of the founding members of the international project to map the horse genome. She was an adjunct professor at the University of California, Davis (UCD), and at the time of her death in 2000 was the executive associate director of the Veterinary Genetics Laboratory (VGL) there. Her unexpected death on December 8, 2000, at age 57 was attributed to a massive stroke.
↑ Thiruvenkadan, AK; Kandasamy N; Panneerselvam S (2008). "Coat colour inheritance in horses". Livestock Science. Elsevier. 117 (2–3): 109–129. doi:10.1016/j.livsci.2008.05.008. There are many mutations that may affect the migration of the cells from the neural crest...Very many different mutants that affect migration of the cells from neural crest region cause lethal white-spotting condition. These mutations affect normal melanocytic and enteric neural crest cell differentiation, proliferation, and migration during development (Searle, 1968). This leads to depigmentation and also lack of neural connections to the colon.
↑ Metallinos DL, Bowling AT, Rine J (1998). "In three unrelated lethal white foals, the EDNRB gene contained a 2-bp nucleotide change leading to a missense mutation (I118K) in the first transmembrane domain of the receptor, a highly conserved region of this protein among different species. Seven additional unrelated lethal white foal samples were found to be homozygous for this mutation. No other homozygotes were identified in 138 samples analyzed, suggesting that homozygosity was restricted to lethal white foals. All (40/40) horses with the frame overo pattern (a distinct coat color pattern that is a subset of overo horses) that were tested were heterozygous for this allele, defining a heterozygous coat color phenotype for this mutation."
1 2 3 4 Australian Equine Genetics Research Center. "Overo-Lethal White Foal Syndrome (OLW)". DNA Screening Tests. University of Queensland. Archived from the original on 2008-07-21. Retrieved 2008-09-05. An individual contains two copies of a gene, one inherited from its father, the other from its mother. When both copies of the EDNRB gene are the mutated form, LWS results. However, when an individual has one copy that is normal (also called the "wild-type" of the gene) and one that is the mutated form, then an overo colour pattern results.
1 2 3 4 5 Overton, Rebecca (2004-03-01). "By A Hair"(PDF). Paint Horse Journal. American Paint Horse Association. Archived from the original(PDF) on March 8, 2008. Retrieved 2008-09-06.
↑ Vrotsos, Paul D.; Elizabeth M. Santschi (1998-07-01). "Stalking the Lethal White Syndrome". Paint Horse Journal. American Paint Horse Association. Archived from the original on 2008-10-26. Retrieved 2008-09-06.
↑ "Overo Pattern". American Paint Horse Association. Archived from the original on 2008-09-06. Retrieved 2008-09-03.
1 2 "Horse coat color tests". Veterinary Genetics Laboratory, University of California, Davis. Retrieved 2008-09-06.
↑ Brooks, Samantha (2006). "Studies of Genetic Variation at the KIT Locus and White Spotting Patterns in the Horse". University of Kentucky. Archived from the original(PDF) on 2012-12-12. Retrieved 2010-12-29. Aside from the scientific benefits of studying coat color in the horse there is a more immediate advantage. People like the look of unusual coat colors, and they are willing to pay for a way to improve their ability to get more of them. The value in a flashy colored horse isn't as easily measured as that in a fast race horse, but it does translate into real dollars at the point of sale. For example, the average price of an APHA registered yearling (young horses with undetermined athletic ability) without a spotting pattern on Equine.com was $1540. A yearling APHA registered horse with the tobiano pattern averaged $2803 (Appendix B). This price difference creates an enormous interest among breeders to increase their production of spotted foals.{{cite journal}}: Cite journal requires |journal= (help)
↑ Finno, Carrie J.; Sharon J. Spier; Stephanie J. Valberg (March 2009). "Equine diseases caused by known genetic mutations". The Veterinary Journal. Elsevier. 179 (3): 336–47. doi:10.1016/j.tvjl.2008.03.016. PMID18472287. Ileocolonic aganglionosis, or overo lethal white foal syndrome (OLWS), is an autosomal recessive trait
↑ Metallinos et al 1998. "Based on the strength of this association and its complete compatibility with simple mendelian recessive inheritance, we inferred that Lethal White Foal Syndrome was tightly linked to the mutation."
↑ Thiruvenkadan et al 2008. "The overo lethal syndrome due to dominant homozygotes (OO) at the overo locus results in death of the foals a few days after birth."
↑ Bowling AT (1994). "Dominant inheritance of overo spotting in paint horses". J. Hered. 85 (3): 222–4. doi:10.1093/oxfordjournals.jhered.a111439. PMID8014463. Analysis of selected studbook records of the American Paint Horse Association, consisting of 687 foals sired by 13 overo stallions from nonovero mares, supports the inheritance of overo spotting as an autosomal dominant gene. More than one gene may control patterns registered as overo.
↑ "Genetic Equation". American Paint Horse Association. Archived from the original on 2008-09-07. Retrieved 2008-09-04. Frame overo behaves as a dominant gene. [T]here are records of frame overos being produced by two nonspotted parents. This is typical of a recessive gene, and it is not logical to have both a recessive and a dominant control over the same pattern.
↑ Laura Behning. "Other Colors". Morgan Colors. Retrieved 2009-05-03.
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