FELINE GENETICS<\/p>\n
R. Roger Breton
\n Nancy J Creek<\/p>\n
——————————<\/p>\n
Cells, Chromosomes, and Genes<\/p>\n
From a 35-pound Main Coon to a 5-pound Devon Rex; from the small
\n folded caps of a Scottish Fold to the great, delicate ears of a Bali-
\n nese; from the 4-inch coat of a Chinchilla Persian to the fuzzy down
\n of a Sphinx; from the deep Ebony of a Bombay to the translucent white
\n of a Turkish Angora; from the solid color of a Havana Brown to the
\n rich tabbiness of a Norwegian Forest Cat: the variety and beauty to
\n be found in the domestic cat is beyond measure. When these character-
\n istics are coupled with the genetically-patterned and environmentally-
\n tailored personalities of the individuals, it can be seen that each
\n animal is as unique as it is possible to be. There truly is a cat for
\n everyone.<\/p>\n
Wide as the range of cats is, it pales when compared with the varie-
\n ties of Other Pet. Why should the dog exhibit such a wide spectrum of
\n body types, looking like completely different creatures in some cases,
\n while cats always look like cats (as horses always look like horses)?
\n The secrets behind the wide variations in possible cats, and why cats,
\n unlike dogs, resist gross changes and always look like cats, can be
\n found in its genetic makeup.<\/p>\n
In order to understand what happens genetically when two cats do their
\n thing, it is necessary to understand a few basic things about genetics
\n in general. To study genetics, is to study evolution in miniature,
\n for it is through the mechanism of genetics that evolution makes
\n itself felt. In chapter 1, we showed how the gross evolution of the
\n cat came about, and how this gross mechanism was applied to the Euro-
\n pean Wildcat to evolve the African Wildcat, the immediate forerunner
\n of our cats. We will examine this mechanism itself to better under-
\n stand how the first domestic cat has become the dozens of breeds
\n available today, and how cat breeders use this mechanism to create new
\n breeds or improve existing ones.<\/p>\n
Cats, like people, are multi-cellular creatures: that is, their
\n bodies are composed of cells, lots and lots of cells. Unlike primi-
\n tive multicellular creatures, cat bodies are not mere colonies of
\n cells, but rather societies of cells, with each type of cell doing a
\n specific task. To one specific type of cells, the germ cells (ova in
\n females and sperm in males), fall the task of passing the genetic code
\n to the next generation. The method the Great Engineer has developed
\n to carry this out is one of the most awesome, most elegant, and most
\n beautiful processes in nature.<\/p>\n
The cells of a cat, with few special exceptions, are eukaryotic, that
\n is, they have a membrane surrounding them (acting as a sort of skin),
\n are composed of cytoplasm (cell stuff) containing specialized orga-<\/p>\n
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\n Feline Genetics Page 1<\/p>\n
nelles (the parts that do the cell’s task), and have an inner membrane
\n surrounding a nucleus. It is this nucleus that contains all the
\n genetic materials.<\/p>\n
Within the nucleus of a cell are found the chromosomes, long irregular
\n threads of genetic material. These chromosomes are arranged in pairs:
\n 19 pairs in a cat, 23 pairs in a human. It is these 38 chromosomes
\n that contain the “blueprint” for the individual cat.<\/p>\n
When inspected under a microscope, the chromosomes reveal irregular
\n light and dark bands: hundreds of thousands, perhaps millions per
\n chromosome. These light and dark bands are the genes, the actual
\n genetic codes. Each gene controls a single feature or group of fea-
\n tures in the makeup of the individual. Many genes interact: a single
\n feature may be controlled by one, two, or a dozen genes. This makes
\n the mapping of the genes difficult, and only a few major genes have
\n been mapped out for the cat.<\/p>\n
The chromosome is itself composed primarily of the macromolecule DNA,
\n (deoxyribonucleic acid): one single molecule running the entire
\n length of the chromosome. DNA is a double helix, like two springs
\n wound within each other. Each helix is composed of a long chain of
\n alternating phosphate and deoxyribose units, connected helix to helix
\n by ladder-like rungs of four differing purine and pyridamine com-
\n pounds.<\/p>\n
It is not the number of differing compounds that provide the secret of
\n DNA’s success, but rather the number of rungs in the ladder (uncounted
\n millions) and the order of the amino acids that make up the rungs.
\n The four different amino acids are arranged in groups of three, form-
\n ing a 64-letter alphabet. This alphabet is used to compose words of
\n varying length, each of which is a gene (one particular letter is
\n always used to indicate the start of a gene). Each gene controls the
\n development of a specific characteristic of the lifeform. There is an
\n all-but-infinite number of possible genes. As a result, the DNA of a
\n lifeform contains its blueprint, no two alike, and the variety and
\n numbers of possible lifeforms has even today barely begun.<\/p>\n
Mitosis and Mendel<\/p>\n
When a cell has absorbed enough of the various amino acids and other
\n compounds necessary, it makes another cell by dividing. This process
\n is called mitosis, and is fundamental to life.<\/p>\n
Not too long ago, it was thought that the chromosomes were generated
\n immediately prior to mitosis, and dissolved away afterwards. This
\n turned out not to be true. The extremely tiny chromosomes, normally
\n invisible in an optical microscope, shorten and thicken during mito-
\n sis, becoming visible temporarily.<\/p>\n
The rather complex process of mitosis can perhaps be explained simply
\n as a step-by-step process:<\/p>\n
Mitosis begins when the cell senses sufficient growth and nutrients to<\/p>\n
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\n Feline Genetics Page 2<\/p>\n
support two cells.<\/p>\n
The invisible chromosomes duplicate themselves through the wonder of
\n DNA replication. Various enzymes are used as keys to unlock and
\n unwind the double helix into two single helices. Each of these he-
\n lices then uses other enzymes to lock the proper parts (the amino
\n acids and other stuff) together to build a new second helix, complete
\n with all transverse rungs, so that the results will be exact replicas
\n of the original double helix. This winding and unwinding of the DNA
\n can take place at speeds up to 1800 rpm! The two daughter chromosomes
\n remain joined at a single point, called the centromere.<\/p>\n
The cromosomes then wind themselves up, shortening and thickening,
\n making them visible under the microscope, and attach themselves to the
\n nuclear membrane.<\/p>\n
The nuclear membrane then dissolves into a fibrous spindle, with at
\n least one fiber passing through each centromere (there are many more
\n fibers than centromeres).<\/p>\n
The fibers then stretch and pull the centromeres apart, pulling the
\n chromosomes to opposite sides of the cell.<\/p>\n
The spindles dissolve into two new nuclear membranes, one around each
\n group of chromosomes.<\/p>\n
The chromosomes unwind back into invisibility, the cell divides, and
\n mitosis is complete. Genetically, each daughter cell is an exact
\n duplicate of the parent cell.<\/p>\n
Since the genetic coding is carried in the rungs of the DNA and only
\n consists of four different materials arranged in groups of three to
\n form words of varying length written with a 64-letter alphabet, the
\n instructions for a “cat” may be considered to consist of two sets of
\n 19 “books,” each millions of words long, one set from each of the
\n cat’s parents. The numbers of possible instructions are more than
\n astronomical: there are far more possible instructions in one single
\n chromosome than there are atoms in the known universe!<\/p>\n
A single gene is a group of instructions of some indeterminate length.
\n Somewhere among all the other codes is a set of instructions composing
\n the “white” gene, and what that set says will determine if the cat is
\n white or non-white.<\/p>\n
Since a cat receives two sets of instructions, one from each parent,
\n what happens when one parent says “make the fur white” and the other
\n says “make the fur non-white”? Will they effect a compromise and make
\n the fur pastel? No, they will not. Each and every single gene has at
\n least two levels of expression (many have more), called alleles, which
\n will determine the overall effect. In the case given, the “make the
\n fur white” allele, “W”, is dominant, while the “make the fur non-
\n white” allele, “w”, is recessive. As a result, the fur may be white
\n or non-white, not pastel (we’re only speaking of the “white” gene
\n here, a gray cat is caused by an entirely different gene).<\/p>\n
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\n Feline Genetics Page 3<\/p>\n
In order to understand how this works, lets run through a couple of
\n simple examples using the white gene. A cat has two and only two
\n white genes. Since each white gene, for the purposes of our examples,
\n consists of one of two alleles, “W” or “w”, a cat may have one of four
\n possible karyotypes (genetic codes) for white: “WW”, “Ww”, “wW”,
\n “ww”. Since “W” is dominant to “w”, the codes “WW”, “Ww”, and “wW”
\n produce white cats, while the code “ww” produces a non-white cat.<\/p>\n
| W w
\n –+——–
\n W | WW Ww
\n w | wW ww<\/p>\n
The double-dominant “WW” white cat has only white alleles in its white
\n genes. It is classed as homozygous (same-celled) for white, and will
\n produce only white offspring, regardless of the karyotype of its mate.<\/p>\n
The single-dominant “Ww” or “wW” white cat has one of each allele in
\n its white genes. It is classed as heterozygous (different-celled) for
\n white, and may or may not produce white offspring, depending upon the
\n karyotype of its mate.<\/p>\n
The recessive “ww” non-white cat has only non-white alleles in its
\n white genes. It is classed as homozygous for non-white, and may or
\n may not produce white offspring, depending upon the karyotype of its
\n mate.<\/p>\n
Assuming these cats mate, there are sixteen different possible karyo-
\n type combinations. Since each cat in these sixteen combinations will
\n pass on to their offspring one and only one allele, there are four
\n possible genetic combinations from each mating. There are sixty-four
\n possible combinations of offspring.<\/p>\n
| WW | Ww | wW | ww
\n | W W | W w | w W | w w
\n ——+——–+——–+——–+——–
\n WW W | WW WW | WW Ww | Ww WW | Ww Ww
\n W | WW WW | WW Ww | Ww WW | Ww Ww
\n ——+——–+——–+——–+——–
\n Ww W | WW WW | WW Ww | Ww WW | Ww Ww
\n w | wW wW | wW ww | ww wW | ww ww
\n ——+——–+——–+——–+——–
\n wW w | wW wW | wW ww | ww wW | ww ww
\n W | WW WW | WW Ww | Ww WW | Ww Ww
\n ——+——–+——–+——–+——–
\n ww w | wW wW | wW ww | ww wW | ww ww
\n w | wW wW | wW ww | ww wW | ww ww<\/p>\n
Inspecting these possible offspring, several patterns emerge. Of the
\n 64 possible offspring, 16, or exactly one-quarter, have any given
\n pattern. This means that one quarter of all possible matings will be
\n homozygous for white, “WW”, two quarters will be heterozygous for
\n white, “Ww” or “wW” (which are really the same thing), and one quarter<\/p>\n
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\n Feline Genetics Page 4<\/p>\n
will be homozygous for non-white, “ww”. Since homozygous white and
\n heterozygous white will both produce white cats, three-quarters of all
\n possible combinations will produce white cats, and only one-quarter
\n will produce non-white cats. This 3:1 ratio is known as the Mendelian
\n ratio, after Gregor Johann Mendel, the father of the science of genet-
\n ics.<\/p>\n
Further inspection leads us to several conclusions. If a homozygous
\n white cat mates, all offspring will be white. If two homozygous white
\n cats mate, all offspring will be homozygous white. If a homozygous
\n white cat mates with a heterozygous white cat, there will be both
\n homozygous white and heterozygous white offspring in a 1:1 ratio. If
\n a homozygous white cat mates with a homozygous non-white cat, all
\n offspring will be heterozygous white. Thus, a homozygous white cat
\n can only produce white offspring, regardless of the karyotype of its
\n mate, and is said to be true breeding for white.<\/p>\n
If two heterozygous white cats mate, there will be homozygous white,
\n heterozygous white, and homozygous non-white offspring in a ratio of
\n 1:2:1. The ratio of white to non-white offspring is the Mendelian
\n ration of 3:1. If a heterozygous white cat mates with a homozygous
\n non-white cat, there will be both heterozygous white and homozygous
\n non-white offspring in a 1:1 ratio.<\/p>\n
If two homozygous non-white cats mate, all offspring will be homozy-
\n gous non-white. Homozygous non-white cats are therefore true-breeding
\n for non-white when co-bred.<\/p>\n
Geneticists differentiate between what a cat is genetically versus
\n what it looks like by defining its genotype versus its phenotype. A
\n homozygous white cat has a white genotype and a white phenotype.
\n Likewise, a homozygous non-white cat has a non-white genotype and a
\n non-white phenotype. A heterozygous white cat, on the other hand, has
\n both a white genotype and a non-white genotype, but only a white
\n phenotype.<\/p>\n
Naturally, in a given litter of four kittens the chances of having a
\n true Mendelian ratio are slim (slightly better than 1:11), so several
\n generations of pure white kittens could be bred, still carrying a
\n recessive non-white allele. In all good faith you then breed your
\n several-generations-all-white-but-heterozygous female to a similar
\n several-generation-all-white-but heterozygous male and voila! A black
\n kitten! The non-white genotype has finally shown itself.<\/p>\n
This Mendelian patterning is the basic rule of genetics. Since the
\n rule is so simple, why is it so hard to predict things genetically?
\n The reason is that we are dealing with more than one gene from each
\n parent. The number of possible offspring combinations is two to the
\n power of the number of genes: one gene from each parent is two genes,
\n two squared is four possibilities; two from each parent is four, two
\n to the fourth is sixteen; three from each is six, two to the sixth is
\n 64;… There are literally hundreds of millions of genes for one cat,
\n yet a mere hundred from each parent produces a 61-digit number for the<\/p>\n
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\n Feline Genetics Page 5<\/p>\n
possible offspring combinations!<\/p>\n
Meiosis<\/p>\n
Since each cell contains the entire chromosome set, 19 pairs, how is
\n it possible for a parent to pass on only the genes from one chromosome
\n of a pair, and not both. This is accomplished via the gametes: the
\n germ cells, ova for females and sperm for males. Within the gonads
\n (ovaries or testes), these special cells go through a division process
\n known as meiosis.<\/p>\n
Unlike the normal process of mitosis, where the chromosomes are faith-
\n fully replicated into duplicates of themselves, in meiosis the result-
\n ant gametes have only half the number of chromosomes, one from each
\n original pair. This involves a double division.<\/p>\n
As in mitosis, meiosis begins when the cell senses sufficient growth
\n and nutrients to support division. The invisible chromosomes are
\n duplicated through DNA replication. As usual, the two daughter chro-
\n mosomes remain joined at the centromere. The chromosomes wind them-
\n selves up, shortening and thickening, becoming visible under the
\n microscope. Each new chromosome twin aligns itself with its homolo-
\n gous counterpart: the twin chromosome from its opposite number in the
\n original chromosome pair. The two twin chromosomes intertwine into a
\n tetrad and exchange genes in a not clearly understood process that
\n randomizes the genes between the twins. The tetrad attaches itself to
\n the nuclear membrane. The nuclear membrane dissolves into a spindle,
\n with at least one fiber passing through both centromeres of each
\n tetrad. The fibers stretch and pull the tetrads apart, pulling the
\n chromosomes twins to opposite sides of the cell. Once the chromosome
\n twins are at the poles of the spindle, the spindle dissolves and
\n reforms as two separate parallel spindles at right angles to the
\n original spindle, with at least one fiber through each centromere. At
\n this time there are effectively two mitoses taking place. The paral-
\n lel spindles pull the centromeres apart, forming four separate groups
\n of chromosomes, each of which consists of one-half the normal number.
\n The spindles dissolve and four new nuclear membranes form, one around
\n each group of chromosomes. The chromosomes unwind back into invisi-
\n bility, the cell divides into four gametes, each having 19 chromo-
\n somes, and meiosis is complete.<\/p>\n
At the moment of conception, a single sperm penetrates a single ovum,
\n the ovum absorbs the sperm, merging the sperm’s nucleus with its own
\n and pairing the two sets of chromosomes. The ovum has now become a
\n zygote, which begins dividing through the normal mitosis process, and
\n a kitten is on its way.<\/p>\n
Male, Female, and Maybe<\/p>\n
The 19 pairs of chromosomes in a cat carry the numbers 1 through 18,
\n plus “X” and “Y”. The “X” and “Y” chromosomes are very special, for
\n they determine the sex of the kitten. A female cat has two “X” chro-
\n mosomes, “XX”, while a male cat has one “X” and one “Y” chromosome,
\n “XY”, so if we follow the Mendelian pattern for sex determination we<\/p>\n
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\n Feline Genetics Page 6<\/p>\n
find that the female parent can provide only an “X” chromosome to her
\n offspring, while the male parent can provide either an “X” chromosome
\n or a “Y” chromosome. The resulting kittens are either “XX” or “XY”,
\n as determined by the father. The same rule also applies to people
\n (Sorry guys, if you and the wife have seven girls, it’s your fault,
\n not hers!).<\/p>\n
Since the sex chromosomes follow the same rules as the other chromo-
\n somes, why bother mentioning them separately? Because they don’t
\n exactly follow the same rules: the “X” chromosome is longer than the
\n “Y” chromosome, and it is this extra length that carries the codes for
\n the female. When there is only one set of these extra codes, they act
\n as recessives, allowing the male characteristic to dominate. When
\n there are two sets, they act as dominants, and suppress the male
\n characteristics. Thus, female and male kittens.<\/p>\n
We could end the argument here if it weren’t for two complications.
\n First, the extra-length of the “X” chromosome carries some genes that
\n are for other than sex characteristics (such as the gene for orange
\n fur): such characteristics are said to be sex-linked, and operate
\n differently in males and females.<\/p>\n
A further complication comes with incomplete separation of the “X”
\n gene twin at the centromere. An “X-X” gene twin has its centromere
\n exactly where “Y”‘s would become “X”‘s. If an “X” were to fracture at
\n the centromere during the process of separation, it would become an
\n effective “Y”. This is rare but by no means unheard of, and produces
\n a “false” “Y” (shown as “y” to differentiate it from a female “XX”
\n parent.<\/p>\n
Another variation is incomplete separation, where only a “false cen-
\n tromere” is separated from the gene twin, with or without a part of
\n the twin, causing one gamete to have 18 chromosomes (neither an “X” or
\n a “y” while the other has 20 (either two “X”‘s, an “Xy”, or two “y”‘s,
\n depending on the point and angle of fracture).<\/p>\n
These variations on the sex chromosomes mean that a female, being “XX”
\n in nature, can produce ova with the following: “XX”, “Xy”, “yy”, “X”,
\n “y”, or “O” (no sex chromosome). A male, being “XY”, can produce
\n sperm with “XY”, “Yy”, “X”, “Y”, “y”, or “O”. A zygote, taking one
\n gamete from each parent, may then be any of the following 36 possibil-
\n ities:<\/p>\n
| XX Xy yy X y O
\n —+——————————–
\n XY | XXXY XXYy XYyy XXY XYy XYO
\n Yy | XXYy XYyy Yyyy XYy Yyy YyO
\n X | XXX XXy Xyy XX Xy XO
\n Y | XXY XYy Yyy XY Yy YO
\n y | XXy Xyy yyy Xy yy yO
\n O | XXO XYO yyO XO yO OO<\/p>\n
Since at least one “X” is required (can’t build a puzzle without all
\n the pieces), we may immediately ignore “Yyyy”, “Yyy”, “yyy”, “YyO”,<\/p>\n
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\n Feline Genetics Page 7<\/p>\n
“yyO”, “Yy”, “yy”, “YO”, “yO”, and “OO”.<\/p>\n
In a like manner, “XXXY”, “XXYy”, and “XYyy” have too many pieces and
\n are unstable, usually dying at conception, in the womb, or soon after
\n birth (and invariably before puberty) from gross birth defects due to
\n over-emphasis of various sex-linked traits.<\/p>\n
Turner females, “XO”, show all normal female characteristics save that
\n they have difficulty reproducing due to the absence of a paired sex
\n chromosome, which inhibits normal meiosis.<\/p>\n
Kleinfelter superfemales, “XXX”, tend to exhibit an unusually strong
\n maternal instinct, often refusing to wean or surrender their young.
\n This leads to psychological damage in the young, usually resulting in
\n antisocial behavior.<\/p>\n
Kleinfelter supermales, “XYy” or “Xyy”, tend to exhibit a generally
\n antisocial behavior, often leading to unnecessary fighting to the
\n point of inhibiting mating. As an interesting aside, among us humans
\n approximately 5 per cent of convicted male felons are supermales.
\n Hermaphrodites, “XXy” and “XXY”, have male bodies but tend to exhibit
\n various female characteristics, often adopting orphan kittens or other
\n young. One such cat adopted a litter of mice, which it lovingly
\n raised while gleefully hunting their relatives. Hermaphrodites are
\n invariably sterile, sometime having both sets of sexual organs with
\n neither fully developed. This is the most common of the aberrant
\n sexual makeups.<\/p>\n
Pseudoparthenogenetic females, “XXO”, or males, “XYO”, are identical
\n to normal cats in every way save that their sex and sex-linked charac-
\n teristics come only from one parent.<\/p>\n
Gene-reversal males, “Xy”, suffer partial gene reversal, receiving a
\n normal “X” from one parent and a “y” from the other parent’s “X”.
\n This is the rarest of the aberrant sexual makeups.<\/p>\n
Pseudoparthenogenetic and gene-reversal animals often suffer from
\n birth defects and other signs of the aberrant genetic construct.<\/p>\n
Normal females, “XX”, and males, “XY”, are by definition the norm and
\n vastly outnumber all other type combined. Chances are less than
\n 1:10000 that any given cat has a genetically aberrant sexual makeup,
\n the most common of which is hermaphroditism, about 1:11000.<\/p>\n
Mutations<\/p>\n
Going back to genes in general, those genes that are found in the
\n African Wildcat, felis lybica, the immediate ancestor of our cats, are
\n termed “wild.” These genes may be considered to be the basic stock of
\n all cats.<\/p>\n
Since all cats do not look like African Wildcats (brown tabbies), it
\n is obvious that some changes have taken place in the genetic codes.
\n These changes occur all the time, and are called mutations. Unlike<\/p>\n
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\n Feline Genetics Page 8<\/p>\n
the distortions shown in cheap post-apocalypse or ecological-disaster
\n movies, mutations rarely occur at the gross level, but rather at the
\n level of the genetic codes themselves.<\/p>\n
Mutations occur when, in the course of mitosis or meiosis, there is an
\n imperfect replication or joining of the components of the DNA macro-
\n molecule. Such imperfections can occur as a result of a chemical
\n imbalance within the body which affects replication. Most commonly
\n these days such an imbalance is caused by the introduction of some
\n foreign agent into the body (such as nicotine or, for an extreme
\n example, thalidomide) which acts as a catalyst and affects the keying
\n action of the enzymes during replication. Such agents are called
\n mutagens.<\/p>\n
The greatest of all mutagens is radiation. It is believed that the
\n vast majority of spontaneous mutations, such as extra toes, long hair,
\n albinism, etc., that keep reoccurring in an otherwise clean gene pool
\n are caused by solar radiation, cosmic rays, the Earth’s own background
\n radiation, and most probably, by radioactive isotopes of the atoms
\n making up DNA itself, most significantly carbon-14. (One of the
\n dangers of nuclear war, other than the obvious, is that the increase
\n in background radiation and atmospheric carbon-14 may increase the
\n numbers of spontaneous mutations to the point where the germ cells
\n lose viability, and whole species, even genera, would go the way of
\n the dinosaur.)<\/p>\n
Mutations are the very essence of evolution (or of a breeding program,
\n which is merely evolution guided by man). It is through mutation that
\n the survival of the fittest takes place.<\/p>\n
To illustrate this, let’s assume a species of striped cat living on
\n the plains. He undergoes a mutation creating a spotted coat (the
\n stripes get broken up). For our plains friend, the spots don’t blend
\n as well as stripes with the long shadows and colors of the grasses,
\n his prey can see and avoid him better, and he soon evolves out. This
\n was a detrimental mutation (most are).<\/p>\n
Now let’s assume the same species of striped cat living in woodlands.
\n He undergoes the same mutation creating a spotted coat. In his case,
\n the spots blend better with the dapple of light and shadow playing
\n through the trees, his prey can’t see or avoid him as well, and spots
\n are soon the “in” thing. This was a beneficial mutation. From the
\n same parent stock we soon have two differing sub-species, one striped,
\n living on the plains, and one spotted, living in the woods.<\/p>\n
In a domestic situation, a litter is born to two normal cats, wherein
\n one of the kittens is hairless. Thinking the hairlessness is differ-
\n ent enough to be a desired feature, especially for those with aller-
\n gies, the kitten is very carefully bred to other cats, back and forth
\n over several generations, until the hairlessness breeds true. Thus
\n the Sphinx, a hairless domestic cat and the ultimate in hypo-allergen-
\n ic cats, was developed.<\/p>\n
The Mapped-out Genes<\/p>\n
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\n Feline Genetics Page 9<\/p>\n
As stated earlier, a few of the common cat genes have been identified
\n and mapped. These genes are grouped according to the effects they
\n have: the body-conformation genes which affect the shape of the body
\n of body parts; the coat-conformation genes which affect the texture
\n and length of the coat; and the color-conformation genes which affect
\n the color and pattern of the coat.<\/p>\n
The color-conformations genes are themselves divided into three
\n groups: the color genes which control the color of the coat and its
\n density; the color-pattern genes which control the pattern of the coat
\n and expression of the color; and the color-masking genes which control
\n the degree and type of masking of the basic color.<\/p>\n
The Body-Conformation Genes<\/p>\n
The body-conformation genes affect the basic conformation of the parts
\n of the body: ears, tail and feet. There are literally thousands of
\n body conformation genes, but only a few have been mapped: normal or
\n Scottish fold ears, normal or Japanese bobtail, normal or Manx tail-
\n lessness and spinal curve, and normal or polydactyl feet.<\/p>\n
The Scottish-fold gene: normal or folded ears. The wild allele,
\n “fd”, is recessive and produces normal ears. The mutation, “Fd”, is
\n dominant and produces the cap-like folded ears of the Scottish Fold.
\n This mutant gene is crippling when homozygous.<\/p>\n
The Japanese Bobtail gene: normal or short tail. The wild allele,
\n “Jb”, is dominant and produces normal-length tails. The mutation,
\n “jb”, is recessive and produces the short tail of the Japanese Bob-
\n tail. Unlike the Manx mutation, this mutation is not crippling and
\n does not cause deformation of the spine.<\/p>\n
The Manx gene: normal or missing tail. The wild allele, “m”, is
\n recessive and produces normal-length tails and proper spinal conforma-
\n tion. The mutation, “M”, is dominant and produces the missing tail
\n and shortened spine of the Manx. This mutation is lethal when homozy-
\n gous. When heterozygous, it is often crippling, sometimes resulting
\n in spinal bifida, imperforate anus, chronic constipation, or inconti-
\n nence.<\/p>\n
The polydactyl gene: normal-number or extra toes. The wild allele,
\n “pd”, is recessive and produces the normal number of toes. The muta-
\n tion, “Pd”, is dominant and produces extra toes, particularly upon the
\n front paws.<\/p>\n
Interestingly, humans also have a similar dominant polydactyl gene
\n controlling the number of fingers. Homozygous people with six fingers
\n on each hand will pass that trait on to all their children, heterozy-
\n gous people to one in four of their children, even with a normal mate:
\n the gene is dominant. Just because a given mutation is dominant,
\n however, doesn’t mean it will dominate the species. If a given muta-
\n tion is not conducive to survival of the individual or inhibits mating
\n in any way, it will never become “popular,” no matter how dominant it<\/p>\n
———————————————————————-
\n Feline Genetics Page 10<\/p>\n
may be.<\/p>\n
The Coat-Conformation Genes<\/p>\n
The coat conformation genes affect such things as the length and
\n texture of the coat.<\/p>\n
The Sphinx gene: hairy or hairless coat. The wild allele, “Hr”, is
\n dominant and produces a normal hairy coat. The mutation, “hr”, is
\n recessive and produces the hairless or nearly hairless coat of the
\n Sphinx.<\/p>\n
The longhaired gene: short or long coat. The wild allele, “L”, is
\n dominant and produces a normal shorthaired coat. The mutation, “l”,
\n is recessive and produces the longhaired coat of the Persians, Ango-
\n ras, Main Coons, and others.<\/p>\n
The Cornish Rex gene: straight or curly coat. The wild allele, “R”,
\n is dominant and produces a normal straighthaired coat. The mutation,
\n “r”, is recessive and produces the very short curly coat, without
\n guard hairs, of the Cornish Rex.<\/p>\n
The Devon Rex gene: straight or curly coat. The wild allele, “Re”,
\n is dominant and produces a normal straighthaired coat. The mutation,
\n “re”, is recessive and produces the very short curly coat of the Devon
\n Rex. Unlike the Cornish Rex, the Devon Rex retains guard hairs in its
\n coat.<\/p>\n
The Oregon Rex gene: straight or curly coat. The wild allele, “Ro”,
\n is dominant and produces a normal straighthaired coat. The mutation,
\n “ro”, is recessive and produces the very short curly coat of the
\n Oregon Rex. Like the Cornish Rex, the Oregon Rex lacks guard hairs.<\/p>\n
The American Wirehair gene: soft or bristly coat. The wild allele,
\n “wh”, is recessive and produces a normal soft straighthaired coat.
\n The mutation, “Wh”, is dominant and produces the short, stiff, wiry
\n coat of the American Wirehair.<\/p>\n
Note that there are three different Rex mutations producing almost
\n identical effect. There are still three different genes involved,
\n however.<\/p>\n
The Color-Conformation Genes<\/p>\n
The color-conformation genes determine the color, pattern, and expres-
\n sion of the coat. Since these characteristics are among the most
\n important of the cat’s features, at least from a breeding point of
\n view, more emphasis is given the color conformation genes than the
\n others.<\/p>\n
These genes fall into three logical groups: those that control the
\n color, those that control the pattern, and those that control the
\n color expression. Each of these groups contains several differing but
\n interrelated genes.<\/p>\n
———————————————————————-
\n Feline Genetics Page 11<\/p>\n
The Color Gene<\/p>\n
The first of the genes controlling coat color is the color gene. This
\n gene controls the actual color of the coat and comes in three alleles:
\n black, dark brown, or light brown. This three-level dominance is not
\n at all uncommon: the albinism gene, for example, has five levels.<\/p>\n
The black allele, “B”, is wild, is dominant, and produces a black or
\n black-and-brown tabby coat, depending upon the presence of the agouti
\n gene. Technically, the black is an almost-black, super-dark brown
\n that is virtually black — true black is theoretically impossible, but
\n often reached in the practical sense (so much for theory).<\/p>\n
The dark-brown allele, “b”, is mutant, is recessive to black but
\n dominant to light brown, and reduces black to dark brown.<\/p>\n
The light-brown allele, “bl”, is mutant, is recessive to both black
\n and dark brown, and reduces black to a medium brown.<\/p>\n
The Orange-Making Gene<\/p>\n
The second of the genes controlling coat color is the orange-making
\n gene. This gene controls the conversion of the coat color into orange
\n and the masking of the agouti gene and comes in two alleles: non-
\n orange and orange.<\/p>\n
The non-orange allele, “o”, is wild and allows full expression of the
\n black or brown colors. The orange allele, “O”, is mutant and converts
\n black or brown to orange and masks the effects of the non-agouti
\n mutation of the agouti gene (all orange cats are tabbies).<\/p>\n
This gene is sex-linked — it is carried on the “X” chromosome beyond
\n the limit of the “Y” chromosome. Therefore, in males there is no
\n homologous pairing, and the single orange-making gene stands alone.
\n As a result there is no dominance effect in males: they are either
\n orange or non-orange. If a male possesses the non-orange allele, “o”,
\n all colors (black, dark brown, or light brown) will be expressed. If
\n he possesses the orange allele, “O”, all colors will be converted to
\n orange.<\/p>\n
In females there is an homologous pairing, one gene being carried on
\n each of the two “X” chromosomes. These two genes act together in a
\n very special manner (as a sort of tri-state gene), and again there is
\n no dominance effect.<\/p>\n
If the female is homozygous for non-orange, “oo”, all colors will be
\n expressed. If she is homozygous for orange, “OO”, all colors will be
\n converted to orange. It is when she is heterozygous for orange, “Oo”,
\n that interesting things begin to happen: through a very elegant
\n process, the black-and-orange tortoiseshell or brindled female is
\n possible.<\/p>\n
Shortly after conception, when a female zygote is only some dozens of<\/p>\n
———————————————————————-
\n Feline Genetics Page 12<\/p>\n
cells in size, a chemical trigger is activated to start the process of
\n generating a female kitten. This same trigger also causes the zygote
\n to “rationalize” all the sex-linked characteristics, including the
\n orange-making genes. In this particular case, suppression of one of
\n the orange-making genes in each cell takes place in a not-quite-random
\n pattern (there is some polygene influence here). Each cell will then
\n carry only one orange-making gene.<\/p>\n
Since the zygote was only some dozens of cells in size at the time of
\n rationalization, only a few of those cells will eventually determine
\n the color of the coat (the orange-making genes in the other cells will
\n be ignored). If the zygote were homozygous for non-orange, “oo”, then
\n all cells will contain “o”, and the coat will be non-orange. Like-
\n wise, if the zygote were homozygous for orange, “OO”, then all cells
\n will contain “O”, and the coat will be orange. If, however, the
\n zygote were heterozygous, “Oo”, then some of the cells will contain
\n “O” and the rest of the cells will contain “o”. In this case, those
\n portions of the coat determined by “O” cells will be orange, while
\n those portions determined by “o” cells will be non-orange. Voila! A
\n tortoiseshell cat!<\/p>\n
A female kitten has two “X” chromosomes, and therefore two orange-
\n making genes, one from each parent. Assuming for the sake of discus-
\n sion an equal likelihood of inheriting either allele from each parent
\n — an assumption that is patently false, but used here for demonstra-
\n tion only — then one quarter of all females would be non-orange, one-
\n quarter would be orange, and one-half would be tortoiseshell. A male
\n kitten, on the other hand, has only one “X” chromosome, and therefore
\n only one orange-making gene. Keeping the same false assumption of
\n equal likelihood, then one-half of all males would be non-orange and
\n one-half would be orange. This means that there would be twice as
\n many orange males as females if our assumption were correct.<\/p>\n
Our equal-likelihood assumption is not correct, however. The orange-
\n making gene is located adjacent to the centromere and is often damaged
\n during meiosis. This damage tends to make an orange allele into a
\n non-orange allele, giving the non-orange allele a definite leg up, so
\n to speak, in a 7:3 ratio. This means that among female kittens 49%
\n will be non-orange, 42% will be tortoiseshell, and only 9% will be
\n orange, while among male kittens 70% will be non-orange and 30% will
\n be orange: there will be more than 3 times as many orange males as
\n females. That’s why there are so many Morris-type males around.<\/p>\n
Since a male has only one orange-making gene, there cannot be a male
\n tortie. An exception to this rule is the hermaphrodite, which has an
\n “XXY” genetic structure. Such a cat can be tortie, since it has two
\n “X” chromosomes, but must invariably be sterile. In fact, despite the
\n presence of male genitalia, a hermaphrodite is genetically an underde-
\n veloped female, and may have both ovaries and testes, with neither
\n fully functional.<\/p>\n
The Color-Density Gene<\/p>\n
The third and last of the genes controlling the coat color is the<\/p>\n
———————————————————————-
\n Feline Genetics Page 13<\/p>\n
color-density gene. This gene controls the uniformity of distribution
\n of pigment throughout the hair and comes in two alleles: dense, “D”,
\n and dilute, “d”.<\/p>\n
The dense allele, “D”, is wild, is dominant, and causes pigment to be
\n distributed evenly throughout each hair, making the color deep and
\n pure. A dense coat will be black, dark brown, medium brown, or or-
\n ange.<\/p>\n
The dilute allele, “d”, is mutant, is recessive, and causes pigment to
\n be agglutinated into microscopic clumps surrounded by translucent
\n unpigmented areas, allowing white light to shine through and diluting
\n the color. A dilute coat will be blue (gray), tan, beige, or cream.<\/p>\n
The Eight Cat Colors<\/p>\n
All possible expressions of the color, orange-making, and color-
\n density genes produce the eight basic coat colors: black, blue
\n (gray), chestnut or chocolate (dark-brown), lavender or lilac (tan),
\n cinnamon (medium brown), fawn (beige), red (orange), and cream.<\/p>\n
| Sex | “BB Bb Bbl bb bbl blbl”
\n —–+——–+——————————————————-
\n ooDD | Either | Black Black Black Chestnut Chestnut Cinna
\n —–+——–+——————————————————-
\n ooDd | Either | Black Black Black Chestnut Chestnut Cinna
\n —–+——–+——————————————————-
\n oodd | Either | Blue Blue Blue Lavender Lavender Fawn
\n —–+——–+——————————————————-
\n oODD | Female | Blk\/Red Blk\/Red Blk\/Red Chs\/Red Chs\/Red Cin\/Red
\n | Male | Black Black Black Chestnut Chestnut Cinna
\n —–+——–+——————————————————-
\n oODd | Female | Blk\/Red Blk\/Red Blk\/Red Chs\/Red Chs\/Red Cin\/Red
\n | Male | Black Black Black Chestnut Chestnut Cinna
\n —–+——–+——————————————————-
\n oOdd | Female | Blu\/Crm Blu\/Crm Blu\/Crm Lav\/Crm Lav\/Crm Fwn\/Crm
\n | Male | Blue Blue Blue Lavender Lavender Fawn
\n —–+——–+——————————————————-
\n OoDD | Female | Blk\/Red Blk\/Red Blk\/Red Chs\/Red Chs\/Red Cin\/Red
\n | Male | Red Red Red Red Red Red
\n —–+——–+——————————————————-
\n OoDd | Female | Blk\/Red Blk\/Red Blk\/Red Chs\/Red Chs\/Red Cin\/Red
\n | Male | Red Red Red Red Red Red
\n —–+——–+——————————————————-
\n Oodd | Female | Blu\/Crm Blu\/Crm Blu\/Crm Lav\/Crm Lav\/Crm Fwn\/Crm
\n | Male | Cream Cream Cream Cream Cream Cream
\n —–+——–+——————————————————-
\n OODD | Either | Red Red Red Red Red Red
\n —–+——–+——————————————————-
\n OODd | Either | Red Red Red Red Red Red
\n —–+——–+——————————————————-
\n OOdd | Either | Cream Cream Cream Cream Cream Cream<\/p>\n
The brown and dilute colors are rarer (hence generally more prized)<\/p>\n
———————————————————————-
\n Feline Genetics Page 14<\/p>\n
because they are recessive. A table of all possible combinations of
\n the three genes controlling color will show all eight basic coat
\n colors, among which are six female or twelve male black cats but only
\n one female or two male fawn:<\/p>\n
Note that although tortoiseshell females are two-color they introduce
\n no new colors.<\/p>\n
It may also be noted that red and cream dominate any of the true
\n (black or brown) colors: a red coat is red regardless of whether the
\n color gene is black, dark brown, or light brown. The color gene is
\n masked by the orange-making gene. This, coupled with the fact that
\n males are either red or non-red require that the color chart show “oO”
\n and “Oo” as distinctly separate. A male has only the first of the two
\n genes: “o” from “oO” or “O” from “Oo”. In some texts, the orange-
\n making genes are indicated as “o(O)” and “O(o)” to emphasize the
\n sexual distinction.<\/p>\n
The Albinism Gene<\/p>\n
The first of the color-conformation genes affect coat pattern is the
\n albinism gene. This gene controls the amount of body color and comes
\n in five alleles: full color, “C”, Burmese, “cb”, Siamese, “cs”, blue-
\n eyed albino, “ca”, and albino, “c”.<\/p>\n
The full color allele, “C” is wild, is dominant, and produces a full
\n expression of the coat colors. This is sometimes called the non-
\n albino allele.<\/p>\n
The Burmese allele, “cb”, is mutant, is recessive to the full color
\n allele, codominant with the Siamese allele, and dominant to the blue-
\n eyed albino and albino alleles, and produces a slight albinism, reduc-
\n ing black to a very dark brown, called sable in the Burmese breed, and
\n producing green or green-gold eyes.<\/p>\n
The Siamese allele, “cs”, is mutant, is recessive to the full color
\n allele, codominant with the Siamese allele, and dominant to the blue-
\n eyed albino and albino alleles, and produces an intermediate albinism,
\n reducing the basic coat color from black\/brown to a light beige with
\n dark brown “points” in the classic Siamese pattern and producing
\n bright blue eyes.<\/p>\n
The Burmese and Siamese alleles are codominant, that is they each have
\n exactly as much dominance or recessivity. It is possible to have one
\n of each allele, “cbcs”, producing a Siamese-patterned coat with a
\n darker base body color and turquoise (aquamarine) eyes: the Tonkinese
\n pattern.<\/p>\n
The blue-eyed albino allele, “ca”, is mutant, is recessive to the full
\n color, Burmese and Siamese alleles and dominant to the albino allele,
\n and produces a nearly complete albinism with a translucent white coat
\n and very washed-out pale blue eyes.<\/p>\n
The albino allele, “c”, is mutant, is recessive to all others, and<\/p>\n
———————————————————————-
\n Feline Genetics Page 15<\/p>\n
produces a complete albinism with a translucent white coat and pink
\n eyes.<\/p>\n
The albanism genes combine in some rather interesting ways:<\/p>\n
| C cb cs ca c
\n —+———————————————————–
\n C | full color full color full color full color full color
\n cb | full color Burmese Tonkinese Burmese Burmese
\n cs | full color Tonkinese Siamese Siamese Siamese
\n ca | full color Burmese Siamese B-E Albino B-E Albino
\n c | full color Burmese Siamese B-E Albino Albino<\/p>\n
Notice how the dominance characteristics among the alleles are normal
\n except for the combination of Burmese and Siamese, which produce the
\n Tonikinese pattern.<\/p>\n
The Agouti Gene<\/p>\n
The next gene controlling the pattern of the coat is the agouti gene.
\n This gene will control ticking and comes in two alleles: agouti, “A”,
\n and non-agouti, “a”.<\/p>\n
The agouti allele, “A”, is wild, is dominant, and produces a banded
\n or ticked (agouti) hair, which in turn will produce a tabby coat
\n pattern.<\/p>\n
The non-agouti allele, “a”, is mutant, is recessive, and suppresses
\n ticking, which in turn will produce a solid-color coat. This gene
\n only operates upon the color gene (black, dark brown, or light brown)
\n in conjunction with the non-orange allele of the orange-making gene
\n and is masked by the orange allele of the orange-making gene.<\/p>\n
The Tabby Genes<\/p>\n
The last of the genes affecting the coat pattern is the tabby gene.
\n This gene will control the actual coat pattern (striped, spotted,
\n solid, etc.) and comes in three alleles: mackerel or striped tabby,
\n “T”, Abyssinian or all-agouti-tabby, “Ta”, and blotched or classic
\n tabby, “tb”.<\/p>\n
The mackerel-tabby allele, “T”, is wild, is co-dominant with the
\n spotted tabby and Abyssinian alleles and dominant to the classic-tabby
\n allele, and produces a striped cat, with vertical non-agouti stripes
\n on an agouti background. This is the most common of all patterns and
\n is typical grassland camouflage, where shadows are long and strait.<\/p>\n
A spotted tabby is genetically a striped tabby with the stripes broken
\n up by polygene influence. There is no specific “spotted-tabby” gene.
\n This spotted coat is a typical forest camouflage, where shadows are
\n dappled by sunlight shining through the trees. Do not confuse the
\n spots of our domestic cats with the rosettes of the true spotted cats:
\n entirely different genes are involved.<\/p>\n
———————————————————————-
\n Feline Genetics Page 16<\/p>\n
The Abyssinian allele, “Ta”, is mutant, is codominant to the mackerel-
\n tabby allele and dominant to the classic-tabby allele, and will pro-
\n duce an all-agouti coat without stripes or spots. This all-agouti
\n coat is a basic type of bare-ground camouflage, seen in the wild
\n rabbit and many other animals.<\/p>\n
A special case occurs when both the mackerel-tabby and Abyssinian
\n alleles are expressed, “TTa”. This will produce a unique coat con-
\n sisting of the beige ground color with each hair tipped with the
\n expressed color. By selective breeding, the ground color has become a
\n soft gold, producing the beautiful golden chinchilla cats.<\/p>\n
The blotched- or classic-tabby allele, “tb”, is recessive to both the
\n mackerel-tabby and the Abyssinian alleles and will produce irregular
\n non-agouti blotches or “cinnamon-roll” sworls on an agouti background.
\n When the “cinnamon-rolls” are clean and symmetrical, and nicely cen-
\n tered on the sides, a strikingly beautiful coat is achieved.<\/p>\n
The “coat of choice” in Europe is the classic tabby (hence the name),
\n probably because of the similarity in appearance of a large mackerel
\n tabby domestic cat and the European Wildcat, the former being soft and
\n cuddly and the latter prone to remove fingers. In the U.S., the
\n reverse is true.<\/p>\n
The Color-Inhibitor Gene<\/p>\n
The first of the color-conformation genes controlling color expression
\n is the color-inhibitor gene. This gene controls the expression of
\n color within the hair and comes in two alleles: the non-inhibitor,
\n “i”, and the inhibitor, “Y”.<\/p>\n
The non-inhibitor allele, “i”, is wild, is recessive, and allows
\n expression of the color throughout the length of the hair, producing a
\n normally colored coat.<\/p>\n
The inhibitor allele, “I”, is mutant, is dominant, and inhibits ex-
\n pression of the color over a portion of the hair.<\/p>\n
The inhibitor allele is variably-expressed. When slightly expressed,
\n the short down hairs (underfur) are merely tipped with color, while
\n the longer guard and awn hairs are clear for about the first quarter
\n of their lengths: the coat is said to be smoked. When moderately
\n expressed, the down hairs are completely clear and the longer hairs
\n are clear for about half their lengths: the coat is shaded. When
\n heavily expressed, the down hairs are completely clear and the longer
\n hairs are clear for about three-quarters (or more) of their lengths:
\n the coat is then tipped or chinchilla.<\/p>\n
Neither allele has anything to do with the actual color or pattern,
\n only with whether that color is laid upon a clear undercoat or one of
\n the beige ground color.<\/p>\n
The Spotting Gene<\/p>\n
———————————————————————-
\n Feline Genetics Page 17<\/p>\n
The next gene controlling color expression is the white-spotting gene.
\n This gene controls the presence and pattern of white masking the
\n normal coat pattern, and has four alleles: non-spotted, “s”, spotted,
\n “S”, particolor, “Sp”, and Birman, “sb”. The presence of the parti-
\n color and Birman alleles of this gene are still subject to argument at
\n this time: their effect is not.The non-spotted allele, “s”, is wild,
\n is recessive, and produces a normal coat without white.<\/p>\n
The spotted allele, “S”, is mutant, is dominant, and produces white
\n spotting which masks the true coat color in the affected area. This
\n is a variably-expressed allele with a very wide expression range:
\n From a black cat with one white hair to a white cat with one black
\n hair.<\/p>\n
The particolor allele, “Sp”, if it exists, is a variation of the
\n spotted allele affecting the pattern of white. The classic particolor
\n pattern is an inverted white “V” starting in the center of the fore-
\n head and passing through the centers of the eyes. The chin, chest,
\n belly, legs and feet are white. Variable expressions of this allele
\n range downward to a simple white locket or a white spot on the fore-
\n head.<\/p>\n
The Birman allele, “Sb”, if it exists, is a variation of the spotted
\n allele producing white feet. Variable expression ranges from white
\n legs and feet to white toes only.<\/p>\n
Unlike the white gene or the albinism gene, the white-spotting gene
\n does not affect eye color: if your all white cat has green eyes, it
\n is most definitely a colored cat with one big white spot all over.<\/p>\n
The Dominant-White Gene<\/p>\n
The final gene controlling color expression is the dominant-white
\n gene. This gene determines whether the coat is solid white or not,
\n and comes in three alleles: non-white, “w”, white, “W”, and van,
\n “Wv”. The existence of the van allele is open to argument: it may be
\n a separate gene.<\/p>\n
The non-white allele, “w”, is wild, is recessive, and allows full
\n expression of the coat color and pattern.<\/p>\n
The white allele, “W”, is mutant, is dominant, and produces a translu-
\n cent all-white coat with either orange or pale blue. Blue-eyed domi-
\n nant-white cats are often deaf, orange-eyed cats occasionally so.
\n Interestingly, a white cat may be odd-eyed, having one blue and one
\n orange eye. Such a cat is often deaf on the blue side.<\/p>\n
The van allele, “Wv”, if it exists, is a variation of the white allele
\n allowing color in the classic van pattern: on the crown of the head
\n (often a two small half-caps separated by a thin white line), on the
\n ears, and on the tail. Variable expression controls cap size and
\n shape and the presence of color on the ears and tail. Occasionally,
\n the caps will be missing and only the ears and\/or tail will be col-
\n ored.<\/p>\n
———————————————————————-
\n Feline Genetics Page 18<\/p>\n
It is important to remember that, genetically speaking, white is not a
\n color, but rather the suppression of the pigment that would normally
\n be present. A heterozygous white cat can an often does produce col-
\n ored kittens, sometimes with no white at all.<\/p>\n
Polygenes<\/p>\n
The genes described above control color and coat, and several breed-
\n specific body features, but what about the genes that control the body
\n structure itself? Can we not develop a cat with long floppy ears
\n (sort of a bassett-cat)? The answer is a qualified no. Not within
\n the realms of normal breeding, and not without a much better means of
\n genetic engineering than is currently available to us. The reason
\n cats (and horses) resist major changes, whereas dogs do not, is be-
\n cause the genes controlling these features are scattered among the
\n genetic codes of other genes (remember, a gene is not a physical
\n entity but rather a series of instructions). This type of scattered
\n gene is called a “polygene”. Polygenes are in firm control of many of
\n those things that define the cat, and breeding programs can only
\n change these characteristics slowly, bit-by-bit.<\/p>\n
The Eye Colors<\/p>\n
There are no specific genes for the eye colors. Rather, the color of
\n the eyes is intimately linked to the color and pattern of the coat via
\n several polygenes.<\/p>\n
There is much about eye color that is not yet understood. As an
\n example, the British Blue usually has orange or copper eyes while
\n those of the Russian Blue are usually green, in spite of the fact that
\n the breeds have identical coat genotypes.<\/p>\n
The range of eye color is from a deep copper-orange through yellow to
\n green. The blue and pink eyed cats are partial or full albinos, with
\n suppression of the eye color.<\/p>\n
Color Abr Description
\n ————————————————————-
\n Copper cpr Deep copper-orange
\n Orange org Bright orange
\n Amber amb Yellow-orange
\n Yellow yel Yellow
\n Gold gld Dark yellow with hint of green
\n Hazel hzl Dark greenish-yellow
\n Green grn Green
\n Turquoise trq Bluish-green (common in Tonkinese)
\n Siamese Blue sbl Royal Blue to medium-pale grayish-blue
\n Dominant-White Blue wbl Medium blue
\n Dominant-White Odd odd One blue, one orange
\n Albino Blue abl Very pale blue, almost gray
\n Albino Pink pnk Pink<\/p>\n
There is a definite interaction between the color genes, “B”, “b”, and<\/p>\n
———————————————————————-
\n Feline Genetics Page 19<\/p>\n
“bl”, the color density genes, “D” and “d”, and eye color. This
\n interaction is especially evident in those cats with Siamese coats
\n where the eye color can range from a strikingly deep, rich blue for a
\n Seal Point coat to a medium-pale, grayish blue for a lilac point coat.<\/p>\n
Naming the Colors<\/p>\n
When it came to naming the colors, those who did so were firm believ-
\n ers in using the thesaurus: never call a color brown when you can
\n call it chocolate or cinnamon.<\/p>\n
The colors naturally fall into distinct groups: the “standard” col-
\n ors, the shaded colors, the “exotic” colors, the oriental colors, and
\n the whites. Each group may then be subdivided into several distinct
\n smaller groups, each with a common characteristic. Each color name is
\n followed by its karyotype in three groups (as they were discussed
\n above), and the usual eye colors. Bear in mind that all possible
\n combinations of color and pattern will eventually be realized, but not
\n necessarily recognized: especially by the various cat fancies.<\/p>\n
The Standard Solid Colors<\/p>\n
The solids form the basis for all other colors in nomenclature and
\n karyotypes: these are the fundamental rendition of the eight basic
\n coat colors. Solids are called “selfs” in Britain.<\/p>\n
The black solid technically has a brown undercoat, but selective
\n breeding has managed to eliminate the brown undercoat and has produced
\n cats that are “black to the bone.”<\/p>\n
The subtle differences possible in blues (grays) has made this one of
\n the most popular colors among breeders, with several breeds being
\n exclusively blue. Blues, regardless of pattern, are often referred to
\n as “dilutes.”<\/p>\n
The terms “chestnut” and “chocolate” are synonymous, as are the terms
\n “lavender” and “lilac.”<\/p>\n
Since the orange allele of the orange-making gene also masks the non-
\n agouti allele of the agouti gene, red and cream solids are genetically
\n identical to red and cream tabbies. Careful selective breeding has
\n made cause the non-agouti areas (the stripes) to widen and overlap,
\n effectively canceling the paler agouti background and obscuring the
\n tabby pattern. A generation or two of random breeding, however, and
\n the stripes will return.<\/p>\n
The patched solids, solid-and-whites or bi-colors, are formed by
\n adding the white-spotting gene, “S*”, to the solids. If, instead of
\n the normal random white spotting gene, the particolor gene, “Sp*”, is
\n present, then the coat will show white in the particolor pattern. If
\n both the random white-spotting and particolor genes, “SSp”, are
\n present, then a composite pattern will be evident. If the Birman
\n gene, “sbsb”, is present, then the pattern will be white feet only.<\/p>\n
———————————————————————-
\n Feline Genetics Page 20<\/p>\n
The tortoiseshells or torties are formed by combining both the domi-
\n nant and recessive sex-linked orange genes, “Oo”, with the solids.
\n Because of the sex-linking of the orange genes, the tortie is always
\n female. A tabby pattern may be visible in the orange areas, with any
\n tabby pattern being permitted. In some individuals, the agouti and
\n non-agouti orange areas may offer such contrast as to produce a false
\n tri-color (black-orange-cream).<\/p>\n
The patched tortoiseshells or calicos are formed by combining both the
\n dominant and recessive sex-linked orange-making genes, “Oo”, to the
\n solids and adding the white-spotting gene, “S*”. Like the torties,
\n the calicos are always female, and like the patches, any white-
\n spotting pattern is permitted.<\/p>\n
Color | Karyotype | Usual eye color
\n ———————+————————–+—————-
\n Black | B*ooD* C*aa** iissww | cpr org grn
\n Blue | B*oodd C*aa** iissww | cpr org grn
\n Chestnut | b*ooD* C*aa** iissww | cpr org
\n Lavender | b*oodd C*aa** iissww | cpr org gld
\n Cinnamon | blblooD* C*aa** iissww | org
\n Fawn | blbloodd C*aa** iissww | org gld
\n Red | **OOD* C***T* iissww | cpr org
\n Cream | **OOdd C***T* iissww | cpr org
\n ———————+————————–+—————-
\n Black patch | B*ooD* C*aa** iiS*ww | cpr org grn
\n blue patch | B*oodd C*aa** iiS*ww | cpr org grn
\n chestnut patch | b*ooD* C*aa** iiS*ww | cpr org
\n lavender patch | b*oodd C*aa** iiS*ww | cpr org grn
\n cinnamon patch | blblooD* C*aa** iiS*ww | org
\n fawn patch | blbloodd C*aa** iiS*ww | org grn
\n red patch | **OOD* C***T* iiS*ww | cpr org
\n cream patch | **OOdd C***T* iiS*ww | cpr org<\/p>\n
The Standard Tabby Colors<\/p>\n
The tabbies are formed by adding the agouti gene, “A*”, to the solids.
\n This causes the otherwise solid color to show the pattern dictated by
\n the tabby gene: light and dark stripes (mackerel allele, “T*”) or
\n blotches (blotched allele, “tbtb”).<\/p>\n
The brown tabby corresponds to the black solid: sufficient undercoat
\n color shows in the agouti areas to provide a brownish cast. When in
\n mackerel pattern, this is the “all wild” genotype, and represents the
\n natural state of the cat.<\/p>\n
The red tabby, when in mackerel pattern, presents an alternate stable
\n coat often found on feral domestic cats, usually as a pale ginger.<\/p>\n
The patched tabbies or tabby-and-whites are formed by adding the white
\n spotting gene, “S*”, to the tabbies. Like the patched solids, any
\n white spotting pattern is permitted.<\/p>\n
The tabby-tortoiseshells or torbies are formed by combining both the<\/p>\n
———————————————————————-
\n Feline Genetics Page 21<\/p>\n
dominant and recessive sex-linked orange genes, “Oo”, with the tabbies
\n colors. Like the torties, the torbies are always female.<\/p>\n
Color | Karyotype | Usual eye color
\n ———————–+————————-+—————-
\n tortie | B*OoD* C*aaT* iissww | cpr org
\n blue tortie | B*Oodd C*aaT* iissww | cpr org grn
\n chestnut tortie | b*OoD* C*aaT* iissww | cpr org
\n lavender tortie | b*Oodd C*aaT* iissww | cpr org grn
\n cinnamon tortie | blblOoD* C*aaT* iissww | org
\n fawn tortie | blblOodd C*aaT* iissww | org grn
\n ———————–+————————-+—————-
\n calico | B*OoD* C*aaT* iiS*ww | cpr org
\n blue calico | B*Oodd C*aaT* iiS*ww | cpr org grn
\n chestnut calico | b*OoD* C*aaT* iiS*ww | cpr org
\n lavender calico | b*Oodd C*aaT* iiS*ww | cpr org grn
\n cinnamon calico | blblOoD* C*aaT* iiS*ww | org
\n fawn calico | blblOodd C*aaT* iiS*ww | org grn
\n ———————–+————————-+—————-
\n brown tabby | B*ooD* C*A*T* iissww | cpr org yel hzl
\n blue tabby | B*oodd C*A*T* iissww | cpr org yel hzl
\n chestnut tabby | b*ooD* C*A*T* iissww | cpr org yel hzl
\n lavender tabby | b*oodd C*A*T* iissww | cpr org yel hzl
\n cinnamon tabby | blblooD* C*A*T* iissww | org yel hzl
\n fawn tabby | blbloodd C*A*T* iissww | org yel hzl
\n red tabby | **OOD* C***T* iissww | cpr org yel hzl
\n cream tabby | **OOdd C***T* iissww | cpr org yel hzl
\n ———————–+————————-+—————-
\n brown patched tabby | B*ooD* C*A*T* iiS*ww | cpr org yel hzl
\n blue patched tabby | B*oodd C*A*T* iiS*ww | cpr org yel hzl
\n chestnut patched tabby | b*ooD* C*A*T* iiS*ww | cpr org yel hzl
\n lavender patched tabby | b*oodd C*A*T* iiS*ww | cpr org yel hzl
\n cinnamon patched tabby | blblooD* C*A*T* iiS*ww | org yel hzl
\n fawn patched tabby | blbloodd C*A*T* iiS*ww | org yel hzl
\n red patched tabby | **OOD* C***T* iiS*ww | cpr org yel hzl
\n cream patched tabby | **OOdd C***T* iiS*ww | cpr org yel hzl
\n ———————–+————————-+—————-
\n torbie | B*OoD* C*A*T* iissww | cpr org yel hzl
\n blue torbie | B*Oodd C*A*T* iissww | cpr org yel hzl
\n chestnut torbie | b*OoD* C*A*T* iissww | cpr org yel hzl
\n lavender torbie | b*Oodd C*A*T* iissww | cpr org yel hzl
\n cinnamon torbie | blblOoD* C*A*T* iissww | org yel hzl
\n fawn torbie | blblOodd C*A*T* iissww | org yel hzl
\n ———————–+————————-+—————-
\n torbico | B*OoD* C*A*T* iiS*ww | cpr org yel hzl
\n blue torbico | B*Oodd C*A*T* iiS*ww | cpr org yel hzl
\n chestnut torbico | b*OoD* C*A*T* iiS*ww | cpr org yel hzl
\n lavender torbico | b*Oodd C*A*T* iiS*ww | cpr org yel hzl
\n cinnamon torbico | blblOoD* C*A*T* iiS*ww | org yel hzl
\n fawn torbico | blblOodd C*A*T* iiS*ww | org yel hzl<\/p>\n
The patched tabby-tortoiseshells, or patched torbies or torbicos, are
\n formed by combining the dominant and recessive orange-making genes,
\n “Oo”, with the standard tabbies and adding the white spotting gene,<\/p>\n
———————————————————————-
\n Feline Genetics Page 22<\/p>\n
“S*”, to the torbie colors. Like the patched solids, any white-
\n spotting pattern is permitted.<\/p>\n
The Shaded Colors<\/p>\n
The shaded colors are formed by adding the inhibitor gene, “I*”, to
\n the standard solids. If the expression is light, a smoked coat is
\n produced, if moderate, a shaded coat, and if heavy, a tipped or chin-
\n chilla coat. Only six of the eight possible colors are recognized.<\/p>\n
The tortie chinchillas are formed by adding a moderate-to heavy ex-
\n pression of the inhibitor gene, “I*”, to the standard torties. Only
\n four of the six possible colors are recognized.<\/p>\n
Color | Karyotype | Usual eye color
\n ———————–+————————-+—————-
\n (silver) smoke | B*ooD* C*aa** I*ssww | cpr org yel
\n blue smoke | B*oodd C*aa** I*ssww | cpr org yel
\n chestnut smoke | b*ooD* C*aa** I*ssww | cpr org yel
\n lavender smoke | b*oodd C*aa** I*ssww | cpr org yel
\n red smoke | **OOD* C***T* I*ssww | cpr org yel
\n cream smoke | **OOdd C***T* I*ssww | cpr org yel
\n ———————–+————————-+—————-
\n (silver) shade | B*ooD* C*aa** I*ssww | cpr grn
\n blue shade | B*oodd C*aa** I*ssww | cpr grn
\n chestnut shade | b*ooD* C*aa** I*ssww | cpr grn
\n lavender shade | b*oodd C*aa** I*ssww | cpr grn
\n red shade | **OOD* C***T* I*ssww | cpr grn
\n cream shade | **OOdd C***T* I*ssww | cpr grn
\n ———————–+————————-+—————-
\n (silver) chinchilla | B*ooD* C*aa** I*ssww | grn
\n blue chinchilla | B*oodd C*aa** I*ssww | grn
\n chestnut chinchilla | b*ooD* C*aa** I*ssww | grn
\n lavender chinchilla | b*oodd C*aa** I*ssww | grn
\n red chinchilla | **OOD* C***T* I*ssww | grn
\n cream chinchilla | **OOdd C***T* I*ssww | grn
\n ———————–+————————-+—————-
\n tortie chinchilla | B*OoD* C*aaT* I*ssww | cpr org yel
\n blue tortie chinchilla | B*Oodd C*aaT* I*ssww | cpr org yel
\n chestnut tortie chinch | b*OoD* C*aaT* I*ssww | cpr org yel
\n lavender tortie chinch | b*Oodd C*aaT* I*ssww | cpr org yel<\/p>\n
The Golden Chinchilla Colors<\/p>\n
The golden chinchillas are formed by combining the mackerel and Abys-
\n sinian alleles of the tabby gene, “TTa”, with the standard solids.
\n This produces a coat of undercoat-colored hairs tipped with the stand-
\n ard colors. Selective breeding has altered the undercoat polygenes to
\n produce a striking warm-gold color. Only three of the eight possible
\n colors are recognized.<\/p>\n
The golden chinchilla torties are formed by combining the mackerel and
\n Abyssinian alleles of the tabby gene, “TTa”, with the standard
\n torties. This produces a coat with hairs of undercoat color tipped<\/p>\n
———————————————————————-
\n Feline Genetics Page 23<\/p>\n
with the standard tortie colors. While any combination is possible,
\n only two colors are recognized.<\/p>\n
Color | Karyotype | Usual eye color
\n ———————–+————————-+—————-
\n golden chinchilla | B*ooD* C*A*TTa iissww | gld
\n honey chinchilla | b*ooD* C*A*TTa iissww | gld
\n copper chinchilla | **OOD* C***TTa iissww | cpr gld
\n ———————–+————————-+—————-
\n golden tortie chinch | B*OoD* C*A*TTa iissww | gld
\n honey tortie chinch | b*OoD* C*A*TTa iissww | gld<\/p>\n
The Silver Tabby Colors<\/p>\n
The silver tabbies are obtained by adding a moderate expression of the
\n inhibitor gene, I*, to the standard tabbies. Only six of the eight
\n possible colors are recognized.<\/p>\n
Color | Karyotype | Usual eye color
\n ———————–+————————-+—————-
\n silver tabby | B*ooD* C*A*T* I*ssww | hzl grn
\n silver blue tabby | B*oodd C*A*T* I*ssww | hzl grn
\n silver chestnut tabby | b*ooD* C*A*T* I*ssww | hzl grn
\n silver lilac tabby | b*oodd C*A*T* I*ssww | hzl grn
\n silver red tabby | **OOD* C***T* I*ssww | hzl grn
\n silver cream tabby | **OOdd C***T* I*ssww | hzl grn<\/p>\n
The Spotted Tabby Colors<\/p>\n
The bronze spotted tabbies are genetically standard mackerel tabbies
\n with the mackerel striping broken into spots by the effects of various
\n polygenes. Ideal coats have evenly spaced round spots. Only six of
\n the eight possible colors are recognized.<\/p>\n
The silver spotted tabbies are bronze spotted tabbies with a moderate
\n expression of the inhibitor gene, “I*”, added. This produces a pat-
\n tern of jet black spots on a silvery agouti background. Only six of
\n the eight possible colors are recognized.<\/p>\n
Color | Karyotype | Usual eye color
\n ———————–+————————-+—————-
\n bronze | B*ooD* C*A*T* iissww | gld
\n bronze blue | B*oodd C*A*T* iissww | cpr gld
\n bronze chocolate | b*ooD* C*A*T* iissww | cpr gld
\n bronze lavender | b*oodd C*A*T* iissww | cpr gld
\n copper | **OOD* C***T* iissww | cop
\n bronze cream | **OOdd C***T* iissww | gld
\n ———————–+————————-+—————-
\n silver | B*ooD* C*A*T* I*ssww | hzl grn
\n silver blue | B*oodd C*A*T* I*ssww | hzl grn
\n silver chocolate | b*ooD* C*A*T* I*ssww | hzl grn
\n silver lilac | b*oodd C*A*T* I*ssww | hzl grn
\n silver red | **OOD* C***T* I*ssww | org hzl grn
\n silver cream | **OOdd C***T* I*ssww | org hzl grn<\/p>\n
———————————————————————-
\n Feline Genetics Page 24<\/p>\n
The Abyssinian Colors<\/p>\n
The Abyssinians are primarily standard tabbies with the Abyssinian
\n allele of the tabby gene, “Ta*”. This produces an all-agouti coat,
\n similar to that of the wild rabbit.<\/p>\n
The silver Abyssinians are Abyssinians with a moderate expression of
\n the inhibitor gene, “I*”. This produces the all-agouti ticking on a
\n pale silver undercolor.<\/p>\n
It should be noted that among Abyssinians there are two genetically
\n different reds that are virtually identical in appearance: “red,”
\n which is in reality cinnamon, and “true red,” which is red.<\/p>\n
Color | Karyotype | Usual eye color
\n ———————–+————————-+—————-
\n ruddy | B*ooD* C*A*Ta* iissww | org amb grn
\n blue | B*oodd C*A*Ta* iissww | org amb grn
\n chestnut | b*ooD* C*A*Ta* iissww | org amb grn
\n lavender | b*oodd C*A*Ta* iissww | org amb grn
\n red | blblooD* C*A*Ta* iissww | org amb
\n fawn | blbloodd C*A*Ta* iissww | org amb
\n true red | **OOD* C***Ta* iissww | cpr org amb
\n cream | **OOdd C***Ta* iissww | cpr org amb
\n ———————–+————————-+—————-
\n silver | B*ooD* C*A*Ta* I*ssww | grn
\n silver blue | B*oodd C*A*Ta* I*ssww | grn
\n silver chestnut | b*ooD* C*A*Ta* I*ssww | grn
\n silver lilac | b*oodd C*A*Ta* I*ssww | grn
\n silver red | blblooD* C*A*Ta* I*ssww | yel
\n silver fawn | blbloodd C*A*Ta* I*ssww | yel
\n true silver red | **OOD* C***Ta* I*ssww | org yel
\n silver cream | **OOdd C***Ta* I*ssww | org yel<\/p>\n
The Oriental Solid Colors<\/p>\n
The oriental solids are identical in every way to the standard solids
\n except in their names. Oriental color names tend to be used with cats
\n of oriental build, effectively solid-color Siamese.<\/p>\n
Color | Karyotype | Usual eye color
\n ———————-+————————–+—————-
\n ebony | B*ooD* C*aa** iissww | grn
\n blue | B*oodd C*aa** iissww | grn
\n chocolate | b*ooD* C*aa** iissww | grn
\n lilac | b*oodd C*aa** iissww | grn
\n caramel | blblooD* C*aa** iissww | grn
\n fawn | blbloodd C*aa** iissww | grn
\n red | **OOD* C***T* iissww | grn
\n cream | **OOdd C***T* iissww | grn<\/p>\n
———————————————————————-
\n Feline Genetics Page 25<\/p>\n
The Burmese Colors<\/p>\n
The Burmese colors are formed from the standard solid colors by the
\n reduction in color expression from full, “C*”, to the Burmese alleles,
\n “cbcb”. This is a partial albinism and causes a slight reduction in
\n color intensity: black becomes sable. These colors are used almost
\n exclusively for the Burmese and related breeds, such as the Malayan
\n and Tiffany.<\/p>\n
Color | Karyotype | Usual eye color
\n ———————-+————————–+—————-
\n sable | B*ooD* cbcbaa** iissww | gld
\n blue | B*oodd cbcbaa** iissww | gld
\n champagne | b*ooD* cbcbaa** iissww | gld
\n platinum | b*oodd cbcbaa** iissww | gld
\n cinnamon | blblooD* cbcbaa** iissww | gld
\n fawn | blbloodd cbcbaa** iissww | gld
\n red | **OOD* cbcb**T* iissww | gld
\n cream | **OOdd cbcb**T* iissww | gld<\/p>\n
The Tonkinese Colors<\/p>\n
The Tonkinese colors are formed from the standard solid colors by the
\n reduction of color expression from full, “C*”, to combined Burmese and
\n Siamese, “cbcs”. This is a partial albinism and causes a downgrade in
\n color expression, the body color becoming a light-to-medium brown and
\n the points becoming Burmese. These colors are used only with the
\n Tonkinese breed.<\/p>\n
Color | Karyotype | Usual eye color
\n ———————-+————————–+—————-
\n natural mink | B*ooD* cbcsaa** iissww | trq
\n blue mink | B*oodd cbcsaa** iissww | trq
\n honey mink | b*ooD* cbcsaa** iissww | trq
\n champagne mink | b*oodd cbcsaa** iissww | trq
\n cinnamon mink | blblooD* cbcsaa** iissww | trq
\n fawn mink | blbloodd cbcsaa** iissww | trq
\n red mink | **OOD* cbcs**T* iissww | trq
\n cream mink | **OOdd cbcs**T* iissww | trq<\/p>\n
The Siamese Colors<\/p>\n
The Siamese solid-point formed from the standard colors by the reduc-
\n tion of color expression from full, “C*”, to Siamese, “cscs”. This is
\n a partial albinism and causes a downgrade in color expression, the
\n body color becoming fawn and the points becoming Burmese. The solid-
\n point colors are formed from the standard solids, the tortie-point
\n from the standard torties, the lynx-point from the standard tabbies,
\n and the torbie-point from the standard torbies. Only six of the eight
\n possible solid- or lynx-point and four of the six possible tortie- or
\n torbie-point colors are recognized.<\/p>\n
———————————————————————-
\n Feline Genetics Page 26<\/p>\n
Color | Karyotype | Usual eye color
\n ———————–+————————-+—————-
\n seal point | B*ooD* cscsaa** iissww | sbl
\n blue point | B*oodd cscsaa** iissww | sbl
\n chocolate point | b*ooD* cscsaa** iissww | sbl
\n lilac point | b*oodd cscsaa** iissww | sbl
\n red point | **OOD* cscsT* iissww | sbl
\n cream point | **OOdd cscsT* iissww | sbl
\n ———————–+————————-+—————-
\n seal tortie point | B*OoD* cscsaaT* iissww | sbl
\n blue tortie point | B*Oodd cscsaaT* iissww | sbl
\n chocolate tortie point | b*OoD* cscsaaT* iissww | sbl
\n lilac tortie point | b*Oodd cscsaaT* iissww | sbl
\n ———————–+————————-+—————-
\n seal lynx point | B*ooD* cscsA*T* iissww | sbl
\n blue lynx point | B*oodd cscsA*T* iissww | sbl
\n chocolate lynx point | b*ooD* cscsA*T* iissww | sbl
\n lilac lynx point | b*oodd cscsA*T* iissww | sbl
\n red lynx point | **OOD* cscs**T* iissww | sbl
\n cream lynx point | **OOdd cscs**T* iissww | sbl
\n ———————–+————————-+—————-
\n seal torbie point | B*OoD* cscsA*T* iissww | sbl
\n blue torbie point | B*Oodd cscsA*T* iissww | sbl
\n chocolate torbie point | b*OoD* cscsA*T* iissww | sbl
\n lilac torbie point | b*Oodd cscsA*T* iissww | sbl<\/p>\n
The Van Colors<\/p>\n
The van colors are formed from the standard solid colors by the addi-
\n tion of the van gene, “Wv”. This is a masking gene, covering the
\n effects of the agouti, color-expression, tabby, inhibitor, and white-
\n spotting genes. The van gene, a modified dominant-white gene, causes
\n the coat to be white with color on the crown of the head, ears, and
\n tail only. The preferred van color is auburn (orange). The tail is
\n often tabby-ringed.<\/p>\n
Color | Karyotype | Usual eye color
\n ———————-+————————–+—————-
\n black van | B*ooD* ****** ****Wv* | org wbl odd
\n blue van | B*oodd ****** ****Wv* | org wbl odd
\n chestnut van | b*ooD* ****** ****Wv* | org wbl odd
\n lavender van | b*oodd ****** ****Wv* | org wbl odd
\n cinnamon van | blblooD* ****** ****Wv* | org wbl odd
\n fawn van | blbloodd ****** ****Wv* | org wbl odd
\n auburn van | **OOD* ****** ****Wv* | org wbl odd
\n cream van | **OOdd ****** ****Wv* | org wbl odd<\/p>\n
The Whites<\/p>\n
White is not a color, but rather a masking of the color genes result-
\n ing in an absence of color. There are five ways a cat can have an all
\n white coat: be full-inhibited white, be full-spotted white, be domi-
\n nant white, be blue-eyed albino, or be albino. Each of these ways is
\n genetically different.<\/p>\n
———————————————————————-
\n Feline Genetics Page 27<\/p>\n
The full-inhibited white coat comes from a 100% expression of the
\n inhibitor gene, “I*”, masking all colors and patterns. Since the
\n current trend in chinchilla coats is to have just a hint of tipping,
\n certain kittens are bound to be born where the “hint” is effectively
\n zero, creating an all-white cat. Since the colors still exist, the
\n eyes will be the proper color for the masked “true” coat colors, and
\n may be anything except dominant-white blue, albino blue, or pink.<\/p>\n
The full-spotted white coat comes from a 100% expression of the white
\n spotting gene, “S*”, masking all colors and patterns. This coat may
\n have a few non-white hairs, especially on a kitten. Like the full-
\n inhibited white, the eyes will be the proper color for the masked
\n “true” coat colors, and may be anything except dominant-white blue,
\n albino blue, or pink.<\/p>\n
The dominant white coat comes from expression of the dominant-white
\n gene, “W*”, masking all colors and patterns. The eyes are always
\n orange, dominant-white blue, or odd.<\/p>\n
The blue-eyed albino comes from expression of the blue-eyed albino
\n allele of the albino gene, “ca*”, masking all colors and patterns.
\n The eyes are always albino blue.<\/p>\n
The albino coat comes from expression of the albino allele of the
\n albino gene, “cc”, masking all colors and patterns. The eyes are
\n always pink.<\/p>\n
Color | Karyotype | Usual eye color
\n ———————-+————————–+—————-
\n full-inhibited white | ****** ****** I***** | not wbl\/abl\/pnk
\n full-spotted white | ****** ****** **S*** | not wbl\/abl\/pnk
\n dominant white | ****** ****** ****W* | org wbl odd
\n blue-eyed albino | ****** ca***** ****** | alb
\n albino | ****** cc**** ****** | pnk<\/p>\n
———————————————————————-
\n Feline Genetics Page 28<\/p>\n
