Dominant white explained

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.

White-colored horses are born with unpigmented pink skin and white hair, usually with dark eyes. Under normal conditions, at least one parent must be dominant white to produce dominant white offspring. However, most of the currently-known alleles can be linked to a documented spontaneous mutation that began with a single ancestor born of non-dominant white parents. Horses that exhibit white spotting will have pink skin under the white markings, but usually have dark skin beneath any dark hair.

There are many different alleles that produce dominant white or white spotting; they are labeled W1 through W28 and W30 through W35, plus the first W allele discovered was named Sabino 1 (SB-1) instead of W1.[1] [2] [3] They are associated with the KIT gene. The white spotting produced can range from white markings like those made by W20, to the irregularly-shaped or roaning patterns previously described as Sabino, to a fully white or almost fully white horse.

For many of the W alleles, the white coats are, as the name suggests, inherited dominantly, meaning that a horse only needs one copy of the allele to have a white or white spotted coat. In fact, some such alleles may be embryonic lethal when homozygous. Others, such as SB-1 and W20, are incomplete dominants, capable of producing viable offspring with two copies of the gene, and who generally have more white than horses with only one copy. In addition, different alleles which on their own give a white-spotted but not completely white horse, such as W5 and W10, can combine to make a horse completely white.

White can occur in any breed, and has been studied in many different breeds. Because of the wide range of patterns produced, some suggest the family be called “white spotting” rather than “white.” Other researchers suggest the term "dominant white" be used only for the W alleles thought to be embryonic lethal when homozygous.[4]

White is both genetically and visually distinct from gray and cremello. Dominant white is not the same as lethal white syndrome, nor are white horses "albinos"—Tyrosinase negative albinism has never been documented in horses.

Description

Although the term "dominant white" is typically associated with a pure white coat, such horses may be all-white, near-white, partially white, or exhibit an irregular spotting pattern similar to that of sabino horses.[5] To add to the confusion, at least some horses in each of those groups might be referred to as "dominant white", "white spotted", or "sabino". The amount of white hair depends on which KIT alleles are involved. At birth, most of the white hair is rooted in unpigmented pink skin. The pink skin lacks melanocytes, and appears pink from the underlying network of capillaries. White spotting is not known to affect eye color, and most white horses have brown eyes.[6]

White or near-white

White horses are born with pink skin and a white coat, which they retain throughout their lives.[7] The genetic factors that produce an all-white horse are often also capable of producing a near-white horse, which is mostly white but has some areas that are pigmented normally. Near-white horses most commonly have color in the hair and skin along the topline (dorsal midline) of the horse, in the mane, and on the ears. The color is often interspersed as specks or spots on a white background. In addition, the hooves are usually white, but may have striping if there is pigmented skin on the coronary band just above the hoof.[8] [9] In some cases, foals born with residual non-white hair may lose some or all of this pigment with age, without the help of the gray factor.[10]

White spotting

White spotting from a W allele is difficult to identify visually, as it can range from small white markings in the case of a heterozygous W20 horse all the way to an obvious pinto pattern. In addition, even completely white horses can have genes which by themselves would only give white spotting, such as W20 combined with W22 or W5 combined with W10. As such, the only reliable way to find out whether a horse has one of the known white spotting patterns from an allele on KIT is to have it genetically tested.

Prevalence

Dominant white is one of several potential genetic causes for horses with near-white or completely white coats; it may occur through spontaneous mutation, and thus may be found unexpectedly in any breed, even those that discourage excessive white markings. To date, forms of dominant white have been identified in Thoroughbreds, Standardbreds, American Quarter Horses, Frederiksborg horses, Icelandic horses, Shetland ponies, Franches Montagnes horses, South German Draft horses, and the Arabian horse. The American White Horse, which is descended primarily from one white stallion crossed on non-white mares, is known for its white coat, as is the Camarillo White Horse.[11]

Inheritance

The W locus was mapped to the KIT gene in 2007. KIT is short for "KIT proto-oncogene receptor tyrosine kinase".[12] White spotting is caused by multiple forms, or alleles, of the KIT gene. All horses possess the KIT gene, as it is necessary for survival even at the earliest stages of development. The presence or absence of dominant white is based on the presence of certain altered variants of KIT. Each unique form is called an allele, and for every trait, all animals inherit one allele from each parent. The original or "normal" form of KIT, which is expected in horses without dominant white spotting, is called the "wild type" allele. Thus, a dominant white horse has at least one KIT allele with a mutation associated with dominant white spotting.

Allelic series

The KIT gene contains over 2000 base pairs, and a change in any of those base pairs results in a mutant allele. Over forty seven such alleles have been identified by sequencing the KIT genes of various horses. The resultant phenotype of many of these alleles is not yet known, but over 30 have been linked to white spotting.[13] [14] DNA tests can identify if a horse carries the identified W alleles.

W20 has been found in many breeds including the German Riding Pony, German Warmblood, Thoroughbred, Oldenburger, Welsh pony, Quarter horse, Paint horse, Appaloosa, Noriker, Old-Tori, Gypsy horse, Morgan horse, Clydesdale horse, Franches-Montagnes, Marwari horse, South German Draft, Paso Peruano, Camarillo White Horse, and Hanoverian horse.[29]

W20 is a missense mutation on exon 14 (c.2045G>A; p.Arg682His).[24]

These alleles do not account for all dominantly inherited white spotting in horses. More KIT alleles are expected to be found with roles in white spotting. Most W alleles occur within a specific breed or family and arise as spontaneous mutations. KIT appears to be prone to mutation, in part due to its many exons, so new alleles of W can occur in any breed.[13] There are likely many KIT variants in the global horse population that have not yet been investigated.

Relation to sabino

See main article: Sabino horse. Sabino can refer either specifically to Sabino 1 (SB1) or to a variety of visually similar spotting patterns. SB1 creates a nearly pure white horse when homozygous, and bold spotting when heterozygous. To add to the confusion, white spotting created by several W alleles, such as W5, W15, and W19 creates patterns that historically were called sabino. For that reason, the use of the word "sabino" is evolving. Genetically, Sabino 1 is simply another allele on KIT,[51] and thus can be classified in the same “family” of KIT mutations as the alleles labeled W or dominant white.[52]

In its homozygous form, Sabino 1 can be confused with dominant white alleles such as W1, W2, W3, or W4 that create a white or near-white horse with only one copy. Both dominant white and "Sabino-White" horses are identified by all-white or near-white coats with underlying pink skin and dark eyes, often with residual pigment along the dorsal midline. However, it takes two copies of Sabino 1 to produce a Sabino-white horse, and Sabino 1 is not homozygous lethal.[53]

Initially, dominant white was separated from sabino on the grounds that the former had to be entirely white, while the latter could possess some pigment.[54] However, the 2007 and 2009 studies of dominant white showed that many dominant white alleles produce a range of white phenotypes that include horses with pigmented spots in their hair and skin. Each of the larger families of dominant white studied included pure-white horses, horses described as having "sabino-like" white markings, as well as white horses described as "maximal sabino".

More recently, dominant white and sabino were distinguished from one another on the grounds that dominant white alleles produce nonviable embryos in the homozygous state, while Sabino 1 was viable when homozygous.[55] However, not all KIT alleles currently identified as "dominant white" have been proven lethal,[56] and in fact W20 is known to be viable in the homozygous form.[57]

The similarities between Dominant White and Sabino 1 reflect their common molecular origin: The W series and SB1 have both been mapped to KIT. The researchers who mapped Sabino 1 in 2005 suggested that other sabino-like patterns might also map to KIT,[51] which has been the case for many other alleles discovered since that time, including major alleles for white leg and facial markings that have also been mapped to or near to the KIT gene.

Molecular genetics

See main article: CD117.

The KIT gene encodes a protein called steel factor receptor, which is critical to the differentiation of stem cells into blood cells, sperm cells, and pigment cells. A process called alternative splicing, which uses the information encoded in the KIT gene to make slightly different proteins (isoforms) for use in different circumstances, may impact whether a mutation on KIT affects blood cells, sperm cells, or pigment cells. Steel factor receptor interacts chemically with steel factor or stem cell factor to relay chemical messages. These messages are used during embryonic development to signal the migration of early melanocytes (pigment cells) from the neural crest tissue to their eventual destinations in the dermal layer. The neural crest is a transient tissue in the embryo that lies along the dorsal line. Melanocytes migrate along the dorsal line to a number of specific sites: near the eye, near the ear, and the top of the head; six sites along each side of the body, and a few along the tail. At these sites, the cells undergo a few rounds of replication and differentiation, and then migrate down and around the body from the dorsal aspect towards the ventral aspect and the limb buds.[58]

The timing of this migration is critical; all white markings, from a small star to a pure white coat, are caused by the failed migration of melanocytes.[59]

A certain degree of the eventual amount of white, and its "design", is completely random. The development of an organism from single-celled to fully formed is a process with many, many steps. Even beginning with identical genomes, as in clones and identical twins, the process is unlikely to occur the same way twice. A process with this element of randomness is called a stochastic process, and cell differentiation is, in part, a stochastic process.[60] The stochastic element of development is partly responsible for the eventual appearance of white on a horse, potentially accounting for nearly a quarter of the phenotype.[61] The research team that studied dominant white cited "subtle variations in the amount of residual KIT protein" as a potential cause for the variability in phenotype of horses with the same allele. They also speculated that variability in the phenotype of horses with W1 might be caused by "different efficacies of [nonsense-mediated decay] in different individuals and in different body regions." That is, some horses destroy more of the mutant KIT protein than others.

Lethality

See also: Lethal allele. Early embryonal lethality, also known as early embryonic death or a non-viable embryo, may occur when the embryo possesses two copies of certain dominant white alleles.[62] The reason for this is that several mutations of W are caused by nonsense mutations, frameshift mutations or DNA deletions, which, if homozygous, would make it impossible to produce a functional KIT protein. However, it appears that not all W alleles are embryonic lethals. Homozygous embryos from alleles of certain missense and splice site mutations are sometimes viable, apparently because they have less effect on gene function.[13] For instance, W1 is a nonsense mutation and it is thought that horses with the genotype W1/W1 would die in utero, while W20 is a missense mutation and living horses with the W20/W20 genotype have been found. A 2013 study also located horses that were compound W5/W20 heterozygotes, almost completely white, essentially with greater depigmentation than could be accounted for by either allele alone.[24]

"White" horses that are not dominant white

See also: White (horse). White horses are potent symbols in many cultures.[63] An array of horse coat colors may be identified as "white", often inaccurately, and many are genetically distinct from "dominant white".

"Albino" horses have never been documented, despite references to so-called "albino" horses.[64] [65] Dominant white is caused by the absence of pigment cells (melanocytes), whereas albino animals have a normal distribution of melanocytes.[66] Also, a diagnosis of albinism in humans is based on visual impairment, which has not been described in horses with dominant white nor similar coat colors.[67] In other mammals, the diagnosis of albinism is based on the impairment of tyrosinase production.[68] No mutations of the tyrosinase gene are known in horses, however, cream and pearl colors result from mutations to a protein involved in tyrosinase transport.[69]

Non-white colors

Lethal white overo

See main article: Lethal white syndrome. Foals with lethal white syndrome (LWS) have two copies of the frame overo gene and are born with white or nearly white coats and pink skin. However, unlike dominant white horses, foals with LWS are born with an underdeveloped colon that is untreatable, and if not euthanized, invariably die of colic within a few days of birth.[80] Horses that carry only one allele of the LWS gene are healthy and typically exhibit the "frame overo" spotting pattern. In cases of "solid" horses with frame overo ancestry, uncertain "overo" (non-tobiano) phenotype, or horses with multiple patterns, the LWS allele can be detected by DNA test.[81]

Mosaicism

Mosaicism in horses is thought to account for some spontaneous occurrences of white, near-white, spotted, and roan horses.[82] Mosaicism refers to mutations that occur after the single-cell stage, and therefore affect only a portion of the adult cells.[83] Mosaicism may be one possible cause for the rare occurrence of brindle coloring in horses.[84] Mosaic-white horses would be visually indistinguishable from dominant whites. Mosaicism could produce white or partially white foals if a stem cell in the developing foal underwent a mutation, or change to the DNA, that resulted in unpigmented skin and hair. The cells that descend from the affected stem cell will exhibit the mutation, while the rest of the cells are unaffected.

A mosaic mutation may or may not be inheritable, depending on the cell populations affected.[85] Though this is not always the case, genetic mutations can occur spontaneously in one sex cell of a parent during gametogenesis.[86] In these cases, called germline mutations, the mutation will be present in the single-celled zygote conceived from the affected sperm or egg cell, and the condition can be inherited by the next generation.

History of dominant white research

Dominant white horses were first described in scientific literature in 1912. Horse breeder William P. Newell described his family of white and near-white horses to researcher A. P. Sturtevant of Columbia University:

"The colour of skin is white or so-called pink, usually with a few small dark specks in skin. Some have a great many dark spots in skin. These latter usually have a few dark stripes in hoofs; otherwise the hoofs are almost invariably white. Those that do not have dark specks in skin usually have glass or watch eyes, otherwise dark eyes ... I have one colt coming one year old that is pure white, not a coloured speck on him, not a coloured hair on him, and with glass [blue] eyes."

Sturtevant and his contemporaries agreed that this colt's blue eyes were inherited separately from his white coat.[87] In 1912, Sturtevant assigned the "white" trait to the White or W locus. At the time there was no means of assigning W to a position on the chromosome, or to a gene.

This family of white horses produced Old King in 1908, a dark-eyed white stallion that was purchased by Caleb R. and Hudson B. Thompson. Old King was bred to Morgan mares to produce a breed of horse known today as the American White Horse.[88] A grandson of Old King, Snow King, was at the center of the first major study of the dominant white coat color in horses, conducted in 1969 by Dr. William L. Pulos of Alfred University and Dr. Frederick B. Hutt of Cornell. They concluded, based on test matings and progeny phenotype ratios, that the white coat was dominantly inherited and embryonic lethal in the homozygous state.[89] Other factors, such as variations in expressivity and the influence of multiple genes, may have influenced the progeny ratios that Pulos and Hutt observed. The white coat of the American White Horse has not yet been mapped.

A 1924 study by C. Wriedt identified a heritable white coat color in the Frederiksborg horse.[90] Wriedt described a range of what he considered to be homozygote phenotypes: all-white, white with pigmented flecks, or weißgraue, which transliterates to "white-gray."[91] The German term for gray horse is schimmel, not weißgraue.[92] Heterozygotes, according to Wriedt, ranged from roaned or diluted to more or less solid white horses. Reviewers, such as Miguel Odriozola, reinterpreted Wriedt's data in successive years, while Pulos and Hutt felt that his work had been "erroneous" because Wriedt never concluded that white was lethal when homozygous.[93]

Other researchers prior to modern DNA analysis developed remarkably prescient theories. The gene itself was first proposed and named W in 1948.[13] In a 1969 work on horse coat colors, A los colores del caballo, Miguel Odriozola suggested that various forms of dominantly inherited white spotting might be arranged sequentially along one chromosome, thus allowing for the varied expression of dominant white. He also proposed that other, distant genes might also influence the amount of white present.[94]

The embryonic lethality hypothesis was originally supported by Pulos and Hutt's 1969 study of Mendelian progeny ratios. Conclusions about Mendelian traits that are controlled by a single gene can be drawn from test breedings with large sample sizes. However, traits that are controlled by allelic series or multiple loci are not Mendelian characters, and may not be subject to Mendelian ratios.[95]

Pulos and Hutt knew that if the allele that created a white coat was recessive, then white horses would have to be homozygous for the condition and therefore breeding white horses together would always result in a white foal. However, this did not occur in their study and they concluded that white was not recessive. Conversely, if a white coat was a simple autosomal dominant, ww horses would be non-white, while both Ww and WW horses would be white, and the latter would always produce white offspring. But Pulos and Hutt did not observe any white horses that always produced white offspring, suggesting that homozygous dominant (WW) white horses did not exist. As a result, Pulos and Hutt concluded that white was semidominant and lethal in the homozygous state: ww horses were non-white, Ww were white, and WW died.[96]

Pulos and Hutt reported that neonatal death rates in white foals were similar to those in non-white foals, and concluded that homozygous white fetuses died during gestation.[97] No aborted fetuses were found, suggesting that death occurred early on in embryonic or fetal development and that the fetus was "resorbed."[98]

Prior to Pulos and Hutt's work, researchers were split on the mode of inheritance of white and whether it was deleterious (harmful).[99] Recent research has discovered several possible genetic pathways to a white coat, so disparities in these historical findings may reflect the action of different genes. It is also possible that the varied origins of Pulos and Hutt's white horses might be responsible for the lack of homozygotes. It now appears that not all equine dominant white mutations cause embryonic lethality in the homozygous state.[100]

The white (W) locus was first recognized in mice in 1908.[101] The mutation of the same name produces a belly spot and interspersed white hairs on the dorsal aspect of the coat in the heterozygote (W/+) and black-eyed white in the homozygote (W/W). While heterozygotes are healthy, homozygous W mice have severe macrocytic anemia and die within days.[102] A mutation which affects multiple systems is "pleiotropic." Following the mapping of the KIT gene to the W locus in 1988, researchers began identifying other mutations as part of an allelic series of W.[103] There are dozens of known alleles, each representing a unique mutation on the KIT gene, which primarily produce white spotting from tiny head spots to fully white coats, macrocytic anemia from mild to lethal, and sterility. Some alleles, such as splash produce white spotting alone, while others affect the health of the animal even in the heterozygous state. Alleles encoding small amounts of white are no more likely to be linked with anemia and sterility than those encoding conspicuous white. Presently, no anecdotal or research evidence has suggested that equine KIT mutations affect health or fertility.[104] A recent study showed that blood parameters in horses with the W1 mutation were normal.[105]

Between the time of Pulos and Hutt's study in 1969 and the beginning of molecular-level research into dominant white in the 21st century, a pattern known as "Sabino" began to describe certain white phenotypes.[106] The first allele of the W series identified by researchers was an incomplete dominant that was named Sabino-1 (SB-1). It is found on the same locus as other W alleles. When homozygous, SB-1 can produce nearly all-white horses.

In 2007, researchers from Switzerland and the United States published a paper identifying the genetic cause of dominant white spotting in horses from the Franches Montagnes horse, Camarillo White Horse, Arabian horse and Thoroughbred breeds. Each of these dominant white conditions had occurred separately and spontaneously in the past 75 years, and each represents a different allele (variation or form) of the same gene. These same researchers identified a further seven unique causes of dominant white in 2009: three in distinct families of Thoroughbreds, one Icelandic horse, one Holsteiner, a large family of American Quarter Horses and a family of South German Draft horses.

Homologous conditions

See also: Homology (biology). In humans, a skin condition called piebaldism is caused by more than a dozen distinct mutations in the KIT gene. Piebaldism in humans is characterized by a white forelock, and pigmentless patches of skin on the forehead, brow, face, ventral trunk and extremities. Outside of pigmentation, piebaldism is an otherwise benign condition.[107] In pigs, the "patch," "belted," and commercial "white" colors are caused by mutations on the KIT gene.[108] The best-known model for KIT gene function is the mouse, in which over 90 alleles have been described. The various alleles produce everything from white toes and blazes to black-eyed white mice, panda-white to sashed and belted. Many of these alleles are lethal in the homozygous state, lethal when combined, or sublethal due to anemia. Male mice with KIT mutations are often sterile.[109]

External links

Notes and References

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  43. Esdaile . Elizabeth . Till . Brad . Kallenberg . Angelica . Fremeux . Michelle . Bickel . Leslie . Bellone . Rebecca R. . 2022-05-31 . A de novo missense mutation in KIT is responsible for dominant white spotting phenotype in a Standardbred horse . Animal Genetics . 53 . 4 . en . 534–537 . 10.1111/age.13222 . 35641888 . 249233588 . 0268-9146.
  44. Patterson Rosa . Laura . Martin . Katie . Vierra . Micaela . Lundquist . Erica . Foster . Gabriel . Brooks . Samantha A. . Lafayette . Christa . A KIT Variant Associated with Increased White Spotting Epistatic to MC1R Genotype in Horses (Equus caballus) . Animals . 1958 . en . 10.3390/ani12151958 . January 2022. 12 . 15 . 35953947 . 9367399 . free .
  45. Web site: Etalon Discovers New White Marking Variant W35 "Holiday" in Horses.
  46. 10.1016/j.jevs.2023.104563. 5'UTR Variant in KIT Associated With White Spotting in Horses. 2023 . 37182614 . McFadden . A. . Martin . K. . Foster . G. . Vierra . M. . Lundquist . E. W. . Everts . R. E. . Martin . E. . Volz . E. . McLoone . K. . Brooks . S. A. . Lafayette . C. . Journal of Equine Veterinary Science . 127 . 104563 .
  47. A Genome-Wide Association Analysis in Noriker Horses Identifies a SNP Associated With Roan Coat Color . 2020. 10.1016/j.jevs.2020.102950. Grilz-Seger. Gertrud. Reiter. Simone. Neuditschko. Markus. Wallner. Barbara. Rieder. Stefan. Leeb. Tosso. Jagannathan. Vidhya. Mesarič. Matjaz. Cotman. Markus. Pausch. Hubert. Lindgren. Gabriella. Velie. Brandon. Horna. Michaela. Brem. Gottfried. Druml. Thomas. Journal of Equine Veterinary Science. 88. 102950. 32303326. 212861746.
  48. Coat Color Roan Shows Association with KIT Variants and No Evidence of Lethality in Icelandic Horses. 2020. 10.3390/genes11060680. free. Voß. Katharina. Tetens. Julia. Thaller. Georg. Becker. Doreen. Genes. 11. 6. 680. 32580410. 7348759.
  49. A chromosome inversion near the KIT gene and the Tobiano spotting pattern in horses . Brooks . Lear . Adelson . Bailey. Cytogenetic and Genome Research . 2007 . 119 . 3–4 . 225–30 . 10.1159/000112065 . 18253033 . 22835035 .
  50. Whole-genome sequencing reveals a large deletion in the MITF gene in horses with white spotted coat colour and increased risk of deafness . Henkel J, Lafayette C, Brooks SA, Martin K, Patterson-Rosa L, Cook D, Jagannathan V, Leeb T . 2019 . Animal Genetics . 50 . 2 . 172–174 . 10.1111/age.12762. 30644113 . 58656314 .
  51. Brooks . Samantha . Ernest Bailey . 2005 . Exon skipping in the KIT gene causes a Sabino spotting pattern in horses . Mammalian Genome . 16 . 893–902 . Chapter 3 . 10.1007/s00335-005-2472-y . 16284805 . 11. 32782072 .
  52. Web site: Sabino-1. Centerforanimalgenetics.com. 27 April 2019. https://web.archive.org/web/20190106042046/https://www.centerforanimalgenetics.com/services/horse-genetic-testing/phenotype-testing-for-horses/sabino-1/. 6 January 2019.
  53. Web site: Sabino 1 . January 5, 2018 . UC Davis . Veterinary Genetics Laboratory . University of California - Davis. Horses with 2 copies of the Sabino1 gene, are at least 90% white and are referred to as Sabino-white..
  54. Castle, Nancy (2009). "It has been the belief of horse enthusiasts that true “white” horses were always completely white with no retained pigment, and that if a horse retained some pigment of the skin and/or hair, it was genetically some form of sabino if it were not the result of other known white spotting patterns (tobiano, frame overo, splash white, etc.)"
  55. Castle, Nancy (2009). "KIT mutations that cause depigmentation generally ranging from approximately 50% depigmented to all white phenotypes, and are also predicted to be embryonic lethal when homozygous, are classified as Dominant White. Mutations that are viable in the homozygous state are categorized as Sabino."
  56. Haase, B. et al (2007) "While [homozygous lethality] is certainly likely for the two nonsense mutations found in Franches-Montagnes Horses and Arabians, it should not necessarily be assumed for the two reported missense mutations or for any of the other as-yet unknown W mutations."
  57. Web site: Dominant White - Horse Coat Color.
  58. Thiruvenkadan . AK . N Kandasamy. S Panneerselvam . Review: Coat colour inheritance in horses . Livestock Science . 117 . 2008 . 2–3 . 109–129 . During embryogenesis the pigment cells (melanocytes) migrate to specific sites on either side of the body as well as the backline. There are three such sites on the head (near the eye, ear, and top of the head), and six sites along each side of the body, and several along the tail. A few pigment cells migrate to each of these sites, there they proliferate and migrate outwards, joining up to form larger patches, spreading down the legs and down the head until they meet up under the chin, and down the body until they meet up on the belly (Cattanach, 1999). . 10.1016/j.livsci.2008.05.008.
  59. Rieder S, Hagger C, Obexer-Ruff G, Leeb T, Poncet PA . Genetic analysis of white facial and leg markings in the Swiss Franches-Montagnes Horse Breed . The Journal of Heredity . 99 . 2 . 130–6 . 2008 . 18296388 . 10.1093/jhered/esm115 . Phenotypes may vary from tiny depigmentated body spots to white head and leg markings, further on to large white spotting and finally nearly complete depigmentation in white-born horses ... White markings result from the lack of melanocytes in the hair follicles and the skin ... A completely pigmented head or leg depends on the complete migration and clonal proliferation of the melanoblasts in the mesoderm of the developing fetus, thus ensuring that limbs and the head acquire a full complement of melanocytes. free .
  60. Kurakin A . Self-organization vs Watchmaker: stochastic gene expression and cell differentiation . Development Genes and Evolution . 215 . 1 . 46–52 . January 2005 . 15645318 . 10.1007/s00427-004-0448-7. 10728304 .
  61. Woolf CM . Influence of stochastic events on the phenotypic variation of common white leg markings in the Arabian horse: implications for various genetic disorders in humans . The Journal of Heredity . 86 . 2 . 129–35 . 1995 . 7751597 . 10.1093/oxfordjournals.jhered.a111542 .
  62. Haase, B. et al. (2007) "In one study, white horses were shown to be obligate heterozygous (W/+), as the W/W genotype was hypothesized to cause early embryonal lethality [4]."
  63. Encyclopedia: Cooper . JC . An Illustrated Encyclopedia of Traditional Symbols . Horse . 1978 . Thames & Hudson . London . 978-0-500-27125-4 . 85–6 . ... [T]he white horse ... represents pure intellect; the unblemished; innocence; life and light, and is ridden by heroes. . registration .
  64. Castle . William E . The ABC of Color Inheritance in Horses . Genetics . 33 . 1 . 22–35 . 17247268 . No true albino mutation of the color gene is known among horses, though several varieties of white horse are popularly known as albinos. . 1948 . 10.1093/genetics/33.1.22 . 1209395.
  65. Book: O'Hara, Mary . My Friend Flicka . registration . 1941 . Lippincott . 978-0-06-080902-7.
  66. Book: Silvers, Willys K. . The Coat Colors of Mice: A Model for Mammalian Gene Action and Interaction . 3: The b-Locus and c (Albino) Series of Alleles . Springer Verlag . 1979 . http://www.informatics.jax.org/wksilvers/chapters/chapter3-2.shtml . 2009-07-07 . 59 . ... the inability of albino animals to produce pigment stems not from an absence of melanocytes.
  67. Web site: What is Albinism? . The National Organization for Albinism and Hypopigmentation . 2009-07-07 . https://web.archive.org/web/20120514003907/http://www.albinism.org/publications/what_is_albinism.html . 2012-05-14 . dead .
  68. Book: Cheville, Norman F . Introduction to veterinary pathology . August 2006 . Wiley-Blackwell . 978-0-8138-2495-6 . 3 . Albinism results from a structural gene mutation at the locus that codes for tyrosinase; that is, albino animals have a genetically determined failure of tyrosine synthesis..
  69. A Missense Mutation in SLC45A2 Is Associated with Albinism in Several Small Long Haired Dog Breeds . Wijesen . Schmutz . Journal of Heredity . 106 . 3 . 285–8 . May–June 2015 . 10.1093/jhered/esv008. 25790827 . free .
  70. Web site: Facts and Myths . Cream Gene Information . Cremello and Perlino Education Association . 2009-07-08 . dead . https://web.archive.org/web/20120207114059/http://www.doubledilute.com/cremecolors.htm . 2012-02-07 .
  71. Mariat . Denis . Sead Taourit. Gérard Guérin . A mutation in the MATP gene causes the cream coat colour in the horse. . Genet. Sel. Evol. . 35 . 2003 . 119–133 . 10.1051/gse:2002039 . 12605854 . 1 . 2732686.
  72. Web site: Champagne-Cream Combinations . International Champagne Horse Registry . 2009-06-04.
  73. Rosengren Pielberg G, Golovko A, Sundström E . A cis-acting regulatory mutation causes premature hair graying and susceptibility to melanoma in the horse . Nature Genetics . 40 . 8 . 1004–9 . August 2008 . 18641652 . 10.1038/ng.185. 6666394 . etal.
  74. Bellone . Rebecca R . Samantha A Brookers. Lynne Sandmeyer. Barbara A Murphy. George Forsyth. Sheila Archer. Ernest Bailey. Bruce Grahn . Differential Gene Expression of TRPM1, the Potential Cause of Congenital Stationary Night Blindness and Coat Spotting Patterns (LP) in the Appaloosa Horse (Equus caballus) . Genetics . 179 . August 2008 . 1861–1870 . 10.1534/genetics.108.088807 . A single autosomal dominant gene, leopard complex (LP), is thought to be responsible for the inheritance of these patterns and associated traits, while modifier genes are thought to play a role in determining the amount of white patterning that is inherited (Miller 1965; Sponenberg et al. 1990; S. Archer and R. R. Bellone, unpublished data) . 18660533 . 4 . 2516064.
  75. Web site: Rules & Knabstrupper Breed Standard of the German ZfDP Registry . UK Knabstrupper Association . 2009-06-20. https://web.archive.org/web/20090529235857/http://www.ukknabstrupperassociation.co.uk/zfdpbreedstandardandrules.htm. 2009-05-29.
  76. Web site: Die Farbmerkmale . Knabstrupper.de . de . 2009-06-20 . https://web.archive.org/web/20090618075846/http://www.knabstrupper.de/content.php?content.4 . 2009-06-18 . dead .
  77. Book: Sponenberg, Dan Phillip . 2003 . 94 . Equine color genetics . 5. Patterns Characterized by Patches of White . 2 . Wiley-Blackwell . 978-0-8138-0759-1 . ... most Appaloosas have a blanket or varnish roan phenotype ... In the Noriker breed most horses with LpLp are leopard, and the few varnish roans or blanketed horses in the breed tend to produce leopards more than their own blanket or varnish roan pattern.
  78. The Impact of the Mutation Causing Overo Lethal White Syndrome on White Patterning in Horses . Vrotsos . Paul D. . Elizabeth M. Santschi. James R. Mickelson . Proceedings of the Annual Convention of the AAEP . 2001 . 47 . 385–391 . This is a rare color pattern in which the coat is almost entirely white (Fig. 6). Pigmented areas are found primarily on the ears and poll, but may also appear on the thorax, flank, dorsal midline, and tail head. Medicine hat horses can arise from overo or tovero bloodlines; when of overo bloodlines, medicine hat horses may have pigment that is quite faint on the dorsal midline..
  79. Web site: Breed Close Up Part II . The Colorful World of Paints & Pintos . Janet Piercy . International Registry of Colored Horses . 2001 . 2009-07-03 . The perfectly marked medicine hat is usually a tovero, but these horses can be overos and tobianos too . https://web.archive.org/web/20090224162732/http://www.coloredhorses.com/PP2new.html . 2009-02-24 . dead .
  80. Metallinos . DL . Bowling AT. Rine J . June 1998 . A missense mutation in the endothelin-B receptor gene is associated with Lethal White Foal Syndrome: an equine version of Hirschsprung Disease . Mammalian Genome . 9 . 6 . 426–31 . 9585428 . 10.1007/s003359900790 . 19536624 .
  81. Web site: Equine Coat Color Tests . Veterinary Genetics Laboratory . UC Davis . 2009-07-08.
  82. Haase, B. et al (2009). "Whenever a white foal is born out of solid-coloured parents, the most likely explanation is a KIT mutation in the germline of one of its parents or alternatively a mutation in the early developing embryo itself, which might lead to mosaic foals."
  83. Book: Strachan . Tom . Read . Andrew . Fran . Kingston . BIOS Scientific Publishers . Human Molecular Genetics . 2009-07-08 . 2 . 1999 . 1996 . John Wiley & Sons . New York . 978-1-85996-202-2 . 297 . Genes in pedigrees: 3.2 Complications to the basic pedigree patterns . https://www.ncbi.nlm.nih.gov/books/bv.fcgi?highlight=mosaic&rid=hmg.section.286#297 . Post-zygotic mutations produce mosaics with two (or more) genetically distinct cell lines. [...] Mutations occurring in a parent's germ line can cause de novo inherited disease in a child. When an early germ-line mutation has produced a person who harbors a large clone of mutant germ-line cells (germinal, or gonadal, mosaicism), a normal couple with no previous family history may produce more than one child with the same serious dominant disease . amp .
  84. Web site: Brindle Information . American Brindle Equine Association . Kay L. Isaac . 2009-07-08 . One only outwardly appearing brindle that is likely the result of a mosaic or chimeric equine ... .
  85. Haase, B. et al (2009) "our study included several founder animals where mosaicism cannot be excluded. One example for such a scenario is the W8 allele observed in a single "mottled" Icelandic horse, which represents the founder animal for this mutation (Fig. 1g). This horse might be a mosaic, and it remains to be determined whether it will consistently produce offspring with the mottled phenotype."
  86. Strachan, Tom & Andrew Read (1999) "A common assumption is that an entirely normal person produces a single mutant gamete. However, this is not necessarily what happens. Unless there is something special about the mutational process, such that it can happen only during gametogenesis, mutations may arise at any time during post-zygotic life."
  87. Sturtevant, AH (1912). "Since "glass" eyes occur not infrequently in pigmented horses it seems probable that this white-eyed albino [sic] is really an extreme case of spotting, plus an entirely independent "glass" eye."
  88. Web site: American Creme and White . Breeds of Livestock . Oklahoma State University . 1999-05-03 . 2009-06-20 . dead . https://web.archive.org/web/20091209065550/http://www.ansi.okstate.edu/breeds/horses/americancremeandwhite/index.htm . 2009-12-09 .
  89. Lethal Dominant White in Horses . Pulos . WL . FB Hutt . Journal of Heredity . 60 . 2 . 59–63 . 1969. 10.1093/oxfordjournals.jhered.a107933 . 5816567 .
  90. Wriedt . C . Vererbungsfaktoren bei weissen Pferden im Gestut Fredriksborg . Zeitschrift für Tierzuchtung und Zuchtungsbiologie . 1 . 2 . 231–242 . 1924 . 10.1111/j.1439-0388.1924.tb00195.x.
  91. WL Pulos & FB Hutt (1969). "Although Wriedt referred to Sturtevant's report in his genetic analysis of records of the Frederiksborg white horses, he considered the latter to be recessive whites, with homozygotes white, white with gray spots, or gray white ("weissgraue"). Heterozygotes were believed to vary all the way from dilute gray to full color."
  92. Web site: International Horse & Pony Colour Term Dictionary Online (Part 2) . 2009-07-08 . 2005-09-09 . Beth Mead.
  93. WL Pulos & FB Hutt (1969). "In the light of more recent evidence, these conclusions now seem to have been erroneous ..."
  94. WL Pulos & FB Hutt (1969). "Odriozola added no new data on dominant white, but ... suggested that different forms of W arranged linearly in the chromosome might be responsible for the differing degrees of white ... and that the expression of white is also influenced by modifying genes."
  95. Book: Strachan . Tom . Read . Andrew . Fran . Kingston . BIOS Scientific Publishers . Human Molecular Genetics . 2009-07-10 . 2 . 1999 . 1996 . John Wiley & Sons . New York . 978-1-85996-202-2 . 333 . Genes in pedigrees: 3.4 Nonmendelian characters . https://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=hmg.section.333 . amp .
  96. Pulos & Hutt (1969). "Each of the five white stallions used in the stud sired one or more colored foals. Similarly, all of the eight white mares that were adequately tested produced at least one colored foal. The fact that these 13 white horses were all proven to be heterozygotes agrees with previous reports that white horses with colored eyes did not breed true to type, but always produced some colored progeny. This, in turn, suggests that the genoytpe WW is not viable."
  97. Pulos & Hutt (1969). "Among six white foals (from parents both white) that died soon after birth, one had been unable to stand and nurse; death of another was attributed to exposure, one was strangled and another killed by the mare. The possibility that any of these might have been homozygotes is refuted by the fact that similar conditions caused death of several foals from the colored pony mares. Some of those foals were white, and some colored, but none could have been WW."
  98. Pulos & Hutt (1969). "As aborted foetuses were not found although a constant watch was maintained for them, it is possible that the homozygotes die early in gestation and are resorbed."
  99. Pulos & Hutt (1969). "... in his genetic analysis of records of the Frederiksborg white horses, [Wriedt] considered [them] to be recessive whites, with homozygotes white, white with gray spots, or gray white ("weissgraue") ... He considered that the gene for white could not itself be lethal because four fertile white mares produced from 46 matings a total of 37 foals, none of which was dead or weak, and that good record (80 percent fertility) was better than could have been expected if the gene for white color were lethal. Subsequently von Lehmann-Mathildenhoh reported evidence of a dominant white in the Bellschwitz and Ruschof studs ... He did not consider the possibility that it might be associated with any lethal action ... [Salisbury] made no reference to effects of the gene in homozygotes ... Berge lists dominant white horses as heterozygotes, and follows Castle in suggesting that homozygosity for W is lethal."
  100. Haase, B. et al (2007). "However, this report on the embryonic lethality was derived from the analysis of offspring phenotype ratios in a single herd segregating one or more unknown mutations."
  101. Durham, F.M. A preliminary account of the inheritance of coat colour in mice. Reports to the Evolution Committee IV: 41-53, 1908.
  102. Book: Silvers, Willys K. . The Coat Colors of Mice: A Model for Mammalian Gene Action and Interaction . 10: Dominant Spotting, Patch, and Rump-White . Springer Verlag . 1979 . http://www.informatics.jax.org/wksilvers/ . 2009-07-03 . 978-0-387-90367-5.
  103. Chabot . Benoit . Dennis A. Stephenson. Verne M. Chapman. Peter Besmer. Alan Bernstein . The proto-oncogene c-kit encoding a transmembrane tyrosine kinase receptor maps to the mouse W locus . Nature . 1988-09-01 . 335 . 6185 . 88–9 . 2457811 . 10.1038/335088a0. 1988Natur.335...88C . 4344521 .
  104. Haase, B. et al (2009). "Currently, there is little known about possible pleiotropic effects of KIT mutations in horses."
  105. Haase . B . Obexer-Ruff G . Dolf G . Rieder S . Burger D . Poncet PA . Gerber V . Howard J . Leeb T . Veterinary Journal . 9 April 2009. 19362501 . Haematological parameters are normal in dominant white Franches-Montagnes horses carrying a KIT mutation. . 10.1016/j.tvjl.2009.02.017 . 184 . 3 . 315–7.
  106. Web site: Sabino. https://web.archive.org/web/20081225170354/http://www.equinecolor.com/sabino.html. 2008-12-25. Equine Color. 2011-12-09 .
  107. Web site: Piebaldism . Michael D. Fox . Camila K. Janniger . 2009-01-30 . eMedicine . WebMD . 2009-06-20.
  108. Pielberg G, Olsson C, Syvänen AC, Andersson L . Unexpectedly high allelic diversity at the KIT locus causing dominant white color in the domestic pig . Genetics . 160 . 1 . 305–11 . January 2002 . 10.1093/genetics/160.1.305 . 11805065 . 1461930.
  109. Book: Silvers, Willys K. . The Coat Colors of Mice . Springer Verlag . 1979 . 978-0-387-90367-5.

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