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Robinow-like Syndrome (DLV2), also known as screw tail, is a hereditary trait that affects skeletal development. It is caused by a mutation in the DVL2 gene, leading to a non-functional protein and disruption of normal spine formation. This mutation is found in Boston Terriers, Bulldogs, and French Bulldogs, where it contributes to the characteristic shortened, kinked “screw” tail and the typical bulldog-type body shape.
Ichthyosis is a disease of the skin, causing itch, hair loss and the formation of dry, flaky “scales”. It also leaves the skin vulnerable to yeast infection. This variant of the disorder, known as Autosomal Recessive Congenital Ichthyosis (ARCI) is found in the American Bulldog and American Bully. It is caused by a recessive mutation to the gene NIPAL4.
Hypertrophic Cardiomyopathy (HCM) is a serious disorder characterized by an enlarged heart, which can lead to weakness, fatigue and potentially fatal heart failure. This specific variant of the disease is found in the Maine Coon, Munchkin, Scottish Fold, Siberian and Pixiebob Longhair. It is caused by a mutation to the gene MYBPC3. It seems to inherit in an autosomal recessive way. A related variant has also been observed in the Ragdoll.
Birman cats have clearly defined white feet (“gloves”) as part of their breed standard. This characteristic gloving is caused by a variant in the KIT gene and is inherited as an autosomal recessive trait. A cat must have two copies of the mutation in order to have the gloved white feet. Besides the Birman cats, this genetic variant occurs in lower frequencies in other breeds without leading to the typical Birman gloving.
Disproportionate Short-Limbed Chondrodysplasia is a developmental disorder of the skeleton that results in disproportionate dwarfism. The specific variant of the disorder analysed in this test is found in the Karelian Bear Dog and the Norwegian Elkhound Grey. It is caused by a recessive mutation to the gene ITGA10.
Panda is a coat colour variation that adds large, distinctive black and white patches to the normal brown of a German Shepherd’s coat. It is the result of a very recent mutation to the KIT gene, first arising in the year 2000. The coat colour inherits dominantly; however, the mutation is believed to be embryonic lethal, meaning that no puppies will be born carrying two copies of the mutation.
The White Spotting coat colour pattern in horses can be caused by any in a wide array of related mutations. The resulting pattern can vary anywhere between white markings on the face and legs, up to a completely white coat. Depending on both breed and pattern, variants of the White Spotting phenotype may be referred to as Splashed White, Dominant White, Tobiano or Sabino, among others.
The specific variant analysed in this test, known as Dominant White 21 (W21), is caused by an autosomal dominant mutation to the gene KIT. It has been observed in the Icelandic horse and the Icelandic word for the pattern is ýruskjóttur.
The White Spotting coat colour pattern in horses can be caused by any in a wide array of related mutations. The resulting pattern can vary anywhere between white markings on the face and legs, up to a completely white coat. Depending on both breed and pattern, variants of the White Spotting phenotype may be referred to as Splashed White, Dominant White, Tobiano or Sabino, among others.
The specific variant analysed in this test, known as White Spotting 15 (W15), is caused by an incomplete dominant mutation to the gene KIT. It has been observed in the Arabian horse.
Autosomal, dominant inheritance means that an animal may be clear (normal homozygote), affected (abnormal homozygote) or carrier (heterozygote). Carriers and affected will both have the symptoms of the mutation.
Explanation for veterinarians:
• An animal is CLEAR/NORMAL and has two healthy alleles (normal homozygote). The animal will not acquire any symptoms.
• An animal is a CARRIER and has one healthy allele and one defective allele (heterozygote). The animal will acquire symptoms of the disease.
• An animal is AFFECTED and therefore has two defective alleles (abnormal homozygote). The animal will acquire symptoms of the disease.
Explanation for breeders:
• An animal is CLEAR/NORMAL, and in that case will have two healthy alleles (normal homozygote). This animal will not acquire any abnormalities when breeding and cannot pass on the abnormality to the next generation.
• An animal is a CARRIER, where it will have a healthy allele and a defective allele (heterozygote). The animal will pass on the mutant allele to half of its offspring. Carriers can themselves also become sick.
• An animal is a AFFECTED, which means it has two defective alleles (abnormal homozygote). Affected animals pass on the defective allele to all their offspring in the next generation, and will also develop symptoms associated with the disease.
| Inheritance autosomal dominant: | Parents: | Reproductive cells: | Offspring: | Interpretation breeding: | Interpretatie veterinatian: |
|---|---|---|---|---|---|
| NORMAL x NORMAL | AA and AA | A/A x A/A | 100% AA | 100% NORMAL | 100% HEALTHY |
| NORMAL x CARRIER | AA and AB | A/A x A/B | 50% AA
50% AB |
50% NORMAL
50% CARRIER |
50% HEALTY
50% AFFECTED |
| NORMAL x AFFECTED | AA and BB | A/A x B/B | 100% AB | 100% CARRIER | 100% AFFECTED |
| CARRIER x CARRIER | AB and AB | A/B x A/B | 25% AA
50% AB 25% BB |
25% NORMAL
50% CARRIER 25% AFFECTED |
25% HEALTHY
75% AFFECTED |
|
CARRIER x AFFECTED |
AB and BB | A/B x B/B | 50% AB
50% BB |
50% CARRIER
50% AFFECTED |
100% AFFECTED |
| AFFECTED x AFFECTED | BB and BB | B/B x B/B | 100% BB | 100% AFFECTED | 100% AFFECTED |
Coat colour in cats is controlled by a wide range of different loci working together. One of these is the B-locus. On this locus there are several mutations known to be involved in the dilution or modification of the coat colour. Two of these coat colours are Chocolate and Cinnamon. These are both known to be autosomal recessive and caused by a mutation in the TYRP1 gene.
The Chocolate colour in cats is a dilution of black and occurs when the cat has two copies of the mutated allele (b). It presents itself as a warm, brown coat color that is lighter than black but still solid and deep in tone. The Cinnamon colour is an even lighter dilution of the chocolate colour and is governed by the cinnamon allele (b’). It’s considered a further modification of the brown pigment that creates a soft, warm, reddish-brown coat.
Cinnamon is recessive to Chocolate, which means that a cat with one mutated allele of both variants (b/b’) will appear Chocolate. Both variants are tested here.
The Hermansky-Pudlak syndrome 3 (HPS3) gene, also known as cocoa coat colour or co-locus is responsible for the brown colour in French Bulldogs. Mutations of the HPS3 gene interfere with the eumalin (black pigment) synthesis, which results in brown-pigmentation. The brown colour caused by the HPS3-variants is known to darken over age and to be slightly darker in adults that the brown colour caused by the TYRP1-related variants (B-locus). The co-locus is recessive and therefore needs two copies of the gene to present the phenotype. This co-locus can be present in French Bulldogs with various coat colours; brown, lilac, black, blue, cream, fawn or white, but the phenotype might be less visible in some cases. The complete phenotype of the coat, footpads and nose also depends on the A-, E-, K- and B-locus genes. Right now, no interaction in French Bulldogs between the co- and B-locus have been reported. Therefore it is not possible to predict what phenotype the combination of these variants would cause.
N/N = cocoa variant not present. The cocoa phenotype is not expressed, the offspring won’t inherit a copy of the co-locus.
N/co = carrier of the cocoa variant. Phenotype is not present. 50% of the offspring will inherit one copy of the co-locus.
co/co = the cocoa phenotype is present. The display of this phenotype depends on the interaction between other colour genes (loci). 100% of the offspring will get one copy of the co-locus.
The growth and maintenance of a dog’s coat, including the degree to which it sheds its coat, is a complex trait affected by multiple different genes. One such gene is the melanocortin 5 receptor (MC5R). A mutation to MC5R has been found to have a link to decreased shedding. Selecting for this mutation may therefore be of interest for the breeding of dogs that shed less hair.
Roan coat colour is a white patterning with a mixture of white and colored hairs over the body while the head, lower legs, mane and tail remain colored. In horses that inherit the classic Roan gene, the white and colored hairs are evenly mixed in comparison to horses that have an uneven distribution of white hairs called Roaning pattern. For this roaning pattern, the inheritance has not been defined.
In literature it is suggested that coat colour Roan is homozygous lethal, but evidence from studies with the Quarter horse breed indicate otherwise. Roan Quarter horses that produce 100% Roan foals exist in the population.
Amelogenesis Imperfecta (AI), also known as familial enamel hypoplasia (FEH), is an autosomal recessive hereditary condition caused by a mutation in the ENAM gene. This gene is involved in a process known as amelogenesis: the formation and deposition of enamelin, which is an important component of the enamel of the teeth. This variant of the disorder is found in the Italian Greyhound.
Coat colour in dogs is controlled by a wide range of different genes working together. These genes are often referred to as ‘loci’. The Dilution, or D-Locus, corresponds to the gene for melanophilin, MLPH, which is involved in the distribution of pigment. Autosomal recessive mutations of the D-Locus result in a ‘dilution’ of dark coat colours, turning them lighter and more silvery.
Any combination of two mutant alleles will result in a diluted coat. This variant of the D-Locus mutation, designated as d^3, is found in breeds such as the Chihuahua, Hungarian Mudi and Hungarian Pumi, Italian Greyhound and Shih-Tzu.
Delayed Postoperative Hamorrhage (DEPOH) is an inherited bleeding disorder primarily observed in Greyhounds and Scottish Deerhounds. It is associated with a mutation in the Serpin Family F Member 2 (SERPINF2) gene, which affects the function of alpha-2 antiplasmin, a key inhibitor of blood clot breakdown. As a result, affected dogs initially form normal blood clots after surgery or trauma, but these clots are broken down prematurely, leading to delayed bleeding. The condition is inherited in an autosomal dominant manner with incomplete penetrance. Dogs carrying one copy of the variant have a moderately increased risk of developing clinical signs, while dogs with two copies have a higher risk.
The white spotting patterns that occur in many dog breeds do not have a uniform genetic basis. The Microphthalmia Associated Transcription Factor gene (MITF gene) is associated with many white spotting patterns. This gene is also known as the S-Locus. There are three major white spotting patterns described. One pattern is called “Irish spotting” and is a symmetrical pattern with white markings on the undersides, collar and muzzle, and/or blaze as demonstrated by breeds such as the Boston Terrier, Corgi, Bernese Mountain dog and Basenji. Another pattern of less symmetrical white spotting in which random white spots occur on the body of the dog is often called piebald, parti or random white and is observed in several breeds, including the Beagle and Fox Terrier. The third major pattern is called extreme white and results in a dog that is almost entirely white but usually has at least some color on the head. Furthermore, there is a pattern called mantle, this pattern is similar to Irish spotting but with more white extending onto the thigh and up the torso, as seen in some Great Danes. Another pattern that is similar to Irish spotting is called flash or pseudo-Irish and occurs in Boxers. A mutation found in the MITF gene is associated with the piebald spotting pattern in more than 25 different dog breeds. The Coat Colour Piebald test (H326) tests for the genetic status of this mutation. It results in two variants (alleles). The allele N does not produce a piebald pattern, therefor dogs with two copies of the N allele do not display the piebald pattern. The allele S is associated with the piebald pattern, however the amount of white spotting expressed varies from breed to breed and among individuals within a breed. In many breeds such as Collie, Great Dane, Italian Greyhound, Shetland Sheepdog, Boxer and Bull Terrier, piebald behaves as a dosage-dependent trait. In those breeds the allele S is semi-dominant. One copy of the S allele (S/N) results in a limited white spotting pattern. Dogs with two copies of the S allele (S/S) display more extreme white with colour only on the head and perhaps a body spot. In Boxers and Bull Terriers, dogs that have two copies of the S allele (S/S) are completely white while dogs that only have one copy of the S allele (N/S) display the mantle pattern (called flash in these breeds). However, additional mutations in MITF or other white-spotting genes that affect the amount of white being expressed appear to be present in these breeds. In some other breeds, the allele S is recessive and in those breeds two copies are needed to produce the piebald pattern.
The Coat Colour Piebald test encloses the following results:
| MITF gene | Coat Colour |
|---|---|
| S/S | Dog has two copies of the piebald mutation, the amount of white spotting expressed depends on the breed and varies among individuals within a breed, see description above, only allele S will be passed on to an offspring |
| S/N | Dog has one copy of the piebald mutation, the amount of white spotting expressed depends on the breed and varies among individuals within a breed, see description above, either allele S or N will be passed on to an offspring |
| N/N | No piebald spotting, only allele N will be passed on to an offspring |
This product includes parentage verification and DNA profiling of the offspring. If the DNA profile of the (expected) parent(s) is unavailable, a separate DNA profile needs to be ordered.
A DNA profile is established using DNA markers. The profile from each sample is stored in a database and can be represented as a barcode, which is unique to each individual. This DNA profile serves the purpose of parentage verification, involving a comparison of the genetic information present in an offspring with that of the potential parents. For accurate parentage verification, all genetic information in the offspring must be traceable to the combination of the dam and the sire. In the majority of cases, the reliability of this analysis exceeds 99.5 percent.
This product includes parentage verification and DNA profiling of the offspring. If the DNA profile of the (expected) parent(s) is unavailable, a separate DNA profile needs to be ordered.
A DNA profile is established using DNA markers. The profile from each sample is stored in a database and can be represented as a barcode, which is unique to each individual. This DNA profile serves the purpose of parentage verification, involving a comparison of the genetic information present in an offspring with that of the potential parents. For accurate parentage verification, all genetic information in the offspring must be traceable to the combination of the dam and the sire. In the majority of cases, the reliability of this analysis exceeds 99.5 percent.
This product includes maternity verification and DNA profiling of the offspring. If the DNA profile of the (expected) mother is unavailable, a separate DNA profile needs to be ordered.
A DNA profile is established using DNA markers. The profile from each sample is stored in a database and can be represented as a barcode, which is unique to each individual. This DNA profile serves the purpose of parentage verification, involving a comparison of the genetic information present in an offspring with that of the potential parents. For accurate parentage verification, all genetic information in the offspring must be traceable to the combination of the dam and the sire. In the majority of cases, the reliability of this analysis exceeds 99.5 percent.
