Cat coat genetics


Cat coat genetics determine the coloration, pattern, length, and texture of feline fur. Understanding how is challenging because many genes are involved. The variations among cat coats are physical properties and should not be confused with cat breeds. A cat may display the coat of a certain breed without actually being that breed. For example, a Siberian could wear point coloration, the stereotypical coat of a Siamese.

Solid colors

Eumelanin

The browning gene B/b/bl codes for TYRP1, an enzyme involved in the metabolic pathway for eumelanin pigment production. Its dominant form, B, will produce black eumelanin. It has two recessive variants, b, and bl, with bl being recessive to both B and b. Chocolate is a rich brown color, and is referred to as chestnut in some breeds. Cinnamon is a lighter reddish brown.

Sex-linked orange/red

The sex-linked Orange locus, O/o, determines whether a cat will produce eumelanin. In cats with orange fur, phaeomelanin completely replaces eumelanin. This gene is located on the X chromosome. The orange allele is O, and is codominant with non-orange, o. Males can typically only be orange or non-orange due to only having one X chromosome. Since females have two X chromosomes, they have two alleles of this gene. OO results in orange fur, oo results in black or brown fur, and Oo results in a tortoiseshell cat, in which some parts of the fur are orange and others areas non-orange. Male tortoiseshell cats are known to exist, but, as expected from the genetics involved, they are rare and often exhibit chromosomal abnormalities. In one study, less than a third of male calicos had a simple XXY Klinefelter's karyotype, slightly more than a third were complicated XXY mosaics, and about a third had no XXY component at all.
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This color is known as red by breeders. Other names include yellow, ginger, and marmalade. Red show cats have a deep orange color, but it can also present as a yellow or light ginger color. Unidentified "rufousing polygenes" are theorized to be the reason for this variance.
Orange is epistatic to nonagouti, so all red cats are tabbies. "Solid" red show cats are usually low contrast ticked tabbies.
The precise identity of the gene at the Orange locus is unknown. It has been narrowed down to a 3.5 Mb stretch on the X chromosome in 2009.

Dilution and Maltesing

The Dense pigment gene, D/d, codes for melanophilin, a protein involved in the transportation and deposition of pigment into a growing hair. When a cat has two of the recessive d alleles, black fur becomes "blue", chocolate fur becomes "lilac", cinnamon fur becomes fawn, and red fur becomes cream.

Other genes

s are striped due to the agouti gene. Their stripes have an even distribution of pigment, while the background is made up of banded hairs. Tabby cats usually show the following traits:
The Agouti gene, with its dominant A allele and recessive a allele, controls the coding for agouti signaling protein. The wild-type A produces the agouti shift phenomenon, which causes hairs to be banded with black and an orangish/reddish brown, this revealing the underlying tabby pattern. The non-agouti or "hypermelanistic" allele, a, does not initiate this shift in the pigmentation pathway and so homozygotes aa have pigment production throughout the entire growth cycle of the hair—along its full length. As a result, the non-agouti genotype is solid and has no obvious tabby pattern.
A major exception to the solid masking of the tabby pattern exists: the O allele is epistatic over the aa genotype. That is, in red or cream colored cats, tabby striping is displayed despite the genotype at the agouti locus. This explains why you can usually see the tabby pattern in the orange patches of non-agouti tortoiseshell cats, but not in the black or brown patches.
However, some red cats and most cream cats show a fainter tabby pattern when they have no agouti allele to allow full expression of their tabby alleles. That is, in genetically red cats the aa does still have an effect, especially in dilute coats, where the tabby pattern is sometimes not expressed except on the extremities.

Tabby pattern

The tabby gene has three very well known versions, or alleles, which in different combinations account for most tabby patterns seen in domestic cats, including those patterns seen in most breeds. There are additional alleles and even additional genes affecting tabby patterns which have also been both identified and postulated.
The three most common alleles in order of dominance are Ta, the allele for ticked patterns as in the Abyssinian, Tm, for mackerel tabbies, and the recessive tb for classic. Ta is co-dominant to Tm and tb. A cat with the Ta allele will express the ticked tabby pattern and only a cat with two tb alleles will express the classic tabby pattern.
The wild-type is the mackerel tabby, the most common variant is the classic tabby pattern and perhaps the most well known of the less common tabby patterns is the ticked.
The classic tabby is most common in Iran, Great Britain and in lands that were once part of the British Empire and Persian Empire. The gene responsible for this differential patterning has been identified as transmembrane aminopeptidase Q, which also produces the king cheetah coat variant.

Spotted tabby

Spotted tabbies have their stripes broken up into spots, which may be arranged vertically or horizontally. A 2010 study suggests that spotted is caused by the modification of mackerel stripes, and may cause varying phenotypes such as "broken mackerel" tabbies via multiple loci.

Ticked tabby

The Ticked allele Ta generally produces a non-patterned agouti coat having virtually no stripes or bars but still considered a tabby coat. Stripes often remain to some extent on the face, tail, legs, and sometimes the chest in heterozygotes but are nearly or completely nonexistent in homozygotes. The Abyssinian breed is fixed for the ticked allele—all Abyssinians are homozygotes for this gene. The ticked tabby allele is ultimately dominant and therefore completely masks all the other tabby alleles, “hiding” the patterns they would otherwise express.

Other genes

Tortoiseshells are also known as calimanco or clouded tiger cats, and by the abbreviation "tortie". Tortoiseshells have patches of orange fur and black or brown fur, caused by X-inactivation. Because this requires two X chromosomes, the vast majority of tortoiseshells are female, with approximately 1 in 3,000 being male. Male tortoiseshells can occur as a result of chromosomal abnormalities such as Klinefelter syndrome, by mosaicism, or by a phenomenon known as chimerism, where two early stage embryos are merged into a single kitten.
Tortoiseshells with a relatively small amount of white spotting are known as "tortoiseshell and white", while those with a larger amount are known in North America as calicos. Calicos are also known as tricolor cats, mi-ke in Japanese, and lapjeskat in Dutch. The factor that distinguishes tortoiseshell from calico is the pattern of eumelanin and pheomelanin, which is partly dependent on the amount of white, due to an effect of the white spotting gene on the general distribution of melanin. A cat which has both an orange and non-orange gene, Oo, and little to no white spotting, will present with a mottled blend of red/cream and black/blue, reminiscent of tortoiseshell material, and is called a tortoiseshell cat. An Oo cat with a large amount of white will have bigger, clearly defined patches of red/cream and black/blue, and is called a calico. With intermediate amounts of white, a cat may exhibit a calico pattern, a tortie pattern, or something in between, depending on other epigenetic factors.
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A true tricolor must consist of three colors: white; a red, orange, yellow, or cream pheomelanin color; and a black, brownish, or gray eumelanin color. Tricolor should not be mistaken for the natural gradations in a tabby pattern. The shades which are present in the pale bands of a tabby are not considered to constitute a separate color.

Variations

White spotting and epistatic white were long thought to be two separate genes, but in fact they are both on the KIT gene. White spotting can take many forms, from a small spot of white to the mostly-white pattern of the Turkish Van, while epistatic white produces a fully white cat. The Birman-specific recessive "gloving" trait is also located on the KIT gene.
WD causes congenital sensorineural deafness in cats. Domesticated WD cats are often completely deaf.

Colorpoint and albinism

The colorpoint pattern is most commonly associated with Siamese cats, but may also appear in any domesticated cat. A colorpointed cat has dark colors on the face, ears, feet, and tail, with a lighter version of the same color on the rest of the body, and possibly some white. The exact name of the colorpoint pattern depends on the actual color, so there are seal points, chocolate points, blue points, lilac or frost points, red or flame points, and tortie points, among others. This pattern is the result of a temperature sensitive mutation in one of the enzymes in the metabolic pathway from tyrosine to pigment, such as melanin; thus, little or no pigment is produced except in the extremities or points where the skin is slightly cooler. For this reason, colorpointed cats tend to darken with age as bodily temperature drops; also, the fur over a significant injury may sometimes darken or lighten as a result of temperature change.
The tyrosine pathway also produces neurotransmitters, thus mutations in the early parts of that pathway may affect not only pigment, but also neurological development. This results in a higher frequency of cross-eyes among colorpointed cats, as well as the high frequency of cross-eyes in white tigers
The silver series is caused by the Melanin inhibitor gene I/i. The dominant form causes melanin production to be suppressed, but it affects phaeomelanin much more than eumelanin. On tabbies, this turns the background a sparkling silver color while leaving the stripe color intact, making a silver tabby. On solid cats, it turns the base of the hair pale, making them silver smoke.
Silver agouti cats can have a range of phenotypes, from silver tabby, to silver shaded, to tipped silver/chinchilla. This seems to be affected by hypothetical wide band factors, which make the silver band at the base of the hair wider. Breeders often notate wide band as a single gene Wb/wb, but it is most likely a polygenic trait.
If a cat has the wide band trait but no inhibitor, the band will be golden instead of silver. These cats are known as golden tabbies. Shaded golden and tipped golden are also possible. However, there is no golden smoke, because the combination of wide band and nonagouti simply produces a solid cat.
The genetics involved in producing the ideal tabby,, shaded, or smoke cat is complex. Not only are there many interacting genes, but genes sometimes do not express themselves fully, or conflict with one another. For example, the melanin inhibitor gene in some instances does not block pigment, resulting in a grayer undercoat, or in tarnishing. The greyer undercoat is less desirable to fanciers.
Likewise, poorly-expressed non-agouti or over-expression of melanin inhibitor will cause a pale, washed out black smoke. Various polygenes, epigenetic factors, or modifier genes, as yet unidentified, are believed to result in different phenotypes of coloration, some deemed more desirable than others by fanciers.

Tipped or shaded cats

The genetic influences on tipped or shaded cats are:
Fever coat is an effect known in domestic cats, where a pregnant female cat has a fever or is stressed, causing her unborn kittens' fur to develop a silver-type color rather than what the kitten's genetics would normally cause. After birth, over some weeks the silver fur is replaced naturally by fur colored according to the kitten's genetics.

Fur length and texture

Cat fur length is governed by the Length gene in which the dominant form, L, codes for short hair, and the recessive l codes for long hair. In the longhaired cat, the transition from anagen to catagen is delayed due to this mutation. A rare recessive shorthair gene has been observed in some lines of Persian cat where two longhaired parents have produced shorthaired offspring.
Cat coat length is controlled by the fibroblast growth factor 5 gene. The dominant allele codes for the short coat seen in most cats. Long coats are coded for by at least four different recessively inherited mutations, the alleles of which have been identified. The most ubiquitous is found in most or all long haired breeds while the remaining three are found only in Ragdolls, Norwegian Forest Cats, and Maine Coons.
There have been many genes identified that result in unusual cat fur. These genes were discovered in random-bred cats and selected for. Some of the genes are in danger of going extinct because the cats are not sold beyond the region where the mutation originated or there is simply not enough demand for cats expressing the mutation.
In many breeds, coat gene mutations are unwelcome. An example is the rex allele which appeared in Maine Coons in the early 1990s. Rexes appeared in America, Germany and the UK, where one breeder caused consternation by calling them "Maine Waves". Two UK breeders did test mating which indicated that this was probably a new rex mutation and that it was recessive. The density of the hair was similar to normally coated Maine Coons, but consisted only of down type hairs with a normal down type helical curl, which varied as in normal down hairs. Whiskers were more curved, but not curly. Maine Coons do not have awn hairs, and after moulting, the rexes had a very thin coat.

Curly-coated

There are various genes producing curly-coated or "rex" cats. New types of rex arise spontaneously in random-bred cats now and then. Here are some of the rex genes that breeders have selected for:
There are also genes for hairlessness:
Some rex cats are prone to temporary hairlessness, known as baldness, during moulting.
Here are a few other genes resulting in unusual fur: