♞ 𝐆𝐄𝐍𝐄𝐓𝐈𝐂𝐒 𝐋𝐀𝐁𝐎𝐑𝐀𝐓𝐎𝐑𝐘 ♞

[azhefa.]

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𝐂𝐎𝐍𝐓𝐄𝐍𝐓𝐒 • [url]𝐇𝐄𝐋𝐏 & 𝐃𝐈𝐒𝐂𝐔𝐒𝐒𝐈𝐎𝐍[/url] • 𝐌𝐄𝐒𝐒𝐀𝐆𝐄 𝐌𝐄
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welcome to our genetics laboratory. within this laboratory, the genetic code of the different species is unraveled and
studied at length. articles are provided below to help those who wish to learn about the coat color and possible illnesses
or diseases that are caused by genetics in different breeds. please note that these articles are subject to change.

please keep out of the lab, certified workers only
feel free to take copies of our work here

if you are wanting to plan for future offspring in a roleplay, adoptable, or even real life, check out these calculators!
for foals, check out this coat color calculator.
for future puppy [dog] coat colors, check out this coat calculator.
for future rabbit kit colors, check out this coat calculator, though it's still in beta and may not be totally right.

[azhefa.]

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here are all the links to each set of research, more will be added as they are recorded
feel free to take a look at what we have so far
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▼ 𝐄𝐐𝐔𝐈𝐍𝐄 𝐆𝐄𝐍𝐄𝐓𝐈𝐂𝐒 ▼

𝐁𝐀𝐒𝐄 𝐂𝐎𝐀𝐓𝐒 • 𝐃𝐈𝐋𝐔𝐓𝐈𝐎𝐍𝐒 • 𝐖𝐇𝐈𝐓𝐄 𝐆𝐄𝐍𝐄𝐒 • 𝐃𝐈𝐒𝐄𝐀𝐒𝐄𝐒


▼ 𝐂𝐀𝐍𝐈𝐍𝐄 𝐆𝐄𝐍𝐄𝐓𝐈𝐂𝐒 ▼

[url]𝐁𝐀𝐒𝐄 𝐂𝐎𝐀𝐓𝐒[/url] • [url]𝐃𝐈𝐋𝐔𝐓𝐈𝐎𝐍𝐒[/url] • [url]𝐖𝐇𝐈𝐓𝐄 𝐆𝐄𝐍𝐄𝐒[/url] • [url]𝐃𝐈𝐒𝐄𝐀𝐒𝐄𝐒[/url]


▼ 𝐅𝐄𝐋𝐈𝐍𝐄 𝐆𝐄𝐍𝐄𝐓𝐈𝐂𝐒 ▼

[url]𝐁𝐀𝐒𝐄 𝐂𝐎𝐀𝐓𝐒[/url] • [url]𝐃𝐈𝐋𝐔𝐓𝐈𝐎𝐍𝐒[/url] • [url]𝐖𝐇𝐈𝐓𝐄 𝐆𝐄𝐍𝐄𝐒[/url] • [url]𝐃𝐈𝐒𝐄𝐀𝐒𝐄𝐒[/url]

[azhefa.]

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there are 3 types of base coats that a horse can be: black, red [sorrel/chestnut], and bay [red with black points]. the mixing of the extension and agouti genes determines what base color the horse will be and how the dilution and/or white genes will alter their appearance. a horse needs a dominant allele of both the extension and agouti gene to come out as bay in color [ex. AA EE, AA Ee, Aa EE, Aa Ee]. if they have either one dominant allele for only one gene or no dominant alleles at all, then the will be classified as either black or red as explained below.


the extension gene;

'E/e' is the extension gene which is for determining if the horse is black [EE aa or Ee aa] or red [ee aa] based and affects all the other color genes. this gene is mostly for determining what color the horse's legs will be, which is why bay horses have dark points on the legs and face. if a horse has double recessive extension genes, then the horse is automatically a red based horse and is unable to be bay or black based.

the agouti gene;

'A/a' is the agouti gene which is responsible for the bay coloring [AA or Aa] due to the gene forcing the black to the points and showing the red body. this gene is mostly for determining what color the horse's body will be, black or red. if a horse has double recessive agouti genes, then they will be either red or black depending on the dominance of the extension gene.

writing the code;

though it may look quite confusing and complex, writing out the genetic code for a horse is quite easy. first, you look at the base color, then you add on any dilutions the horse may have. it's easier to break it all down by steps. instead of thinking 'blue roan', think 'black base with roan' since this way you can put it together like this: black base [Ee aa or EE aa] with roan [RnRn or nRn]. so now you can just write it out: EE aa RnRn [i chose a higher chance of passing on the black and roan genes]

feel free to message me if you have any questions or difficulties.

[azhefa.]

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these are the dilution genes that affect the base coat colors to create different types of coats of all kinds of colors. most of these genes are dominant and will result in a dilution with only one dominant allele, but some are recessive and are only seen if there are 2 recessive alleles. a heterozygous gene is one where it has two different alleles, such as nD or nCr, one being dominant and the other recessive. a homozygous gene is one where it has two of the same alleles, either both are dominant or both are recessive. double recessive dilution genes are considered void and should just be ignored since there's no dominant allele to trigger that dilution.

the dun dilution; [D]

the dun gene is a dominant gene so either DD or nD will result in a dilution. when both parents are homozygous duns [2 of the same alleles or DD], it will always result in a dun foal of some kind depending on the base coats of the parents. if both parents are heterozygous duns [meaning 2 different alleles or nD] or one parent lacks a dun gene all together, then there's a 50% or less chance of a dun foal depending on the parent's other genes.

○ a black base will produce a grullo dilution
○ a red base will produce a red dun
○ a bay base will produce a classic dun, also called a 'zebra dun'

the silver dilution; [Z]

this is another dominant gene, but it only affects the extension gene [EE/Ee] in black and bay based horses. it doesn't matter if the horse is heterozygous or homozygous, as long as there is one dominant allele, the horse will show the dilution. on black base, the body will lighten to a chocolate and will have a flaxen mane and tail. whereas on bay bases, only the lower legs will lighten and will also have the flaxen mane and tail. though the dilution doesn't show up for red based horses, they can still be a carrier and have a chance to pass it on to their foals.

the champagne dilution; [Ch]

as with other dominant genes, the champagne dilution only needs 1 dominant allele to be able to change the coat. it affects all three base colors and if homozygous, it will pass on to foals regardless of the other parent while heterozygous will have a 50% chance to pass it on. the gene includes pinkish freckled or mottled skin, a shiny coat that is often slightly darker in the winter, and a hazel eye color. the horses are typically born with a blue eye color that evolves to a hazel or an amber color and pink skin that becomes darker and more freckled over time, especially around the eyes and muzzle.

○ on a black base it results in a classic champagne coat
○ on a red base it results in a gold champagne coat
○ on a bay base it results in an amber champagne coat

the cream dilution; [Cr]

the cream dilution is a dominant gene, but can affect at different levels depending on if it's a single [nCr] or double [CrCr] dilution. single dilute horses have a 50% chance of passing on the dilution while a double dilute will always pass on the dilution to foals. this dilution attributes to the lightening or silvering of the coat. breeding a base coat into a single dilute there's a 50% of a dilution in the foal and a 100% chance of single dilution if bred to a double dilute. cremello horses tend to have pale skin and blue eyes. below is what can happen with both dilutions on each of the base coats:

○ a single dilute black base will result in a smokey black coat
○ a double dilute black base will result in a smokey cream coat

○ a single dilute red base will result in a palomino coat
○ a double dilute red base will result in a cremello coat

○ a single dilute on a bay base will result in a buckskin
○ a double dilute on a bay base will result in a perlino

the pearl dilution; [Prl]

this is a recessive gene where it only shows up if there are 2 recessive alleles. a double recessive pearl gene results in a perlino coat while a single recessive results in no change to the coat. a single recessive is considered a carrier for this gene and has a 50% chance of passing it on to a foal where it can add to another single recessive from the other parent to create a perlino foal or it can pair with a single dilute cream gene where it will create a pseudo-double dilute cream. the cream gene is able to react with a recessive pearl allele and trigger the appearance of a double dilute cream. perlinos will have a lightened coat, mane and tail, in addition to bright eye colors due to pigment changes caused by the gene.

the roan dilution; [Rn]

though it is classified as a dominant gene, not much is known about the roan dilution aside from looks. it is the intermixed white and colored hairs in the body while the head, lower legs, mane and tail remain colored. there are 3 basic types of roan which match to the 3 base colors: blue roan for black base, red roan for red base, and bay roan for bay base. the roan dilution can also work off of other dilutions such as palomino and buckskin. it can be difficult to determine if the horse is roan or just greying out with the grey gene.

the sooty dilution; [Sty]

this modifier can display a seasonal effect, which is best seen in lighter animals affected by a creme dilution. the result is darker striping & shading certain times of the year. there is speculation about whether this is related to the primitive striping found in duns as well as dark bays, liver chestnuts & dark palominos (shading can actually conceal the animal’s original color). sooty buckskins can be mistaken for duns, dark bays & even black animals

[azhefa.]

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these are the white genes and are responsible for either total white coats or patches of white. though the coats may seem white, they are actually just devoid of color and aren't truly 'white'. breeding with the white genes can be a very risky practice since several of the genes are lethal if homozygous [2 dominant alleles]. lethal white syndrome [LWS] causes death in foals within a week of birth and can happen when horses carrying the same dominant alleles breed and pass on a double dominant gene. only some breeds of horses seem to have trouble with LWS, but can affect any breed through improper breeding. if it's suspected that horses have these dangerous alleles, they should not breed and risk having a LWS foal.


the dominant white gene;

this is a dominant trait and can also be a very deadly one to foals if the parents are unaware of their genetics. a double dominant gene can result in the death of a foal via lethal white syndrome [LWS]. white horses tend to have pink skin and dark eyes since the gene doesn't affect eyes. having pink skin and a white coat can lead to cancer and sunburns.

the tobiano factor;

one of the white factors that results in patches of white on a coat and is dominant so only one dominant allele is needed to display the gene. tobiano is typically characterized with large, rounded white spots on the body and white legs and the spots typically have sharp, clean edges. the horse's head is usually colored with the base coat color and does not have white caused by the tobiano gene. this gene is often confused with the overo gene.

the frame overo factor;

another gene that contributes to the loss of pigment in areas to leave patches of white which don't pass the 'frame' of the horse [back, neck crest, etc.]. this is a very dangerous gene though and is linked to lethal white syndrome [LWS] like the dominant white gene. a double dominant overo foal will die from lethal white syndrome within a week of birth. two overo horses must not breed due to this risk and can only breed other non-overo horses.

the splash factor;

a possibly lethal gene like many other white factors, but there are several variations of the splash gene in which only a few are dangerous. splashed white horses are characterized by a large blaze, extended white markings on legs, variable white spotting on belly, pink skin and often blue eyes which can lead to deafness. there are 4 types of splash white alleles and only #3 and #4 are homozygous lethal.

○ SW-1 is found in the quarter horse, paint, trakehner, miniature horse, shetland pony and icelandic horse and may be present in other breeds as well. homozygous SW-1 is not lethal.
○ SW-2 and the rare SW-3 may only occur in certain lines of Quarter Horses and Paints with the rare SW-3 being homozygous lethal.
○ SW-4 is very rare and only found in appaloosas, possibly homozygous lethal but not much is known about it.

the sabino factor;

a dominant gene where having two dominant alleles gives more dilution. a heterozygous gene will give white legs and irregular patches on the underbelly with some 'roaning' on the edges. a homozygous gene will result in an almost pure white horse, but without the blue eyes. there is no danger with a double dominant sabino factor.

the leopard complex;

this gene is predominantly associated with appaloosa and knabstrupper horses. this gene is also linked to congenital stationary night blindness (CSNB), a condition making it difficult or even impossible to see in relatively low light. this gene also has several variations to produce different types of white patches and spots on coats. without the PATN1 modifier, coats are more base colored and less white:

○ a LpLp horse tends to be a snow cap appaloosa
○ a nLp horse tends to be a blanket appaloosa
the PATN1 modifier accounts for the spotting of a horse and can be homozygous without having the leopard complex to have it show up on the coat. a double or single dominant PATN1 gene can be passed onto foals with or without the leopard complex. with the leopard complex, the modifier created other styles of spotting:

○ nLp n/PATN1 or PATN1/PATN1 produces a leopard or near leopard pattern
○ LpLp n/PATN1 or PATN1/PATN1 produces a few spot or near few spot pattern

the grey factor;

a dominant gene responsible for the gradual and progressive fading of color from a horse, this is the strongest gene and will dominate all other dilutions or modifiers. they can be born any color with any genes, but if they have the grey gene, they will turn grey with age. some gray horses fade to almost pure white whereas others may be 'fleabitten' with specks of their original base color. having one or two dominant alleles doesn't matter, as long as there's a single dominant allele, the horse will turn grey. it's possible to 'breed out' the grey gene by pairing up horses with only a single dominant allele and by doing this they can uncover coats that were 'hidden' by the grey gene.

[azhefa.]

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these are the different genetic diseases that can be passed on to foals. some are 'sleepers' and only show up after a certain time while others are clear from birth. some of the diseases are also dominant and can affect a horse even if it's heterozygous positive while others are recessive and can be carried as heterozygous positive. these recessive diseases can be very dangerous as the host is unaware and can pass on this disease and possibly breed with another carrier to produce a homozygous foal that shows the disease.

© credit to animalgenetics.us for the info


Hyperkalemic Periodic Paralysis Disease (HYPP);

a muscular disease caused by an inherited genetic mutation and has been traced back to one horse named 'impressive' and has the alternative name, 'impressive syndrome', named after this horse. symptoms of HYPP may include muscle twitching, unpredictable paralysis attacks which can lead to sudden death, and respiratory noises. severity of attacks varies from unnoticeable to collapse or sudden death. the cause of death is usually respiratory failure and/or cardiac arrest. this is a dominant disorder and will affect the horse even if heterozygous. only a percentage of quarter horses are affected by this.

Hereditary Equine Regional Dermal Asthenia (HERDA);

also known as hyperelastosis cutis [HC], it's a genetic skin disease predominantly found in the american quarter horse. researchers believe that the origin of this genetic disorder may be the poco bueno's sire line. the symptom of this disorder is a lack of adhesion within the layers of skin due to a genetic defect in the collagen that holds the skin in place. this defect causes the outer layer of skin to split or separate from the deeper layers, sometimes tearing off completely. this is a recessive disorder so only homozygous carriers are affected, but it can be carried as a recessive trait and passed to foals.

Polysaccharide Storage Myopathy (PSSM1);

a dominant autosomal hereditary condition that can cause a genetic form of tying-up with muscle damage and inability to move. one form of PSSM1 is in part a result of a single base pair substitution in GYS1 gene, thereby changing the amino acid sequence of the glycogen synthase enzyme. at least 20 breeds have been identified with type 1 PSSM. the prevalence of the GYS1 mutation in belgians is as much as 50% of and 8% of the quarter horse-related breeds.

Glycogen Branching Enzyme Deficiency (GBED);

a fatal condition caused by the bodies' inability to properly store sugar. this inherited disorder prevents the body from producing the enzyme needed to branch the glycogen structure, preventing the horse from being able to adequately store the sugars. this means that the horse will not be able to store enough energy to fuel important organs, such as the muscles and brain. foals born which are affected by GBED suffer from a range of symptoms associated with this lack of fuel, such as low energy, weakness and difficulty rising. other symptoms include low body temperature, contracted muscles, seizures, and sudden death. unfortunately, GBED is always fatal; most affected foals will die before the age of 8 weeks. GBED often causes the fetus to be aborted in utero. research suggests that as many as 3% of aborted quarter horse foals were homozygous for the GBED mutation. studies show that the mutation responsible for GBED is carried by as many as 10% of quarter horse, paint horse breeds and related breeds. GBED is an autosomal recessive trait, meaning a foal can only be affected if the foal inherits the disease from both parents. horses that are carriers of the GBED have one copy of the mutation but do not have any symptoms associated with the disorder.

Malignant Hyperthermia (MH);

a genetic muscle disorder that affects quarter horses and related breeds. horses with the MH mutation may not show any physical signs of the disorder until triggered by exposure to anesthesia or extreme exercise or stress. symptoms can include high temperature, increased heart rate, high blood pressure, sweating, acidosis, and muscle rigidity. symptoms develop rapidly, and if not treated quickly, this condition can be fatal.

Junctional Epidermolysis Bullosa (JEB1 and JEB2);

an inherited disease also known as Red Foot Disease or Hairless Foal Syndrome. variations of the disorder affect belgian draft horses, american saddlebred horses and relatives of these breeds. this inherited disorder is caused by a mutation that inhibits the body's ability to produce certain proteins responsible for holding the skin onto the body. affected horses are typically born alive with little symptoms. however, after 4 to 5 days of age the foal begins to develop lesions at the pressure points. these lesions quickly grow larger, creating patches all over the foal's body. because the same protein responsible for skin adhesion is also involved in the hoof attachment, the foal also beings to lose the hoof wall and the hoof may detach. oral ulcers are also seen with JEB, as well as foals being born with front teeth. foals often die from infections, or are euthanized within 3-8 days from birth for humane reasons. it is an autosomal recessive trait, meaning a foal can only be affected if the foal inherits the disease from both parents. parents that are carriers do not have any symptoms associated with JEB. however, they can still pass on a copy of the defective gene to their offspring.

Congenital Stationary Night Blindness (CSNB);

a condition making it difficult or even impossible to see in relatively low light. research has now shown that CSNB is a recessive disorder that is directly linked to the leopard complex in appaloosa horses. homozygous positive horses with the leopard complex will have CSNB.

Hoof Wall Separation Disease (HWSD);

a condition that has been identified in connemara ponies and horses that have been crossed with connemara ponies. it is an autosomal recessive disorder that causes the hoof wall to easily break and crack. all four feet will be affected by the disease. damage can be seen in affected ponies as young 2-3 weeks of age. in rare cases some affected ponies develop less severe form of the disease. this is due to the fact that the mutation is not fully penetrant. in very few case the disease can be managed but in other case the ponies must be euthanized. studies estimate that in the general population the percent of horses carrying a single copy of the disorder is around 15%.

Immune Mediated Myositis (IMM);

an incomplete dominant autoimmune disorder which causes muscular atrophy and stiffness in quarter horses. horses with two copies of the mutation associated with IMM are more likely to develop symptoms than horses with a single copy, although environmental factors can play a role. IMM typically affects horses younger than eight years old and older than seventeen years old. IMM episodes typically last several days to several weeks and can be fatal if mismanaged.

Lethal White Syndrome (LWS);

it occurs when a horse inherits two copies of the mutated gene, one from both parents. whereas horses with just one copy of the gene will live normally and exhibit the desirable pattern. a horse with two copies of the mutated gene will suffer intestinal abnormalities caused by undeveloped nerves of the foal's digestive system. these animals die within the first 72 hours of being born and are typically euthanized sooner for humane reasons.

Lavender Foal Syndrome (LFS);

also known as Coat Color Dilution Lethal (CCDL), is a recessive genetic disorder. affected foals often have a difficult delivery, problems standing at birth and usually have episodes where they rigidly extend their limbs, neck and back. These episodes tend to resemble a seizure, although the affected foal does not seem normal between episodes. all affected foals are usually euthanized within days or weeks of birth. studies show that the prevalence of carriers in the Egyptian Arabian population is around 10%. arabian bloodlines are affected.

Squamous Cell Carcinoma (SCC);

the most common cancer affecting the equine eye. at an increased risk of developing this disease are appaloosas, paints, pintos, haflingers, belgians, shires, clydesdales, and any horse lacing pigment in or around the eye.

Severe Combined Immunodeficiency (SCID);

an inherited disease seen in pure and part-bred arab horses. animals with this inherited condition have an enhanced susceptibility to infection and first show signs of disease at between two days and eight weeks of age. clinical diagnosis of the disease is not straightforward as the symptoms, such as raised temperature, respiratory complications and diarrhea, are typical of new-born foals with a range of infections. foals affected by SCID always die from the disorder within the first six months of life. this happens regardless of the level of veterinary care. the disorder is recessive, which means that a horse must be homozygous positive or have two copies of the defective gene to suffer from the disease. consequently both the sire and the dam must possess at least one copy of the mutated gene in order for the offspring to be afflicted.

Cerebellar Abiotrophy (CA);

also referred to as cerebellar cortical abiotrophy (CCA), is a genetic neurological disease in certain species of animals. to date, CA is known to affect breeds of dogs and horses. the disorder manifests itself when Purkinje cells, the neurons that affect balance and coordination, are present in the cerebellum of the brain. horses affected with CA tend to startle easily and often fall. common symptoms include head tremor, a lack of balance and other neurological issues. affected horses may develop a wide-based stance of the forelegs and difficulty rising from a reclining position. in horses, CA is believed to be linked to an autosomal recessive gene. this means that it is not sex-linked and the allele has to be carried and passed on by both parents in order for an affected animal to be born. horses that only carry one copy of the gene may pass it on to their offspring, despite being perfectly healthy themselves and having no symptoms of the disease. because the disorder is recessive, the allele for CA may pass through multiple generations before it is expressed. CA is sometimes confused with Wobbler's syndrome, Equine Protozoal Myeloencephalitis (EPM) and injury-related problems, such as a concussion. it is a condition known to affect arabian horses as well as miniature horses, the gotland pony and possibly the oldenburg. in most cases, foals appear normal at birth, and symptoms generally become noticeable after four months. there have been reported cases where the condition was observed shortly after birth, while others report symptoms developing after the first year.

Occipitoatlantoaxial Malformation (OAAM);

an autosomal recessive developmental skeletal defect which causes compression of the upper cervical cord. this malformation of the occipital bone of the skull results in a neurologic disorder caused when the first two cervical vertebrae (the atlas and axis), fuse to the base of the skull. this structural change creates pressure on the upper portion of the cervical spinal cord, damaging the tissue. the disease may progress with age from mild incoordination and weakness of the limbs to the inability to stand. depending on the severity of the disorder affected foals may be stillborn, show signs at birth or, in some cases, not show signs until a few weeks after birth. diagnosis of the malformed atlas and axis is generally confirmed with radiographs. affected foals are generally euthanized. in order for a foal to be affected, it must inherit a single copy from each parent. horses that have one copy of the mutated gene are not affected but are considered carriers and, if bred, have a 50% chance of passing on the mutated copy to its offspring. additional, yet unidentified, mutations may exist in arabian foals affected with OAAM.

Foal Immunodeficiency Syndrome (FIS);

a recessive genetic disease that primarily affects two relatively rare native UK pony breeds, the dales and the fell pony. FIS is caused by a single mutation in the sodium/myo-inositol cotransporter gene (SLC5A3). this gene plays a vital role in the regulatory response in many tissues including lymphoid tissues. as much as 10% of all fell ponies born each year suffer from FIS. this has put a strain on the long-term survival of this breed as well as the likely spread of FIS into other breeds. most recently animal genetics has found the mutation that causes FIS in approximately 9% of gypsy horse breeds in the US and europe. foals must have two copies of the mutated gene in order to be affected with FIS. therefore, each parent must be a carrier of the mutated gene in order to have an affected foal. affected foals appear healthy and normal at birth but begin to show signs of weakness, dull coat and anorexia at 2-3 weeks. the first clinical signs of this disease include diarrhea, nasal discharge, poor growth, pale gums and decreased appetite. vision may be affected, presumably due to secondary bacterial infections. mortality rate for foal affected by FIS is 100% despite intensive treatment. all FIS affected foals generally die or are euthanized before they reach the age of 3 months. FIS is an autosomal recessive trait, meaning a foal can only be affected if the foal inherits the disease from both parents. parents that are carriers do not have any symptoms associated with FIS.

Hydrocephalus (Friesian Horse);

a developmental disorder involving an accumulation of cerebrospinal fluid within the skull. this often results in foals born prematurely, stillbirth of affected foals and dystocia in dams. in friesian and other horse breeds, hydrocephalus is inherited as an autosomal recessive mode. hydrocephalus is primarily a result of years of inbreeding in the horse population and the widespread use of some influential ancestors. foals can only be affected by hydrocephalus if the foal inherits the disease from both parents. parents that are carriers do not have any symptoms associated with the disorder.

Dwarfism (Friesian Horse);

a genetic condition in friesian horses results in a disproportionate form of dwarfism. this form of dwarfism is characterized by abnormally short limbs while the size of the head and length of back are normal. affected foals also suffer from flexor tendon laxity. unlike normal foals that grow out of this as they mature, horses impacted by this form of dwarfism continue to be impacted by the condition often resulting in an abnormal gait. dwarfism in friesian horses is inherited as a simple autosomal recessive trait. this means that the disorder is not sex linked and all affected foals must inherit two copies of the defective gene (one from each parent). testing shows that roughly 12% of the friesian horse population carriers the mutated gene.

Naked Foal Syndrome (NFS);

it is inherited as a monogenic autosomal recessive trait where a foal can only be affected if the foal inherits the disease from both parents. parents that are carriers do not have any symptoms associated with NSF. horses affected by NFS are born hairless, and often die within days to months after birth. in most cases it is unclear as to the reason for these early deaths. in some rare cases hairless foals have survived up to 2.5 years. the first records of hairless akhal-teke foals date back to 1938, and since then the number of such foals has increased steadily. this disease affects the akhal-teke breed.

Warmblood Fragile Foal Syndrome (WFFS);

n inherited autosomal recessive disorder caused by a single mutation in PLOD1 gene. WFFS has been identified in a population of horses known as warmbloods. warmbloods are a group of mid-sized horse types often called sport horses and developed with the aim of competing in olympic equestrian sports. an affected WFFS foal is born with a two copies of the mutated LHl gene, one coming from each parent. the affected foal will display extreme skin fragility characterized by tearing, ulceration, etc. from contact with normal surroundings. small skin lesions can occur anywhere on the body, but are most noted on pressure points. in addition to skin wounds, lesions may also be found on the gums and other oral cavity mucous membranes. the limb joints are lax and hyperextensible. fetlocks are the most dramatically affected generally preventing a foal from standing normally. unfortunately there is no cure and all affected foals must be euthanized soon after birth.

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