Cat coat genetics

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The genetics of cat coat coloration, pattern, length, and texture is a complex subject, and many different genes are involved.

Contents

Genes involved in albinism, dominant white, and white spotting

  • The dominant C gene and its recessive alleles determine whether a cat is a complete albino (either pink-eyed or blue-eyed), a temperature sensitive albino (Burmese, Siamese, or a blend known as Tonkinese), or a non-albino. If a cat has the dominant C gene, then the cat is non-albino and the W gene determines its color.
  • The white masking gene, W/w. The dominant allele masks all other colors by preventing pigment producing cell migration to the skin during embryologic development. In other words, the cat has a greatly reduced number of melanocytes. A cat that is WW or Ww will be white, no matter what other color genes it may have. A cat that is homozygous recessive (ww) will express normal pigmentation, and the O gene will determine its color. Some cats with the W gene are deaf and have depigmentation of the iris of one or both eyes, resulting in blue eye color. Cats with W allele are also more likeky to get a skin cancer.
  • The white spotting or piebald spotting gene, S/s, which has variable expression, so that an SS cat has more extensive white patching than an Ss cat. It is this gene that creates the familiar white blaze across the face, a white bib, tuxedo pattern, or dappled paws. This gene can turn a cat's eyes blue if the white spotting occurs over the eyes. A hypothetical Sb allele ("gloving gene") causes the mittens in Birman and Snowshoe breeds. Some researchers believe that there are separate white spotting genes for distinct features, such as the white locket that some cats have on their neck.

Genes involved in orange, black, brown, and diluted colors

  • The sex-linked orange gene, O, determines if there will be orange fur. This gene only appears on the X chromosome. In cats with orange fur, phaeomelanin (orange pigment) completely replaces eumelanin (black pigment).
  • For males, O results in orange fur, and o means that the O gene will determine the color (the black or brown color may be broken up into patterns if the cat has the agouti gene), so this would be epistatic to agouti locus.
  • For females, OO results in orange fur, oo means that the gene will determine the color (patterns if the cat has the agouti gene), and Oo results in a tortoiseshell cat, in which the B gene determines the color of the dark patches. A cat with Oo and white spotting genes will be a calico. The reason for the patchwork effect in female cats heterozygous for the O gene (Oo) is "X chromosome inactivation" - one or the other X chromosome in every cell in the embryo is randomly inactivated, and the gene in the other X chromosome is expressed (see barr body).
  • Rufous polygenes, as yet unidentified, that affect the richness of the orange gene's expression.

For a cat to be tortoiseshell, calico, or one of the diluted variants such as blue-cream, the cat must simultaneously express two alleles, O and o, which are located on the X chromosome. Males normally cannot do this, as they have only one X chromosome, and therefore only one allele, and so calico cats are normally only female. They can be males only is they have chromosomal abnormalities such as XXY, but in this case they are sterile.

  • The browning gene B/b codes for tyrosinase related protein-1, an enzyme involved in the metabolic pathway for eumelanin pigment production, and in its dominant form, B, will produce black color. Recessive variants are b, producing brown (or chocolate), and bl producing light brown or cinnamon.
  • Barrington Brown is a recessive browning gene that dilutes black to mahogany, brown to light brown and chocolate to pale coffee. It is different than the browning gene and has only been observed in laboratory cats.
  • The Dense pigment gene, D/d, corresponds to the dilute phenotype. When a cat has two of the recessive d alleles, black fur becomes "blue" (actually gray), chocolate fur becomes lilac, cinnamon fur becomes fawn, and orange fur becomes cream.
  • Dilution modifier gene, Dm, which caramelizes the dilute colors in its homozygous form (Dm-). The existence of this phenomenon as a discrete gene is a controversial subject among feline enthusiasts.
  • There is also a theoretical "black modifier" gene, Bm, which in its recessive form, bmbm, causes these cats to turn amber or light amber. This gene could be more appropriately called "agouti modifier" and is probably related to the extension locus (the melanocortin receptor) or its ligand, the agouti signaling protein. This phenomenon was first identified in Norwegian Forest Cats. Other forms of extension mutations have been seen in many breeds (and domestic cats), resulting in unique forms of tabby expression.
  • A black modifier has also been found in shaded silver and chinchilla Persians whose fur turns pale golden in adulthood due to elongation of the pigment granules. These cats resemble shaded or tipped goldens, but are genetically shaded or tipped silvers with an additional modifier gene.

One can deduce that a grey male cat with a white bib and paws:

  • has the o variant of the orange gene on its only X chromosome (because the grey color corresponds to black, not orange)
  • has at least one S variant of the white Spotting gene (because it has the white bib and paws)
  • has two w genes (because it expresses a fur color)
  • has the dominant B gene (because its fur color is a shade of black rather than brown)
  • has two d (dilute) genes (because its fur is grey, rather than black)

Genes involved in fur pattern and shading

  • The primary tabby pattern gene, Mc/mc, which sets the basic pattern of stripes that underlies the coat: the basic wild-type tabby gene, Mc, produces what is called a mackerel striped tabby (stripes look like thin fishbones and may break up into bars or spots); while a recessive mutant, mc, produces a blotched or classic tabby pattern (broad bands, whorls, and spirals of dark color on pale background usually with bulls-eye or oyster pattern on flank.) The classic tabby pattern is common in Great Britain and in lands that were once part of the British Empire.
  • Secondary tabby pattern genes such as Ta / ta, at which locus a dominant mutation produces an Abyssinian ticked or non-patterned agouti tabby, having virtually no stripes or bars. (This is one type of unpatterned tabby; the other type of unpatterned tabby is the tipped / shaded / smoke cat. See inhibited pigment gene, below.) The dominant form of the Abyssinian gene masks out all other tabby patterns.
  • Other genes (pattern modifier genes) are theorized to be responsible for creating various type of spotting patterns, many of which are variations on a basic mackeral or classic pattern. There are also hypothetical genes which affect banding frequency, width, and size.
  • The agouti gene, A/a which codes for agouti signaling protein. The dominant, wild-type A causes the agouti shift phenomenon which causes hairs to be black pigmented at the tips and orange pigmented at the roots (revealing the underlying tabby pattern), while the recessive non-agouti or "hypermelanistic" allele, a, prevents this shift in the pigmentation pathway. In its homozygous form, aa, this results in black pigment production throughout the growth cycle of the hair. Thus, the non-agouti genotype (aa) masks or hides the tabby pattern (Mc and mc). The O gene is also epistatic over the aa genotype. That is, the A to a mutation does not have a discernable effect on red or cream colored cats, resulting in these cats displaying tabby striping independent of their genotype at this locus. This explains why you can usually see the tabby pattern in the orange patches of tortoiseshell cats, but not in the black or brown patches.
  • There is an interesting gene, not yet identified but believed to be related to the agouti gene, in the Chausie breed, that produces silver-tipped black fur similar to Abyssinian ticked fur. The "grizzled" phenomenon is purported to have been inherited from the hybridization of these cats to Jungle Cats.
  • The inhibited pigment gene, I/i. The homozygous dominant allele (II) produces tipped hairs that are fully colored only at the tip and have a white base. The homozygous recessive allele (ii), when combined with the agouti gene, produces the "golden tabby" coloration. The melanin inhibitor gene interacts with other genes, especially the agouti gene, to produce various degrees of tipping, ranging from tipped to silver shaded and silver tabby. The inhibitor gene interacts with the non-agouti gene to produce smoke; either silver smokes (dominant Inhibitor gene) or golden smokes (recessive inhibitor gene).

How breeders can identify and separate tabby genes

Cats with tabby genes (AA or Aa) normally have:

  • M on forehead. (Does this disappear in ticked, shaded silver, and tipped cats?)
  • Thin pencil lines on face. (Does this disappear in ticked, shaded silver, and tipped cats?)
  • Black "eyeliner" appearance and white or pale fur around eyeliner.
  • Pigmented lips and paws.
  • A pink nose outlined in darker pigment
  • Torso, leg, and tail banding. (Torso banding disappears in the ticked tabby.)

Most or all banding disappears in the shaded shorthair, but you can still deduce the tabby genes from the other features, such as the "eyeliner" appearance.

The genetics involved in producing the ideal tipped, shaded, or smoke cat is complex. Not only are there dozens of interacting genes, but genes sometimes do not express themselves fully, or conflict with one another. For example, the melanin inhibitor gene sometimes does a poor job blocking pigment, resulting in an excessively gray undercoat, or in tarnishing (yellowish or rusty fur). Likewise, poorly-expressed non-agouti or over-expression of melanin inhibitor will cause a pale, washed out black smoke. Here are the minimum genetic requirements for a tipped or shaded cat to exist:

  • Agouti gene.
  • Genes (such as Ta) causing unstriped body type.
  • Genes affecting number and width of bands of color on each hair.
  • Hypothetical wide band gene(s). Without a wide undercoat, the cat appears as a tabby.
  • Silver or melanin inhibitor gene.
  • Genes causing sparkling appearance (not yet identified?).
  • Genes to clear up residual striping (hypothetical Chaos, Confusion, Unconfused, Erase, and Roan).
  • Various polygenes (sets of related genes), epigenetic factors, or modifier genes, as yet unidentified, believed to result in different degrees of shading, some more desirable than others.

Genes involved in fur length and texture

Cat fur length is governed by the Long hair gene in which the dominant form, L codes for short hair, and the recessive l codes for long hair.

There are many genes resulting in unusual fur. These genes were discovered in random-bred cats and selected for. Some of the genes are in danger of going extinct because the breeders have not marketed their cats effectively, the cats are not sold beyond the region where the mutation originated, or there is simply not enough demand for the mutation.

There are various genes producing curly coated or "rex" cats. New types of rex pop up spontaneously in random-bred cats now and then. Here are some of the rex genes that breeders select for:

  • rr = Cornish rex
  • rere = Devon rex
  • roro = Oregon rex (extinct?)
  • Se = Selkirk rex

There are also genes for hairlessness, which produce the French hairless cat (genotype hh), the British hairless cat (genotype hdhd), and the Canadian Sphynx cat (genotype hrhr). Some rex cats are prone to temporary hairlessness, known as baldness, during moulting.

Here are a few other genes resulting in unusual fur:

  • The Lp gene (dominant) results in LaPerm cats with silky single coats.
  • The Wh gene (dominant, possibly incomplete) results in Wirehair cats. They have bent or crooked hair producing springy, crinkled, coarse fur.
  • The Yuc gene, or York Chocolate undercoat gene, results in cats with no undercoat.

See also

External links