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Feline Genetics
R. Roger Breton
Nancy J Creek

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Continued from page 2

The Mapped-out Genes

As stated earlier, a few of the common cat genes have been identified and mapped. These genes are grouped according to the effects they have: the body-conformation genes which affect the shape of the body of body parts; the coat-conformation genes which affect the texture and length of the coat; and the color-conformation genes which affect the color and pattern of the coat.

The color-conformations genes are themselves divided into three groups: the color genes which control the color of the coat and its density; the color-pattern genes which control the pattern of the coat and expression of the color; and the color-masking genes which control the degree and type of masking of the basic color.

The Body-Conformation Genes

The body-conformation genes affect the basic conformation of the parts of the body: ears, tail and feet. There are literally thousands of body conformation genes, but only a few have been mapped: normal or Scottish fold ears, normal or Japanese bobtail, normal or Manx taillessness and spinal curve, and normal or polydactyl feet.

The Scottish-fold gene: normal or folded ears. The wild allele, "fd", is recessive and produces normal ears. The mutation, "Fd", is dominant and produces the cap-like folded ears of the Scottish Fold. This mutant gene is crippling when homozygous.

The Japanese Bobtail gene: normal or short tail. The wild allele, "Jb", is dominant and produces normal-length tails. The mutation, "jb", is recessive and produces the short tail of the Japanese Bobtail. Unlike the Manx mutation, this mutation is not crippling and does not cause deformation of the spine.

The Manx gene: normal or missing tail. The wild allele, "m", is recessive and produces normal-length tails and proper spinal conformation. The mutation, "M", is dominant and produces the missing tail and shortened spine of the Manx. This mutation is lethal when homozygous. When heterozygous, it is often crippling, sometimes resulting in spinal bifida, imperforate anus, chronic constipation, or incontinence.

The polydactyl gene: normal-number or extra toes. The wild allele, "pd", is recessive and produces the normal number of toes. The mutation, "Pd", is dominant and produces extra toes, particularly upon the front paws.

Interestingly, humans also have a similar dominant polydactyl gene controlling the number of fingers. Homozygous people with six fingers on each hand will pass that trait on to all their children, heterozygous people to one in four of their children, even with a normal mate: the gene is dominant. Just because a given mutation is dominant, however, doesn't mean it will dominate the species. If a given mutation is not conducive to survival of the individual or inhibits mating in any way, it will never become "popular," no matter how dominant it may be.

The Coat-Conformation Genes

The coat conformation genes affect such things as the length and texture of the coat.

The Sphinx gene: hairy or hairless coat. The wild allele, "Hr", is dominant and produces a normal hairy coat. The mutation, "hr", is recessive and produces the hairless or nearly hairless coat of the Sphinx.

The longhaired gene: short or long coat. The wild allele, "L", is dominant and produces a normal shorthaired coat. The mutation, "l", is recessive and produces the longhaired coat of the Persians, Angoras, Main Coons, and others.

The Cornish Rex gene: straight or curly coat. The wild allele, "R", is dominant and produces a normal straighthaired coat. The mutation, "r", is recessive and produces the very short curly coat, without guard hairs, of the Cornish Rex.

The Devon Rex gene: straight or curly coat. The wild allele, "Re", is dominant and produces a normal straighthaired coat. The mutation, "re", is recessive and produces the very short curly coat of the Devon Rex. Unlike the Cornish Rex, the Devon Rex retains guard hairs in its coat.

The Oregon Rex gene: straight or curly coat. The wild allele, "Ro", is dominant and produces a normal straighthaired coat. The mutation, "ro", is recessive and produces the very short curly coat of the Oregon Rex. Like the Cornish Rex, the Oregon Rex lacks guard hairs.

The American Wirehair gene: soft or bristly coat. The wild allele, "wh", is recessive and produces a normal soft straighthaired coat. The mutation, "Wh", is dominant and produces the short, stiff, wiry coat of the American Wirehair.

Note that there are three different Rex mutations producing almost identical effect. There are still three different genes involved, however.

The Color-Conformation Genes

The color-conformation genes determine the color, pattern, and expression of the coat. Since these characteristics are among the most important of the cat's features, at least from a breeding point of view, more emphasis is given the color conformation genes than the others.

These genes fall into three logical groups: those that control the color, those that control the pattern, and those that control the color expression. Each of these groups contains several differing but interrelated genes.

The Color Gene

The first of the genes controlling coat color is the color gene. This gene controls the actual color of the coat and comes in three alleles: black, dark brown, or light brown. This three-level dominance is not at all uncommon: the albinism gene, for example, has five levels.

The black allele, "B", is wild, is dominant, and produces a black or black-and-brown tabby coat, depending upon the presence of the agouti gene. Technically, the black is an almost-black, super-dark brown that is virtually black -- true black is theoretically impossible, but often reached in the practical sense (so much for theory).

The dark-brown allele, "b", is mutant, is recessive to black but dominant to light brown, and reduces black to dark brown.

The light-brown allele, "bl", is mutant, is recessive to both black and dark brown, and reduces black to a medium brown.

The Orange-Making Gene

The second of the genes controlling coat color is the orange-making gene. This gene controls the conversion of the coat color into orange and the masking of the agouti gene and comes in two alleles: non- orange and orange.

The non-orange allele, "o", is wild and allows full expression of the black or brown colors. The orange allele, "O", is mutant and converts black or brown to orange and masks the effects of the non-agouti mutation of the agouti gene (all orange cats are tabbies).

This gene is sex-linked -- it is carried on the "X" chromosome beyond the limit of the "Y" chromosome. Therefore, in males there is no homologous pairing, and the single orange-making gene stands alone. As a result there is no dominance effect in males: they are either orange or non-orange. If a male possesses the non-orange allele, "o", all colors (black, dark brown, or light brown) will be expressed. If he possesses the orange allele, "O", all colors will be converted to orange.

In females there is an homologous pairing, one gene being carried on each of the two "X" chromosomes. These two genes act together in a very special manner (as a sort of tri-state gene), and again there is no dominance effect.

If the female is homozygous for non-orange, "oo", all colors will be expressed. If she is homozygous for orange, "OO", all colors will be converted to orange. It is when she is heterozygous for orange, "Oo", that interesting things begin to happen: through a very elegant process, the black-and-orange tortoiseshell or brindled female is possible.

Shortly after conception, when a female zygote is only some dozens of cells in size, a chemical trigger is activated to start the process of generating a female kitten. This same trigger also causes the zygote to "rationalize" all the sex-linked characteristics, including the orange-making genes. In this particular case, suppression of one of the orange-making genes in each cell takes place in a not-quite-random pattern (there is some polygene influence here). Each cell will then carry only one orange-making gene.

Since the zygote was only some dozens of cells in size at the time of rationalization, only a few of those cells will eventually determine the color of the coat (the orange-making genes in the other cells will be ignored). If the zygote were homozygous for non-orange, "oo", then all cells will contain "o", and the coat will be non-orange. Likewise, if the zygote were homozygous for orange, "OO", then all cells will contain "O", and the coat will be orange. If, however, the zygote were heterozygous, "Oo", then some of the cells will contain "O" and the rest of the cells will contain "o". In this case, those portions of the coat determined by "O" cells will be orange, while those portions determined by "o" cells will be non-orange. Voila! A tortoiseshell cat!

A female kitten has two "X" chromosomes, and therefore two orange- making genes, one from each parent. Assuming for the sake of discussion an equal likelihood of inheriting either allele from each parent -- an assumption that is patently false, but used here for demonstration only -- then one quarter of all females would be non-orange, one- quarter would be orange, and one-half would be tortoiseshell. A male kitten, on the other hand, has only one "X" chromosome, and therefore only one orange-making gene. Keeping the same false assumption of equal likelihood, then one-half of all males would be non-orange and one-half would be orange. This means that there would be twice as many orange males as females if our assumption were correct.

Our equal-likelihood assumption is not correct, however. The orange- making gene is located adjacent to the centromere and is often damaged during meiosis. This damage tends to make an orange allele into a non-orange allele, giving the non-orange allele a definite leg up, so to speak, in a 7:3 ratio. This means that among female kittens 49% will be non-orange, 42% will be tortoiseshell, and only 9% will be orange, while among male kittens 70% will be non-orange and 30% will be orange: there will be more than 3 times as many orange males as females. That's why there are so many Morris-type males around.

Since a male has only one orange-making gene, there cannot be a male tortie. An exception to this rule is the hermaphrodite, which has an "XXY" genetic structure. Such a cat can be tortie, since it has two "X" chromosomes, but must invariably be sterile. In fact, despite the presence of male genitalia, a hermaphrodite is genetically an underdeveloped female, and may have both ovaries and testes, with neither fully functional.

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