Genetics of horse colors
The effects of genetic factors on the coloring of horses are referred to as the genetics of horse colors . For each color variant, the color of the outer hair, the long hair, the eyes and the skin are considered.
First historical classifications based on phenotype
In contrast to the naming for the coat colors of the horses , which used to be based purely on the external appearance, the phenotype , without having sufficient knowledge of genetic connections, and which is still used today for the color names in the papers of the horse one in horse breeding - especially in color breeding - today according to the genetic basis, the genotype of the horse colors.
Color breeding is largely independent of the breeding of the horse breed . In principle, all color variations can occur in all breeds, unless the respective breeder encourages or tries to suppress them through a special selection.
However, in order to understand the most important things in advance, here is a small reference table:
| term | Explanation |
|---|---|
| Eumelanin | black pigment |
| Pheomelanin | red pigment |
| Locus | Location on the chromosome occupied by a gene. |
| Alleles (singular: allele) | Genes that occupy the same locus and influence the same character. |
| homozygous | pure. Gene combination of two identical letter shapes. |
| heterozygous | mischievous. Gene combination of two different letter forms. |
As early as 1912, Adolf Richard Walther laid the basis for a genetic classification of horse colors based on the stud books of Lipizza, Trakehnen, Salzburg and West Prussia. Since the studbooks contain color variations on the basic color of the horse's hide, such as the dark chestnut, cabbage fox and light fox in the case of the fox, his results were limited to the inheritance of the basic colors and their most important variations. Walther attributed the horse colors to a combination of five pairs of factors:
| factor | gene | impact | Inheritance | Overlay | restriction |
|---|---|---|---|---|---|
| Redness (red) | A. | Yellowing | dominant | B (blackening), D (mold), E (spotting) | |
| a | Red color | recessive | |||
| Blackening (rapp) | B. | Blackening | dominant | D (mold), E (spotted) | |
| b | no black | recessive | |||
| Long hair distribution | C. | Lightening | dominant | D (mold), E (spotted) | B (blackening) limited to long hair |
| c | no lightening | recessive | |||
| Mold (gray) | D. | Mould | dominant | ||
| d | no mold | recessive | |||
| Check | E. | Check | dominant | ||
| e | no check | recessive |
Each parent gives the offspring a gene for each pair of factors. Each of the factors is represented by a pair such as B. BB, Bb or bb for the blackening determined. The genes marked with capital letters are always dominant compared to the same factor marked with lower case letters recessive, so they prevail in their effects. Furthermore, gene B overlays the factor basic color (Aa) and both genes D and E overlays the factors basic color (Aa), blackening (Bb) and distribution (Cc). The occurrence of the distribution factor (CC or Cc) causes the blackening to be limited to long hair and legs; its occurrence has no effect on the other factors. These genes are passed on homozygously as 2 dominant genes (e.g. AA or also aa) or heterozygous as a dominant / recessive pair (Aa or aA).
According to Walther, the basic coat color of a horse results as follows:
| Coat color | Base color | Blackening | distribution | Mould | Check |
|---|---|---|---|---|---|
| Fox | any | bb | any | dd | ee |
| Isabell, Palomino | aa | bb | any | dd | ee |
| brown | Aa, AA | Bb, BB | Cc, CC | dd | ee |
| Dun | Aa, AA | Bb, BB | Cc, CC | dd | ee |
| Black | aa | Bb, BB | cc | dd | ee |
| Mould | any | any | any | Dd, DD | any |
| Check | any | any | any | dd | Ee, EE |
This table also shows the possible colors of offspring. The offspring of two blacks, of which at least one is homozygous , i.e. pure breeding in terms of blackening (BB), are always blacks due to the dominance of blackening, while two heterozygous , i.e. mixed breeding blacks (Bb) can have the following types of offspring: Is that the gene causing the black color has not been passed on, according to Walther, depending on the expression of the primary color A, either foxes with neither A nor B (aabb) or isabels with at least one A but no pronounced B (Aabb, AAbb) arise. If, on the other hand, the gene B causing the blackening is passed on from the mixed-genetic black horse, then black horses emerge, which in turn can be either heterozygous (Bb) or homozygous (BB), depending on whether only one parent or both parents inherited the B.
Lethal White Overo
The (Frame) Overo ("frame check") takes a special form; In the heterozygous form (no / on) it forms white flat spots that are framed by colored fur.
If the Overo gene is homozygous (oo), the foal is born white, but is not viable for 72 hours due to an incomplete gastrointestinal tract and dies with colic. This is known as "Lethal White Overo Syndrome".
Molecular genetic research
Molecular genetic research revealed, however, that in addition to the colors that are visible through the phenotype, i.e. the external appearance of a horse, there are also some colors that differ in the genotype, i.e. in the genetic cause, but not in the phenotype, i.e. the appearance . Since this fact, especially in color breeding , can result in different selection criteria for the selection of the parent animals than were previously used, more recent findings in this area are disseminated relatively quickly via the color breeding associations. Research into the genetic basis of horse colors is far from complete. One difficulty arises from the relatively long succession of generations of horses, which sometimes makes the verification of newer findings very tedious. In some cases, attempts have been made and are being attempted to transfer knowledge from color inheritance in mice, in which more than fifty color genes are known, to horses. In horses, only 16 color-relevant genes are currently known.
The position of a gene locus in the DNA is commonly referred to with a capital letter, such as an A .
Due to the notation, it is easy to confuse the expression of the gene located at this position, called the allele , which represents the property that is determined by the gene. They are usually referred to with English names, for example agouti , whereby the dominant form of this expression is indicated with capital letters, while the recessive form is indicated with lowercase letters. In the case of agouti, this would be A in the dominant form that prevails over other hereditary information and a in the recessive form, which is suppressed by dominant hereditary information.
If more than two expressions are possible at a locus, the order of dominance of the alleles is given. Since genetic information always occurs in pairs, one allele comes from the father and one from the mother, there are two alleles for each locus, the interaction of which determines the property. Depending on whether the respective parent inherited a dominant or a recessive form, a horse can therefore have the combinations AA, Aa, aA or aa of the agouti allele.
No allele can appear in two different positions, but is always in the same, very specific position. The alleles are specified below, their respective position on the DNA strand, i.e. the gene location (locus), is only mentioned if known.
Control of dye production
In horses there are two colorants (melanins) that occur in the fur: black eumelanin and red pheomelanin. All coat colors known from horses are caused by different distribution of these two pigments in the coat.
A number of color genes have the function of controlling when and where these dyes should appear in the fur and skin. Of these control loci, the extension locus (E) and the agoutilocus (A) have been researched best .
Agouti
There are four different variants of the gene on the agouti locus. Three of them (A + , A, A t ) lead to browns with black areas of different sizes in the fur, the fourth variant leads to a completely black horse (a), the black horse . The less black the respective allele allows in the horse, the more dominant it is. This means that a horse that has the gene for the color wild-type brown (A + ) looks exactly the same, regardless of whether it has one of the three other genes on the other chromosome or whether there is another gene for wild-type there. Braun has. A horse that has the rapp gene (a) will only become a rappen if the second allele is also the rapp gene, otherwise it will have the color that causes the second gene.
Extension
In the horse there are two alleles on the extension locus. The dominant allele E allows the agoutilocus to influence, so that blacks and browns can arise. The recessive allele e leads to the uniform brown color of the horse, so a fox is created . Since the allele E is dominant over e, a black horse can be homozygous (EE) with respect to E or heterozygous (Ee), while a fox must always be homozygous (ee) with respect to e. In terms of heredity, this means that two heterozygous black horses sire 25% foxes, while two foxes can only sire foxes. If two blacks are mated, of which at least one is homozygous, the descendants will always be blacks.
| Allele combination | Agouti AA | Agouti Aa | Agouti aa |
| Extension EE |
 Brown |
Brown |
 Black |
| Extension Ee |
Brown |
Brown |
Black |
| Extension ee |
 Fox |
Fox |
Fox |
Other mutations that affect the control of melanin synthesis
If a gene affects the control of melanin synthesis, i.e. determines whether and where which melanin should be produced, this can often be recognized by the fact that all colorants can be produced, but appear in different places.
Overview of genes that control melanin synthesis
In addition to the most important data on the genes, the following table also shows what the colors are called that are created when the gene affects the three basic colors of the genes.
| Cross-species gene locus | chromosome | Mutation, allele | Colours |
|---|---|---|---|
| Agouti | ECA22 | Gene for wild type brown A + | Together with E: wild-type brown. With ee: light, yellow-brown fox |
| Agouti | ECA22 | Gene for the color of brown A. | Together with E: normal bay With ee: red-brown fox |
| Agouti | ECA22 | Gene for black brown A t | Together with E: black-brown. With ee: relatively dark fox |
| Agouti | ECA22 | Gene for black color a | Together with E: Black With ee: Cabbage Fox , Dark Fox |
| Extension | ECA3 | Gene for the unimpeded spread of eumelanin E. | Black or brown in all variations |
| Extension | ECA3 | Gene for fox color e | Fox in different shades |
| Extension | ECA3 | Gene for fox color e a | In appearance indistinguishable from animals with the other fox gene. |
| unknown | unknown | Falbgen, engl. Dun (D) |
Falbe Rappe with Falbgen: Rappfalbe , Mausfalbe Brauner with Falbgen: Braunfalbe , normal Falbe fox with Falbgen: Bay roan , Fuchsfalbe |
| unknown | unknown | no lightening, primitive sign (nd1) | Non-fallow horses with eel line / zebra crossing |
| unknown | unknown | no fawn (nd2) | All colors except fallow |
| unknown | unknown | Location for the different characteristics of eel line, shoulder cross, zebra crossing (M or m) | Eel line |
| unknown | unknown | no flaxing (F) | Fox without a light mane |
| unknown | unknown | Flaxen (f) | The fox with flaxes becomes a light fox, black horses and brown ones remain unchanged by the gene. It is assumed that the gene is also responsible for the flour mouth. |
| unknown | unknown | Smutty , Sooty (Sty) | Blacks remain unchanged. Browns turn into dark brown foxes into dark foxes |
| unknown | unknown | no smutty , no sooty (sty) | Color not darkened |
| unknown | unknown | Pangare (P or Pa) | Mehlmaul - The gene has no effect on black horses. |
| unknown | unknown | no pangare (p or pa) | no flour mouth |
| unknown | unknown | unknown | Ben d'or spots : Small round dark spots on brown fur, see badge (horse) |
| unknown | unknown | unknown | Bloodmark : an area of red or brown burin hair in the fur of the white horse , see badge (horse) |
Albinism spectrum: mutated proteins of melanin synthesis
To produce the two melanins, a number of different enzymes, structural proteins and transport mechanisms in the dye-producing cell, the melanocyte, must work together properly. Mutations in the genes of the substances required for this mean that the animals concerned are not able to produce melanin or that they can only produce a little melanin. Even lightening of the coat color is often due to changes in the enzymes involved in melanin synthesis. Mutations at the beginning of the melanin synthesis pathway affect both the red and the black dye. If the black and red dye are lightened to different degrees, this is often due to the fact that the gene intervenes towards the end of melanin synthesis, where the synthesis pathways of eumelanin (black) and pheomelanin have already separated.
Some mutations in this area cause toxic metabolic intermediates to accumulate in the melanocytes, causing the cells to die.
Overview of the change in primary colors caused by genes in the albinism spectrum
| Cross-species gene locus | chromosome | Mutation, allele combination | designation |
|---|---|---|---|
| Thyrosinase blessing / OCA1 ( oculocutaneous albinism type 1 ) | No mutation of this gene locus is known in horses | ||
| MATP ( Oculocutaneous Albinism Type 4 ) | ECA21 | no cream gene , homozygous (cr, cr) | Colors not brightened |
| MATP ( Oculocutaneous Albinism Type 4 ) | ECA21 | Cream gene , heterozygous (cr, Cr) | A Black becomes the light centimes (Engl. Smoky Black) A Brown becomes the earthy (Engl. Buckskin sometimes genetically wrong, also called dun) A fox is for Isabella (ger .: Palomino ) |
| MATP ( Oculocutaneous Albinism Type 4 ) | ECA21 | Cream gene , homozygous (Cr, Cr) |
Weißisabell A black horse becomes Smoky Cream A brown one becomes Perlino A fox becomes Cremello |
| SLC36A1 (Solute Carrier 36 family A1) | ECA14 | Champagne gene, heterozygous or homozygous |
Champagne A black horse becomes a classic Champagne A brown horse becomes an amber champagne A fox becomes a gold champagne Homozygous animals are only slightly lighter. |
| unknown | unknown | Pearl , homozygous | A black horse becomes light gray all over its body due to the gene. A fox becomes sand colored all over its body |
| unknown | unknown | no Pearl (PrlPrl or Prlprl), homozygous or heterozygous | no lightening |
| Silver locus | ECA6 | Silver dapple, wind color genes |
Wind-colored black horse with wind- colored genes : Rappwind- colored brown horse with wind- colored genes : Brown wind-colored genes |
Leucistic color genes
In leucism, the dye-forming cells ( melanocytes ) do not migrate out of the neural crest during embryonic development , in fewer numbers than usual or too late. The following gene loci were known to be the cause of leucism: endothelin receptor B gene (EDNRB), the paired box gene 3 (PAX3), SOX10, the microphthalmia-associated transcription factor (MITF), c-Kit and the steel locus (coded MGF). With complete leucism, the affected animal is completely white and can have normal-colored, slightly brightened, blue or red eyes. Less pronounced leucism leads to piebald animals, to white markings on the head and legs or to animals with white prickly hair in otherwise normal-colored fur.
Every check pattern is possible on every basic color. So there are blacks, foxes, browns, falcons, Isabels and white horses with spotted patterns.
There are also considerable individual differences in the characteristics of the piebald piebald: Most of the same piebald genes range from completely white horses to horses that carry the piebald gene but are not externally recognizable as piebalds or only have an inconspicuous small spot or enlarged Have badges based on this gene.
White markings on the face and legs are also due to leucism in most species.
Black with a Tobiano check
Brauner with a Tobiano check
Fox with Tobiano check
| Cross-species gene locus | chromosome | Name of the mutation | General name |
|---|---|---|---|
| various, leucism | various | various |
Pinto A Black becomes the Piebald A Brown becomes a Brown Take A fox is to Fuchsschecke A mold is used for porcelain Check |
| c-kit (see leucism ) | ECA3 | Dominant white (WW, in fact several different mutations of cKit), homozygous | Fatal in early embryonic development |
| c-kit (see leucism ) | ECA3 | Dominant white (Ww), heterozygous | Dominant white horse |
| c-kit (see leucism ) | ECA3 | Tobiano (Toto or ToTo), heterozygous as well as homozygous | Dominant platter check or tobiano |
| c-kit (see leucism ) | ECA3 | Roan (RnRn), homozygous | probably fatal in early embryonic development |
| c-kit (see leucism ) | ECA3 | Roan (rnRn), heterozygous |
Roan , permanent mold, iron mold A Black becomes the permanent Rappschimmel , permanent blue or black horse with Stichelhaaren (often genetically incorrectly called only Rappschimmel or blue) A Brown becomes the stichelhaarigem brown or time-roan (genetically wrong Brown mold) is a Fuchs Permanent red mold (genetically incorrect red mold) or spiky-haired fox |
| c-kit (see leucism ) | ECA3 | Sabino (Sb1) | Sabino Overo or Sabino |
| c-kit (see leucism ) | ECA3 | White badges | Horse with white markings see markings (horse) |
| c-kit (see leucism ) | ECA3 | Not dominant white, not Roan, no Tobiano or no Sabino (sb1, rn, to or w) | No white hair in the coat Dominant white, Tobiano, Sabino and Roan (prickly hair) are different alleles of the same gene. Therefore the four designations for the wild-type allele refer to the same allele of the same gene. The different names are therefore misleading. |
| EDNRB (see Leucism ) | ECA17 | Overo lethal white gene , homozygous (OO) | Completely white foal that is not viable |
| EDNRB (see Leucism ) | ECA17 | Overo lethal white gene , heterozygous (Oo) | Frame overo |
| EDNRB (see Leucism ) | ECA17 | no overo lethal white gene (oo) | no frame-over check |
| various unknowns ( leucism ) | unknown | Sabino (Sb) | " Sabino Overo " or Sabino |
| unknown ( leucism ) | unknown | Splashed White Gene (SplSpl), homozygous | Splashed White Overo |
| unknown ( leucism ) | unknown | Splashed White Gene (splSpl), heterozygous | Badges on the head and legs, often blue eyes |
| unknown ( leucism ) | unknown | no Splashed White gene (splspl), homozygous | no badges, brown eyes |
| various unknowns, leucism | unknown | various unknowns | White markings on face and legs see markings (horse) |
| various unknowns, leucism | unknown | no name | Small round white dots on light fur: Birdcatcher spots , Chubari spots or Tetrach spots see badge (horse) |
| unknown, leucism | unknown | no name | Reverse Bloodmark : light, spiky- haired area in the dark fur, see badge (horse) |
| unknown, leucism | unknown | Rabicano (RbRb or rbRb) | Rabicano |
| unknown, leucism | unknown | no Rabicano (rb, rb) | no Rabicano |
Other color genes
In addition to the above three groups of color genes, there are some genes that influence color but cannot be classified into these three groups.
| Cross-species gene locus | chromosome | Mutation, allele combination | designation |
|---|---|---|---|
| STX17 ( syntaxin -17) | ECA25 | Gray gene, gray gene, heterozygous or homozygous (Gg or GG) |
Schimmel Rappe in the phase of Ausschimmelung: Rappschimmel , blue Brauner at the stage of Ausschimmelung: roan , roan fox in the phase of Ausschimmelung: roan , Fuchschimmel all colors: if the color is not visible anymore, but the animal is not yet fully ausgeschimmelt is: apple mold Fully moldy: fly mold , Atlas mold |
| STX17 ( syntaxin -17) | ECA25 | no gray gene or gray gene (gg), homozygous | no lightening |
| TRPM1 ( Transient Receptor Potential Cation Channel, Subfamily M, Member 1) | ECA1 | Leopard gene, homozygous (LpLp) | Tiger Piebald Complex : White Born , Full Tiger , Varnish Roan |
| TRPM1 ( Transient Receptor Potential Cation Channel, Subfamily M, Member 1) | ECA1 | Leopard gene, heterozygous (Lplp) | Leopard complex : pelmet tiger , snow tiger , Varnish Roan |
| TRPM1 ( Transient Receptor Potential Cation Channel, Subfamily M, Member 1) | ECA1 | no leopard gene (lp) | No drawing of the tiger piebald complex . |
Health effects of color genes
Eye damage: tiger piebalds that are pure breeding for the gene are night blind.
In the case of Rocky Mountain Horses that wear the wind color gene, malformations of the eyes often occur.
In all horses whose eyes are blue due to albinism or leucism, the visual impairments typical of albinism or leucism can be assumed. In horses, however, only spotting and lightening of the color are known where enough melanin remains in the eye so that the eyesight is good enough for the horse to work normally. The animals do not attract attention because of their unsafe behavior. On the other hand, one can observe that cremellos, which are blinded by bright sunshine, narrow their eyes as a result.
Hearing: Splashed whites are occasionally deaf.
Lethal factors : There are some color genes that are fatal if they are homozygous, whereas the heterozygous expression leads to largely healthy horses. Foals homozygous for the Overo Lethal White gene are snow white and die of colic within the first few days of life. In horses with spiky hair and at least one variant of the horse's dominant white color, homozygous embryos die in a very early phase of pregnancy, the mother mare becomes receptive again and can be mated again.
Insect bites: Dark fur reflects polarized light more strongly than white, and since insects can distinguish polarized and unpolarized light from one another and are attracted by polarized light, white horses are less annoyed by horseflies than dark ones . They can therefore eat more undisturbed and have a lower risk of being attacked by insect-borne diseases.
Color of the wild horse
In genetics, the effects of genes are often compared to the wild type , i.e. the natural color of the wild ancestors of the animals examined. Since most of the subspecies of the wild horse were exterminated before genetic research began, only the Przewalski horse is available for comparison.
A wild-colored horse is a bay with the allele Dun (D) - i.e. a dun with an eel line and possibly also striped legs and a shoulder cross. It usually has a flour mouth, which is caused by the pangare locus. The color of the wild caught varied considerably. There was a light and a dark type. Occasionally foxes and badges appeared, but this can also be traced back to crossbreeding of Mongolian horses .
In the first few days, Przewalski foals have a very light-colored foal coat, which sometimes occurs on Icelandic ponies.
Spots, lightening due to the cream, champagne, pearl, flax and silver, as well as mold, dominantly white horses and roans do not occur in wild horses because these colors are too conspicuous in the wild. In addition, some piebalds and the dominant white bring health disadvantages and the blue eyes caused by the cream gene or dominant white or piebald lead to the visual impairments typical of albinism, which are disadvantageous when discovering predators.
See also
- Coat colors of horses for naming the colors of horses historically based on their appearance.
- Coat color to the genetics of colors
Notes on genetic research on horses
Findings on how exactly a gene is transcribed, i.e. translated into proteins, and how these proteins then control and influence the creation of dyes or other processes in the body, were usually obtained from humans or one of the model organisms for genetic research. When it comes to coat colors, the most important animal model organism is the house mouse, the color mouse . If the cross-species gene locus of a horse gene is not yet known, it always means that one does not know exactly how the gene works, and that much of it is therefore dependent on the knowledge that was already collected before the start of genetic research. In the mouse, around 40 different genes that influence coat color have been located in the genome. In horses, only a fraction of them are known so far, so it can be assumed that the genes whose existence has been postulated so far without knowing the exact location of the gene are more likely to be based on several genes than that one gene has to be discarded The genetic locus is unknown, this also means that the exact function of the gene is not yet known. The fact that the location of a gene is known, but not the cross-species locus or vice versa, occurs in horses because, in contrast to humans and mice, the genome has not yet been completely sequenced and it is therefore not known where each gene is. If both the cross-species gene locus and the location of the gene on the chromosome are unknown, the knowledge about this gene comes from genetic research before genetic engineering. It is then to be expected that it will turn out that several different genes can cause this appearance or that the gene works differently than expected. Presumably, in reality, several mutations and several gene locations are responsible for the different characteristics of the drawing.
Web links
- Website about color breeding in Icelandic horses with detailed explanation and illustration
- Website on color inheritance in horses
- Color tests at the University of California Davis
- Website about the latest genes and their discovery
Individual evidence
- ↑ a b DL Metallinos, AT Bowling, J. Rine: A missense mutation in the endothelin-B receptor gene is associated with Lethal White Foal Syndrome: an equine version of Hirschsprung disease. In: Mamm Genome. 9 (6), 1998 Jun, pp. 426-431. PMID 9585428
- ↑ S. Rieder, p Taourit, D. Mariat, B. Langlois, G. Guerin: Mutations in the agouti (ASIP), the extension (MC1R) and the brown (TYRP1) loci and Their association to coat color phenotypes in horses (Equus caballus). In: Mamm Genome. 12 (6), 2001 Jun, pp. 450-455. PMID 11353392
- ↑ L. Marklund, MJ Moller, K. Sandberg, L. Andersson: A missense mutation in the gene for melanocyte-stimulating hormone receptor (MC1R) is associated with the chestnut coat color in horses. In: Mamm Genome. 7 (12), 1996 Dec, pp. 895-899. PMID 8995760
- ^ American Paint Horse Association's Guide to Coat Color Genetics; Status 12/2006; http://www.apha.com/
- ^ S. Rieder, C. Hagger, G. Obexer-Ruff, T. Leeb, PA Poncet: Genetic analysis of white facial and leg markings in the Swiss Franches-Montagnes Horse Breed. In: J Hered. 99 (2), 2008 Mar-Apr, pp. 130-136. PMID 18296388
- ^ A b c Anna Stachurska, Anne P. Ussing: Coat Color Versus Performance in the Horse (Equus Caballus). In: Polish Journal of Natural Science. Volume 22, Number 1 / March 2007, pp. 43-49. ISSN 1643-9953 doi: 10.2478 / v10020-007-0005-8
- ↑ LS Sandmeyer, CB Breaux, S. Archer, BH Grahn: Clinical and electroretinographic characteristics of congenital stationary night blindness in the Appaloosa and the association with the leopard complex. In: Vet Ophthalmol. 10 (6), 2007 Nov-Dec, pp. 368-375. PMID 17970998
- ^ RR Bellone, SA Brooks, L. Sandmeyer, BA Murphy, G. Forsyth, S. Archer, E. Bailey, B. 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). In: Genetics. 179 (4), 2008 Aug, pp. 1861-1870. Epub 2008 Jul 27. PMID 18660533
- ^ DA Witzel, EL Smith, RD Wilson, GD Aguirre: Congenital stationary night blindness: an animal model. In: Invest Ophthalmol Vis Sci. 17 (8), 1978 Aug, pp. 788-795. PMID 308060
- ^ BH Grahn, C. Pinard, S. Archer, R. Bellone, G. Forsyth, LS Sandmeyer: Congenital ocular anomalies in purebred and crossbred Rocky and Kentucky Mountain horses in Canada. In: Can Vet J. 49 (7), 2008 Jul, pp. 675-681. PMID 18827844
- ↑ Malte M. Harland, Allison J. Stewart, Arvle E. Marshall, Ellen B. Belknap: Diagnosis of deafness in a horse by brainstem auditory evoked potential . In: Can Vet J. 47 (2), 2006 February, pp. 151-154. PMID 16579041
- ↑ L. McCabe, LD Griffin, A. Kinzer, M. Chandler, JB Beckwith, ER McCabe: Overo lethal white foal syndrome: equine model of aganglionic megacolon (Hirschsprung disease). In: Am J Med Genet. 36 (3), 1990 Jul, pp. 336-340. PMID 2363434
- ↑ BD Hultgren: Ileocolonic aganglionosis in white progeny of overo spotted horses. J Am Vet Med Assoc. 180 (3), 1982 Feb 1, pp. 289-292. PMID 7056678
- ↑ C. Mau, PA Poncet, B. Bucher, G. Stranzinger, S. Rieder: Genetic mapping of dominant white (W), a homozygous lethal condition in the horse (Equus caballus). In: Journal of Animal Breeding and Genetics. 121 (6), Volume 121, Issue 6, 2004, pp. 374-383. doi: 10.1111 / j.1439-0388.2004.00481.x .
- ^ Coat color, lethal dominant roan (Phene ID 434, Group 000210) in Equus caballus. In: OMIA - Online Mendelian Inheritance in Animals. http://omia.angis.org.au/retrieve.shtml?pid=434
- ↑ Gábor Horváth1, Miklós Blahó, György Kriska, Ramón Hegedüs, Balázs Gerics, Róbert Farkas, Susanne Åkesson: An unexpected advantage of whiteness in horses: the most horsefly-proof horse has a depolarizing white coat. In: Proc. R. Soc. B. 7 June 2010, vol. 277, no. 1688, pp. 1643-1650 doi: 10.1098 / rspb.2009.2202 .