Cat coat genetics determine the colouration, pattern, length, and texture of feline fur. 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 Neva Masquerade (Siberian colourpoint) could wear point colouration, the coat typically associated with a Siamese.
The browning gene B/b/b<sup>l</sup> codes for TYRP1 (), an enzyme involved in the metabolic pathway for eumelanin pigment production. The dominant form, B, will produce black eumelanin. It has two recessive variants, b (chocolate) and b<sup>l</sup> (cinnamon), with b<sup>l</sup> being recessive to both B and b. Chocolate is a rich dark brown colour, and is referred to as chestnut in some breeds. Cinnamon is a light brown which may be a reddish colour.
The sex-linked red "Orange" locus, O/o, determines whether a cat will produce eumelanin. In cats with orange fur, phaeomelanin (red pigment) completely replaces eumelanin (black or brown pigment). This gene is located on the X chromosome. The orange allele is O, and non-orange is o. Males are typically only 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 fur without any orange (black, brown, etc.), and Oo results in a tortoiseshell cat, in which some parts of the fur are orange and other areas non-orange. One in three thousand tortoiseshell cats are male, making the combination possible but rare - however, due to the nature of their genetics, male tortoiseshells often exhibit chromosomal abnormalities. In one study, less than a third of male tortoiseshells 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.
The coat colour commonly referred to as "orange" is scientifically known as red. Other common names include yellow, ginger, and marmalade. Red show cats have a deep orange colour, but it can also present as a yellow or light ginger colour. Unidentified "rufousing polygenes" are theorised to be the reason for this variance. Orange is epistatic to non-agouti, so all red cats are tabbies. "Solid" red show cats are usually low contrast ticked tabbies.
The identity of the gene at the Orange locus was narrowed down to a 3.5 Mb stretch on the X chromosome in 2009. In 2024 it was discovered that the dominant orange colour associated with the Orange locus is the result of a genomic deletion in a regulatory region of ARHGAP36, a Rho GTPase activating protein. The deletion results in a 13-fold increase in expression of the protein in melanocytes.
The Dense pigment gene, D/d, codes for melanophilin (MLPH; ), a protein involved in the transportation and deposition of pigment into a growing hair. When a cat has two of the recessive d alleles (Maltese dilution), black fur becomes "blue" (appearing grey), chocolate fur becomes "lilac" (appearing light, almost greyish brown-lavender), cinnamon fur becomes "fawn", and red fur becomes "cream". Similar to red cats, all cream cats are tabbies. The d allele is a single-base deletion that truncates the protein. If the cat has d/d genes, the coat is diluted. If the genes are D/D or D/d, the coat will be unaffected.
Tabby cats have a range of variegated and blotched coats, consisting of a dark pattern on a lighter background. This variety is derived from the interplay of multiple genes and resulting phenotypes. Most tabbies feature thin dark markings on the face, including the 'M' on the forehead and an eyeliner effect, pigmented lips and paws, and a pink nose outlined in darker pigment. The following tabby coat patterns are all naturally found in the domestic cat:
The agouti factor determines the "background" of the tabby coat, which consists of hairs that are banded with dark eumelanin and lighter phaeomelanin along the length of the hair shaft. The Agouti gene, with its dominant A allele and recessive a allele, controls the coding for agouti signalling protein (ASIP; ). The wild-type dominant A causes the banding and thus an overall lightening effect on the hair, while the recessive non-agouti or "hypermelanistic" allele a does not initiate this shift in the pigmentation pathway. As a result, homozygous aa have pigment production throughout the entire growth cycle of the hair and therefore along its full length. These homozygotes are solidly dark throughout, which obscures the appearance of the characteristic dark tabby markingsâÂÂsometimes a suggestion of the underlying pattern, called "ghost striping", can be seen, especially on kittens and on adults in bright slanted light, in smokes, and sometimes on the forehead, legs, tail or elsewhere.
A major exception to the solid masking of the tabby pattern exists, as the O allele of the O/o locus is epistatic over the aa genotype. That is, in red or cream coloured cats, tabby marking is displayed regardless of the genotype at the agouti locus. However, some red and most cream tabbies do have a fainter pattern when lacking an agouti allele, indicating that the aa genotype does still have a faint effect even if it does not induce complete masking. The mechanism of this process is unknown.
An example of the Agouti gene can be seen in Bengal cats, which are a hybrid between Asian leopard cats and domestic cats. The breed sports the hybrid 'charcoal' pattern, a pseudomelanistic marking which has a characteristic dark face marking, the "mask", and a broad dorsal stripe down its back, the "cape". According to Gershoney et al., the charcoal mask is indicated to be the result of a heterozygote of A<sup>Pbe</sup>/a. The relationships between the different agouti alleles is not fully understood. More research is required to determine the inheritance modes for charcoal.
The Tabby locus on chromosome A1 accounts for most tabby patterns seen in domestic cats, including those patterns seen in most breeds. The dominant allele Ta<sup>M</sup> produces mackerel tabbies, and the recessive Ta<sup>b</sup> produce classic ('blotched') tabbies. The gene responsible for this differential patterning had been identified as transmembrane aminopeptidase Q (Taqpep, ). The gene name Taqpep has later been replaced by laeverin with symbol LVRN. A threonine to asparagine substitution at residue 139 (T139N) in this protein is responsible for producing the tabby phenotype in domestic cats. In cheetahs, a base pair insertion into exon 20 of the protein replaces the 16 C-terminal residues with 109 new ones (N977Kfs110), generating the king cheetah coat variant.
The wild-type (in African wildcats) is the mackerel tabby (stripes look like thin fishbones and may break up into bars or spots). The most common variant is the classic tabby pattern (broad bands, whorls, and spirals of dark colour on pale background usually with bulls-eye or oyster pattern on flank). Spotted tabbies have their stripes broken up into spots, which may be arranged vertically or horizontally. A 2010 study suggests that spotted coats are caused by the modification of mackerel stripes, and may cause varying phenotypes such as "broken mackerel" tabbies via multiple loci. If the genotype is Sp/Sp or Sp/sp the tabby coat will be spotted or broken. If it is an sp/sp genotype, the tabby pattern will remain either mackerel or blotched. This gene has no effect on cats with a ticked coat.
The Ticked (Ti) locus on chromosome B1 controls the generation of "ticked coats", agouti coats with virtually no stripes or bars. Ticked tabbies are rare in the random-bred population outside Asia, but fixed in certain breeds such as the Abyssinian and Singapura. Ti<sup>A</sup> is the dominant allele that produces ticked coats; Ti<sup>+</sup> is the recessive one. The causative gene for ticked tabby markings is Dickkopf-related protein 4 (DKK4). Both a cysteine to tyrosine substitution at residue 63 (C63Y) and an alanine to valine substitution at residue 18 (A18V) result in decreased DKK4, which is associated with ticking. Both variants are present in the Abyssinian breed, and the A18V variant is found in the Burmese breed. Stripes often remain to some extent on the face, tail, legs, and sometimes the chest ("bleeding through"). Traditionally, this has been thought to happen in heterozygotes (Ti<sup>A</sup>Ti<sup>+</sup>) but be nearly or completely nonexistent in homozygotes (Ti<sup>A</sup>Ti<sup>A</sup>). The ticked tabby allele is epistatic to and therefore completely (or mostly) masks all the other tabby alleles, "hiding" the patterns they would otherwise express.
It was once thought that Ti<sup>A</sup> was an allele of the Tabby gene, called T<sup>a</sup>, dominant to all other alleles at the locus.
Tortoiseshell is a coat pattern that combines two colours, other than white, in an asymmetrical distribution, either closely mixed ('brindled') or in larger patches. The two colours always consist of one eumelanistic (black, blue, chocolate, lilac, cinnamon or fawn) and one phaeomelanistic (red or cream) colour. The pattern is caused by X-inactivation, which requires two X chromosomes, consequently 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 (e.g. Klinefelter syndrome), by mosaicism, or by a phenomenon known as chimaerism (two early stage embryos are merged into a single kitten).
Tortoiseshell should not be mistaken for the natural gradations of colour hues in a tabby pattern. The shades which are present in the ground colour (pale regions) of a tabby are not considered to constitute a separate colour. High degree of warm tones in the ground colour are instead referred to as rufousing factors or rufism.
Tortoiseshells with white spotting are known as "tricolour" or "tortoiseshell and white". Those with approximately 25âÂÂ75% white are known in North America as "calico". A tricolour consist of three colours: white, a phaeomelanin red-based colour (red or cream), and eumelanin black-based colour (e.g. black or blue).
In tricolour cats, the factor that distinguishes brindled patterns from distinct patches is the placement of eumelanin and phaeomelanin pigment, 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 brindled (mottled) blend of black-based and red-based pigments, reminiscent of tortoiseshell material (called tortoiseshell cat in the US). An Oo cat with a large amount of white will have bigger, clearly defined patches of black-based and red-based pigments (called a "calico" in the US).
The KIT gene determines whether or not there will be any white in the coat, except when a solid white coat is caused by albinism, which happens on a different locus (C). White spotting and epistatic white (also known as dominant white) were long thought to be two separate genes (called S and W respectively), but in fact they are both on the KIT gene. The two have been combined into a single white spotting locus (W). White spotting can take many forms of particoloured (bicolour or tricolour) patterns, from a small spot of white to the mostly-white Van pattern of the Turkish Van, while epistatic white produces a completely white cat (solid or self white). The KIT gene W locus has the following alleles:
The colourpoint pattern, also known as acromelanism, oculocutaneous albinism (OCA), and the Himalayan coat-colour pattern, is most commonly associated with Siamese cats, but existed long before the breed's creation and is found worldwide in (non-)pedigree domestic cats. The colloquial point terminology depends on its base colour, e.g. black ("seal", "sable", "brown"), lilac ("frost"), and red ("flame").
A colourpoint cat has dark colours on their extremities âÂÂface, ears, feet, and tailâ with a lighter version of the same colour on the rest of the body. This pattern is the result of a temperature sensitive mutation causing non-functional form of the tyrosinase (TYR) enzyme in the metabolic pathway from tyrosine to pigment, such as melanin; thus, a congenital lack of pigment production in the skin, except in the extremities or points where the skin is slightly cooler. For this reason, colourpoint cats tend to darken with age as bodily temperature drops; also, the fur may sometimes darken or lighten as a result of temperature change due to illness or significant injury.
More specifically, colourpoint is a type of partial albinism found, together with albinism, on the albino locus (C), which contains the gene TYR (). Although the Siamese colourpoint pattern is the most famous colouration produced by TYR, there are colour mutations at the locus.
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 colourpoint 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 (warm red pigment) much more than eumelanin (black or brown pigment). On tabbies, this turns the background colour into a sparkling cold silver tone. The dark hairs that make the tabby pattern will be silvery-white at their roots, whilst leaving the pigmentation at the tip of these hairs intact, resulting in a cold-toned silver tabby. On solid cats, it turns the base of the hair throughout their coat into a depigmented pale silvery-white, whilst the tip stays pigmented, making them (silver) smoke. The term cameo is commonly used for red silver and cream silver (inhibitor gene (I-O-)) coloured coats in cats.
Silver agouti cats can have a range of silver tabby phenotypes depending on the depigmentation ratio of the hair root to tip; from regular silver tabby (over half the hair is pigmented), to the more extreme silver tabby forms of silver shaded (under half the hair is pigmented, approx. â  of hair length), and silver tipped also called 'chinchilla' or 'shell' (only the very tip of the hair is pigmented, approx. â  of hair length). This seems to be affected by hypothetical wide-band factors, which make the silver band at the base of the hair wider in silver tabbies and smokes. 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 silver melanin inhibitor, the band will be golden instead of silver. These cats are known as golden tabbies, or in Siberian cats as sunshine tabbies. The golden colour is caused by the CORIN gene. Shaded golden and tipped golden are also possible, in the same hair length distribution as the silver-gene. However, there is no golden smoke, because the combination of wide-band and non-agouti simply produces a solid cat.
The genetics involved in producing the ideal tabby, tipped, 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 silver melanin inhibitor gene in some instances does not block pigment, resulting in a greyer undercoat, or in tarnishing (yellowish or rusty fur). The greyer undercoat is considered 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 (sets of related genes), epigenetic factors, or modifier genes, as yet unidentified, are believed to result in different phenotypes of colouration, some deemed more desirable than others by fanciers.
The genetic influences on tipped or shaded cats are:
Fever coat is a non-permanent depigmentation effect known in domestic cats, where a female cat experiences health implications during pregnancy (e.g. has a fever or is stressed), causing her unborn kittens' fur to develop a frosty silver-type colour (silver-grey, cream, or reddish) rather than what the kitten's genetics would normally show. The depigmentation is most prominent at the hair tips, rather than the roots as would be the case in actual silver coats. After birth, the frost-like fur is replaced naturally by fur in their actual genetic colours during a moult in their first year; in most cases the full colour is completely grown in at 6âÂÂ8 months old.
Cat fur can be short, long, curly, or hairless. Most cats are short-haired, like their wild ancestor. The fur can naturally come in three types of hairs; guard, awn, and down hair. The length, density and proportions of these three hairs varies greatly between breeds, and in some cats only one or two types are found.
Most oriental breeds only express one single layer of silky coat. However, cats can also have double-layered coats out of two hair types in which the down hairs form the soft, insulating undercoat, and the guard hairs form the protective outer coat.
A typical cat coat exists of all three natural hair types, but due to the equal lengths of two of these hairs, the coat is still considered double-layered. Typically, the down hairs comprise the undercoat while the guard and awn hairs make up the basic top coat. Double-coated cats with thick undercoats require daily grooming as these coats are more prone to matting. Double coats are found in for example the Persian, British Shorthair, Maine Coon and Norwegian Forest Cat.
Additionally, there even exist cats which express all three natural types of cat hair in different lengths and structures, which form three different layers. These cats are called triple-coated. Siberians and Neva Masquerades are known for their unique triple coats, which provided their landrace ancestors with extra insulation to withstand their arctic habitat.
There have been many genes identified that result in unusual cat fur. These genes have been discovered in random-bred and purebred cats worldwide, and are sometimes selectively bred into new breeds or breed varieties. 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 perceived as unfavourable. An example is the rex allele which appeared in Maine Coons in the early 1990s in Germany, the UK and the US.
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 (hair growth) to catagen (cessation of hair growth) is delayed due to this mutation. A rare recessive shorthair gene has been observed in some lines of (silver) Persian where two longhaired parents have produced shorthaired offspring.
The Length gene has been identified as the fibroblast growth factor 5 (FGF5; ) gene. The dominant allele codes for the short coat is 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 are various genes producing curly-coated or "rex" cats. New types of rex arise spontaneously in random-bred cats now and then. Some of the rex genes that breeders have selected for are:
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: