CHIHUAHUA GENETICS ~ SIZE, COLORS AND HAIR COATS

chihuahua-puppies.net/chihuahua-puppy-chihuahua-genetics.html

It's pure genetics.

The gene that controls chihuahua size has six parts, or alleles, and each parent passes on three of theirs to the
offspring. Size alleles can be best described as having a value of either + (positive) or - (negative). The six "values"
of the alleles are combined for a total, which determines size.
For example: +,+,+,-,-,-, = 6 alleles, or 3 positive and 3 negative. Think of + as "up 1", and - as "down 1." The first
three positives cancel out the next three negatives (+1+1+1-1-1-1 = 0), so we end up with 0, or your proverbial
"average".
Another example: +,-,+,-,-,-. Added together, we get 2 up and 4 down, with an end result of -2, "2 down", or below
average size. (+1+1-1-1-1-1 = -2)
One more. +,+,+,+,-,-. 4 up and 2 down = +2, or "2 up". (+1+1+1+1-1-1 = 2) In other words, a bigger than average
pup.
Are you starting to get the idea? Ok, let's start passing things on to the kids.
Take two, average sized parents: Dad = +,+,+,-,-,- and Mom = +,+,+,-,-,-. Let's give them a litter of 3.
Pup #1: Take (at random) 2 minuses and 1 plus from Dad and 1 minus and 2 pluses from Mom. So, Pup #1 is -1,1,+1,-1,+1,+1. The total is 0, or average size... an average size pup from 2 average sized parents. Not surprising.
Pup #2: Take (again, at random) 3 minuses from Dad and three minuses from Mom. What size pup do we get? Pup
#2 is -1,-1,-1,-1,-1,-1. The total is -6, or one very tiny puppy.
Pup #3: Let's have all the pluses that both Mom and Dad can give (this combination can also happen randomly).
That's +1,+1,+1,+1,+1,+1 = 6, and results in a chihuahua much larger than either parent.

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When you see how size is inherited, it all starts to make sense doesn't it? But genetics is only part of the story with
regard to size.
It has been well documented that the human race is getting bigger and taller with each generation. When you look
through museum reproductions of early settler's cottages, the height of doorways and the length of beds stand out
as being quite small by today's standards.
This gradual, but steady increase in the size of humans has been attributed by scientists to improvements in diet
and health care over the years. Diet is just one factor in what is generally referred to as "environment", and
environment plays a major role in the size of chihuahuas as well. Proper nutrition, maternal care, warmth and
exercise all contribute to growth in a puppy.
The last variable in determining size is a congenital factor affecting growth. New research from the Canine Genome
Project has shown a link between size and thyroid development. What is not clear yet is whether size is effecting the
development of the thyroid or the development of the thyroid is effecting size. It is well documented, however, that
the very tiny examples of our breed have more frequent and serious health problems than normal sized chihuahuas.
NO ONE CAN GUARANTEE MATURE WEIGHT!! This is just a tool to be used along with observations of mom and
dad weight, bone structure, previous puppy mature weights and more!

The length of a chihuahua's coat is determined by two genes.

The smooth coat gene is DOMINANT (indicated by capital letters), and the long coat gene is RECESSIVE (indicated
by lower case letters).
The dominant smooth coat gene, if present, will completely hide the recessive long coat gene. So, a dog can be a
smooth coat (the dominant gene is expressed, or seen), and have a hidden long coat gene, which it can pass on to
the offspring.

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Basic Genetics
The basis for order in life lies in a very large molecule called deoxyribonucleic acid, mercifully abbreviated to DNA. A
related molecule, ribonucleic acid (RNA) provides the genetic material for some microbes, and also helps read the
DNA to make proteins.
DNA has a shape rather like a corkscrewed ladder. The "rungs" of the ladder are of four different types. The
information in DNA comes in how those types are ordered along the molecule, just as the information in Morse code
comes in how the dashes and dots are ordered. The information in three adjacent rungs is "read" by a kind of RNA
that hooks onto a particular triad of rungs at one end and grabs a particular amino acid at the other. Special triads
say "start here" and "end here" and mark off regions of the DNA molecule we call discrete genes. The eventual
result is a chain of amino acids that makes up a protein, with each amino acid corresponding to a set of three rungs
along the DNA molecule. There are also genes that tell the cell when to turn on or turn off another gene. The
proteins produced may be structural or they may be enzymes that facilitate chemical reactions in the body.
We now know that chromosomes are essentially DNA molecules. In an advanced (eukaryotic) cell, these
chromosomes appear as threadlike structures packaged into a more or less central part of the cell, bound by a
membrane and called the nucleus. What is more important is that the chromosomes in a body cell are arranged in
pairs, one from the father and one from the mother. Further, the code for a particular protein is always on the same
place on the same chromosome. This place, or location, is called a locus (plural loci.)
There are generally a number of slightly different genes that code for forms of the same protein, and fit into the same

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locus. Each of these genes is called an allele. Each locus, then, will have one allele from the mother and one from
the father. How?
When an animal makes an egg or a sperm cell (gametes, collectively) the cells go through a special kind of division
process, resulting in a gamete with only one copy of each chromosome. Unless two genes are very close together
on the same chromosome, the selection of which allele winds up in a gamete is strictly random. Thus a dog who has
one gene for black pigment and one for brown pigment may produce a gamete which has a gene for black pigment
OR for brown pigment. If he's a male, 50% of the sperm cells he produces will be B (black) and 50% will be brown
(b).
When the sperm cell and an egg cell get together, a new cell is created which once again has two of each
chromosome in the nucleus. This implies two alleles at each locus (or, in less technical terms, two copies of each
gene, one derived from the mother and one from the father,) in the offspring. The new cell will divide repeatedly and
eventually create an animal ready for birth, the offspring of the two parents. How does this combination of alleles
affect the offspring?
There are several ways alleles can interact. In the example above, we had two alleles, B for black and b for brown. If
the animal has two copies of B, it will be black. If it has one copy of B and one of b, it will be just as black. Finally, if it
has two copies of b, it will be brown, like a chocolate Labrador. In this case we refer to B as dominant to b and b as
recessive to B. True dominance implies that the dog with one B and one b cannot be distinguished from the dog with
two B alleles. Now, what happens when two black dogs are bred together?
We will use a diagram called a Punnett square. For our first few examples, we will stick with the B locus, in which
case there are two possibilites for sperm (which we write across the top) and two for eggs (which we write along the
left side. Each cell then gets the sum of the alleles in the egg and the sperm. To start out with a very simple case,
assume both parents are black not carrying brown, that is, they each have two genes for black. We then have:
B

BB (black)

BB (black)

BB (black)

BB (black)

All of the puppies are black if both parents are BB (pure for black.
Now suppose the sire is pure for black but the dam carries a recessive gene for brown. In this case she can produce
either black or brown gametes, so
B

BB (pure for black)

BB (pure for black)

Bb (black carrying brown)

Bb (black carrying brown)

This gives appoximately a 50% probability that any given puppy is pure for black, and a 50% probability that it is
black carrying brown. All puppies appear black. We can get essentially the same diagram if the sire is black carrying
brown and the dam is pure for black. Now suppose both parents are blacks carrying brown:
B

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BB (pure for black

Bb (black carrying brown)

Bb (black carrying brown)

bb (brown)

This time we get 25% probabilty of pure for black, 50% probability of black carrying brown, and - a possible surprise
if you don't realize the brown gene is present in both parents - a 25% probability that a pup will be brown. Note that
only way to distinguish the pure for blacks from the blacks carrying brown is test breeding or possibly DNA testing they all look black.
Another possible mating would be pure for black with brown:
B

Bb (black carrying brown)

Bb (black carrying brown)

Bb (black carrying brown)

Bb (black carrying brown)

In this case, all the puppies will be black carrying brown.

Suppose one parent is black carrying brown and the other is brown:
B

Bb (black carrying brown)

bb (brown)

Bb (black carrying brown)

bb (brown)

In this case, there is a 50% probability that a puppy will be black carrying brown and a 50% probability that it will be
brown.
Finally, look at what happens when brown is bred to brown:
b

bb (brown)

bb (brown)

bb (brown)

bb (brown)

Recessive to recessive breeds true - all of the pups will be brown.

Note that a pure for black can come out of a mating with both parents carrying brown, and that such a pure for black
is just as pure for black as one from ten generations of all black parentage. THERE IS NO MIXING OF GENES.
They remain intact through their various combinations, and B, for instance, will be the same B no matter how often it
has been paired with brown. This, not the dominant-recessive relationship, is the real heart of Mendelian genetics.
This type of dominant-recessive inheritance is common (and at times frustrating if you are trying to breed out a
recessive trait, as you can't tell by looking which pups are pure for the dominant and which have one dominant and
one recessive gene.) Note that dominant to dominant can produce recessive, but recessive to recessive can only
produce recessive. The results of a dominant to recessive breeding depends on whether the dog that looks to be the
dominant carries the recessive. A dog that has one parent expressing the recessive gene, or that produces a puppy

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that shows the recessive gene, has to be a carrier of the recessive gene. Otherwise, you really don't know whether
or not you are dealing with a carrier, bar genetic testing or test breeding.
One more bit of terminology before we move on - an animal that has matching alleles (BB or bb) is called
homozygous. An animal that has two different alleles at a locus (Bb) is called heterozygous.
A pure dominant-recessive relationship between alleles implies that the heterozygous state cannot be distinguished
from the homozygous dominant state. This is by no means the only possibility, and in fact as DNA analysis
advances, it may become rare. Even without such analysis, however, there are many loci where three phenotypes
(appearances) come from two alleles. An example is merle in the dog. This is often treated as a dominant, but in
fact it is a type of inheritance in which there is no clear dominant - recessive relationship. It is sometimes called
overdominance, if the heterozyote is the desired state. I prefer incomplete dominance, recognising that in fact
neither of the alleles is truly dominant or recessive relative to the other.
As an example, we will consider merle. Merle is a diluting gene, not really a color gene as such. If the major
pigment is a dog with two non-merle genes (mm) is the expected color - black, liver, blue, tan-point, sable, recessive
red. If the dog is Mm, it has a mosaic appearance, with random patches of the expected eumelanin pigment in full
intensity against a background of diluted eumelanin. Phaeomelanin (tan) shows little visual effect, though there is a
possibility that microscopic examination of the tan hair would show some effect of M. Thus a black or black tan-point
dog is a blue merle, a brown or brown tan-point dog is red merle, and a sable dog is, though the last color, with
phaeomelanin dominating, may be indistinguishable from sable in an adult. (The effect of merle on recessive red is
unknown, and I can't think of a breed that has both genes.) What makes this different from the black-brown situation
is that an MM dog is far more diluted than is an Mm dog. In those breeds with white markings in the full-color state
the MM dog is often almost completely white with a few diluted patches, and has a considerable probablity of being
deaf, blind, and/or sterile. Even in the daschund, which generally lacks white markings, the so-called double dapple
(MM) has extensive white markings and may have reduced eye size. with a number of combinations of merle with
other genes are available on this site, but the gene also occurs in Australian Shepherds, Collies, Border Collies,
Cardiganshire Welsh Corgis, (French herding breed), harlequin Great Danes, Catahoula leopard dogs, and
Daschunds, at the least.
Note that both of the extremes - normal color and double merle white - breed true when mated to another of the
same color, very much like the Punnett squares above for the mating of two browns or two pure for blacks. I will skip
those two and go to the more interesting matings involving merles.
First, consider a merle to merle mating. Remember both parents are Mm, so we get:
M

MM (sublethal double merle)

Mm (merle)

Mm (merle)

mm (non-merle)

Assuming that merle is the desired color, this predicts that each pup has a 25% probability of inheriting the sublethal
(and in most cases undesirable by the breed standards) MM combination, only 50% will be the desired merle color,
and 25% will be acceptable full-color individuals. (In fact there is some anecdotal evidence that MM puppies make
up somewhat less than 25% of the offspring of merle to merle breedings, but we'll discuss that separately.) Merle,
being a heterozygous color, cannot breed true.
Merle to double merle would produce 50% double merle and is almost never done intentionally. The Punnet square
for this mating is:

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MM (sublethal double merle)

MM (sublethal double merle)

Mm (merle)

Mm (merle)

Merle to non-merle is the "safe" breeding, as it produces no MM individuals:

m

Mm (merle)

Mm (merle)

mm (non-merle)

mm (non-merle)

We get exactly the same probability of merle as in the merle to merle breeding (50%) but all of the remaining pups
are acceptable full-colored individuals.
There is one other way to breed merles, which is in fact the only way to get an all-merle litter. This is to breed a
double merle (MM) to a non-merle (mm). This breeding does not a use a merle as either parent, but it produces all
merle puppies. (The occasional exception will be discussed elsewhere.) In this case,
M

Mm (merle)

Mm (merle)

Mm (merle)

Mm (merle

The problem with this breeding is that it requires the breeder to maintain a dog for breeding which in most cases
cannot be shown and which may be deaf or blind. Further, in order to get that one MM dog who is fertile and of
outstanding quality, a number of other MM pups will probably have been destroyed, as an MM dog, without testing
for vision and hearing, is a poor prospect for a pet. In Shelties, the fact remains that several double merles have
made a definite contribution to the breed. This does not change the fact that the safe breeding for a merle is to a
nonmerle.
Thus far, we have concentrated on single locus genes, with two alleles to a locus. Even something as simple as coat
color, however, normally involves more than one locus, and it is quite possible to have more than two alleles at a
locus. What happens when two or more loci are involved in one coat color?

Canine Color Genetics

Dogs have a wide variety of genes that influence color. Further, the same genes may give a very different effect on
different types and lengths of coats.
One of the biggest problems people have with genetics is the assumption that a defined trait - size, ear type, color,
yappiness - is due to a single gene. In fact, genes code for two types of things. One, which is relatively well
understood, is the structure of a particular protein. The normal equivalent of the albino gene, for instance, codes for
tyrosinase, an enzyme which breaks up the amino acid tyrosine as a first step in producing melanin, the major
pigment in mammalian skin and hair. In an albino, this enzyme cannot be produced, and as a result melanin cannot
be produced. A second type of gene controls when and where other genes are turned on or off. These genes are the

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subject of vigorous ongoing study, and probably have a major impact on such things on the number of vertebrae in
the spine or the age at which growth is complete. Right now, let's look at some of the gene series (loci) known to
influence canine color, and try to get a feel for what they do.
Before starting our list, we need to know that mammals have two forms of melanin in their coats. One, eumelanin, is
dark, though it can vary somewhat in color due to variations in the protein that forms the framework of the pigment
granule. The base form of melanin is black. Melanin can also appear brown (often called liver in dogs) or blue-gray.
The second pigment, which varies from pale cream through shades of yellow, tan and red to mahogany (as in the
Irish Setter), is called phaeomelanin. There are at least two and possibly as many as four gene series that
determine where, on the dog and along the length of the hair, eumelanin and phaeomelanin appear.
The generally recognised color series (loci) in dogs are called A(agouti), B (brown), C (albino series), D (blue
dilution) E (extension), G (graying), M(merle), R (roaning), S(white spotting) and T (ticking.) There may be more,
unrecognised gene series, and in a given breed modifying factors may drastically affect the actual appearance.
Thus one school of thought holds that the round spots on a Dalmation are due to the same gene that produces the
roaned areas on a German Shorthair Pointer, but with vastly different modifiers.
A, the agouti series. The standard assumption, based on Little's research, is that this series contains four alleles
(different forms of the gene). A fifth allele may exist in Shetland Sheepdogs, and a sixth in certain "saddle-tan"
breeds.
As produces black without any tan on the dog. White markings are due to a different gene, and there are
other genes that can modify the black to liver (chocolate Lab) or blue dilute (blue Great Dane.) If As is
present, in most cases the dog will be able to produce only eumelanin pigment (but see the E series). Note
that the agouti series is known in a number of mammals, and dominant black is almost always found in a
different series, so there is a strong possibility that dominant black is not really in the agouti series.
ay in the absense of A s produces a dog which is predominantly tan (phaeomelanin) sometimes with black
tipped hairs or interspersed black hairs. The usual term for this color is "sable." In examining dogs from ay
breeds, I have generally found that even if there is no other black on the coat, the whiskers (the course, stiff
vibrissae, not the "beard" seen with some terrier coats) are black if they originate in a pigmented area.
Examples of a y dogs include Collies, fawn Boxers and Great Danes, and some reds (Basenji red is thought to
be ay, for instance.) a y is recessive to As, but incompletely dominant to a t. That is, an ayat dog is on average
darker (more black hairs) than an ayay dog, but the difference is generally within the range of color for ayay
within the breed.
at, present in double dose, produces a dog which is predominantly black, with tan markings on the muzzle,
over the eyes, on the chest, legs, and under the tail. A Dobermann or Rottweiler is a good example of the
classic black and tan pattern. The Bernese Mountain Dog shows the effect of black and tan combined with
white markings, often called tricolor.
aw is the fourth allele considered by Little. This is the wild "wolf-color" seen in Norwegian Elkhounds and
possibly in some salt-and pepper breeds. It differs from sable in two ways. First, the tan is replaced by a pale
cream to pale gray color. Second, the hairs are normally banded - not just the scattering of black-tipped hairs
sometimes seen in a sable, but several bands of alternating light and black pigment along the length of the
hair. Little was unable to determine the dominance relationship of this gene, or even to say with certainty that
the banding and the reduction of tan pigment were due to the same gene.
Although Little did not make any distinction between the Dobermann black and tan and the "saddle tan" seen in
many terrier breeds (black "saddle" but extensive tan on legs and head), it seems likely that a fifth gene exists in the
a series. For the moment I'll call it "saddle tan," asa. It seems recessive to a y sable, but other dominance
relationships in the series need more investigation.

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Finally, at least two breeds (Shetland Sheepdog and German Shepherd) have a fully recessive black. Since black is
the bottom recessive of the A series in many other mammals, it seems logical to assign this color to recessive black,
a, and state that recessive black is caused by aa at the agouti locus. There is an alternative theory in Shelties which
suggests the existence of a recessive gene that removes tan points from a genetic black and tan or a dominant,
widespread gene that forms tan points on all colors but dominant black.
Little's assignment of dominant black in dogs to the A locus (A s) is totally against experience with this locus in other
species, where more yellow is generally dominant to more black. There may be a third locus controlling dominant
black, in which case A y would be the top dominant in the A series.
B, the brown series. This series is relatively simple. B, in single or double dose, allows the production of black
pigment. A bb dog produces brown pigment wherever the dog would otherwise have produced black. The gene
apparently codes for one of the proteins that makes up the eumelanin pigment granule, so the bb granules are
smaller and rounder in shape as well as appearing a lighter color than those of a dog carrying B. This gene is
responsible for a number of liver and chocolate colors, especially in the sporting breeds. The same gene produces
some "reds" (in Australian Shepherds, Border Collies, and Dobermanns, for example), and probably the bronze
Newfoundland. It has some effect on the iris of the eye and on the skin color, including the eye rims and the nose
leather. Phaeomelanin (tan) is very little affected, so the color of the tan points on a red Dobermann (atatbb), for
instance, is little affected. I have seen little discussion of the effect of brown on a sable dog, but I would expect a
brown nose leather and eye rims, with the coat shaded brown rather than black. Probably the dog would closely
resemble a sable, perhaps with an orangey cast and a light nose. Note that some shades of liver, though a
eumelanin pigment, overlap some shades of tan, a phaeomelanin pigment. In particular the deadgrass color
(bbcchcch) can overlap recessive yellow (ee)
C, the albino series. This again is a fairly complex locus, especially in other mammals. The top dominant, C, allows
full color to develop, and is probably the structural gene for tyrosinase. The bottom recessive, c, does not appear to
occur in dogs, but in other mammals it completely prevents the formation of any melenin in the coat or the irises of
the eyes, giving a pink-eyed or red-eyed white. It is worth pointing out that human albinos from dark-skinned parents
often show some yellowish or reddish hair and even skin color, but it seems this is not due to granular melenin. c,
therefore, is a form of tyrosinase which cannot act as it is intended to in the formation of melanin. Since c is simply a
non-working form, there may be more than one form of c gene (lots of ways to get something not to work), and there
is some evidence that when two different forms are mated, colored offspring may result.
There are a number of intermediate genes where the mutation apparently produces a partly active form of
tyrosinase. Some C alleles known in other mammals are:P>
C full color, allows full expression of whatever pigment is prescribed by other genes. Most dogs are CC.
cch, chinchilla or silver, when present in double dose removes most or all of the phaeomelanin pigment with
only a slight effect on black pigment. This is named after a small fur-bearing South American rodent called
the chinchilla. Black and silver replacing black and tan, or a wolf-like color without the extra banding (see aw,
above) may also be due to a cchcch genotype. Dogs with very light tan probably are cchcch or something
similar. Liver dogs show lightening even of eumelanin pigment, and the "deadgrass" color of the Chesapeake
Bay Retriever is thought to be due to a bbcchcch genetic makeup. The possibility of other, rufous modifiers
affecting the shade of phaeomelanin pigment needs to be kept in mind, as does the possibility of more than
one form of chinchilla in the dog - rabbits are thought to have three.
ce, extreme dilution, has also been proposed for the dog. This gene may be part of the makeup of some
"white" dog breeds where the white color is due to extreme dilution of tan. The West Highland White Terrier
may be ceceee. A cross to a black and tan breed would be interesting from the point of view of color genetics.
Eyes may be lightened in some species, but this is doubtful in dogs.

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ch, Himalyan, is not known to occur in the dog. In homozygous form, it makes the formation of eumelanin
dependant on the temperature of the skin. Thus a genetically solid black animal will have reduced black on
the extremities (seal brown) and an almost white color on the body. The effect on tan/orange pigment is
confusing - the tan in agouti hairs is removed, but that resulting from the orange gene in cats (not in dogs)
remains intense on the extremities. There is reason to suspect that this gene, as well as some forms of
chinchilla, also affects the organization of the brain, particularly in the neural pathways from the eyes to the
brain. There may be a reason for Siamese cats to be cross-eyed. Eyes are normally blue or pink.
cp, platinum, is optically similar to albino but retains very slight tysonase activity and in the mouse is
described as retaining some luster in the coat as opposed to the pure white seen in albino. Although there is
a total absense of proof one way or the other, I would hypothesize that the white Doberman, with pale blue
eyes and pink nose, is due to a homologous gene.
c, albino, is not known to occur in the dog as a regular part of any breed color, though possible candidates for
mutations to c have been recorded. As mentioned above, the c gene cannot produce working tyrosinase, and
a cc individual cannot produce melanin pigment.
As seen from the above, C is known to have a number of different forms and effects. The usual assumption is that
dogs have at least one mutant allele, cch which when homozygous lightens phaeomelanin (yellow) pigment to
cream and more weakly affects liver and longhaired black. A second proposed allele, ce may be responsible for
further reduction of cream to white in some breeds, or modifying alleles may be responsible for the further lightening
in these cases. While some forms of C modify eye pigment (e.g., blue eyes in Siamese cats) there is little evidence
for this in dogs unless "white" Dobermans are indeed due to a C-locus mutation. Although C appears to be fully
dominant over any of the other alleles, the dominance relationship between the others generally goes in the
direction of more color incompletely dominant over less color, the heterozygote generally resembling but not
necessarily identical to the homozygote with more pigment
D, the dilution series. This, again, is a relatively simple series, containing D (dominant, full pigmentation) and d
(recessive, dilute pigment). In contrast to C, which has its strongest effect on phaeomelanin, or B, which effects only
eumelanin, D affects both eumelanin and phaeomelanin pigment. It is thought to act by causing the clumping of
pigment granules in the hair. Like B, it often affects skin and eye color, and in some breeds dd has been associated
with skin problems. "Maltese blue" is a term often used to describe dd blacks. If a solid liver dog also is dd, the result
is the silvery color seen in Weimararners and known as "fawn" in Dobermans. (In most breeds, fawn refers to ay
yellows.)
While dd acting on black or liver is a part of the genotype of several breeds, dd acting on sable is relatively rare. For
one thing, the action of dd on phaeomelanin has been described as a flattening or dulling of color. The cinnamon
color in Chows is probably due to an ayaydd genotype, but otherwise the combination of dd with phaeomelanin coat
color seems limited to breeds in which color is of little importance (e.g., blue brindle in Whippets.)
Although D is usually described as completely dominant to d, I have seen one blue merle Sheltie bitch who
suggested that this may not always be the case. The black merling patches in this bitch were actually an extremely
dark blue-gray. Other than this she was an excellently colored blue merle. The owner insisted that she was not a
maltese blue, but that she had relatives who were. I suspect that this bitch may have been Dd, with the additional
diluting effect of the merle gene allowing the normally hidden effect of a single dose of d to show through.
E, the extension series. This series is probably the least satisfactory of those generally assumed to exist in the dog.
In most mammals, the E series includes Ed (dominant black), E (normal extension) and e (recessive red or yellow,
and sometimes some intermediate alleles called Japanese brindles. In dogs, this is clearly not the case; breeding
experiments have conclusively proven that dominant black and recessive red are not in the same series. This has
led to dominant black being thrust into the A series, which as already mentioned conflicts with results in other

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mammals.
In this summary, I will give the genes as postulated by Little, followed by a brief discussion of other possible
explanations and a suggestion for matings that might clarify the situation. Note that the question is not in whether
the genes occur, but whether they are in fact alleles in the same gene series. With regard to e and E, recent
sequencing of the e and E genes in dogs show definite homology with those in other species.
Em, mask factor. This gene replaces phaeomelanin (tan) with eumelanin (black) over part of the dog. There is
considerable variation in the area of replacement, probably affected by modifiers but possibly involving more
than one form of Em. At its weakest the mask factor may produce black hair fringing the mouth, or a slightly
smutty muzzle. At its strongest (Belgian Tervuren) most of the head is black, and there is considerable
blackening of chest and legs. The effect of Em shows to its fullest extent on clear sable dogs (ayay), but is
visible on the tan points of black and tan dogs (atat) as well. In its strongest version, it can change a black
and tan to a pseudo-black, with tan so restricted in its distribution that it may not be immediately apparent that
the dog is not black. The occasional "black" puppy produced by two Tervuren parents is probably this type of
black, with two ayatEmEm parents producing an a tatEmEm puppy. A similar but not quite as strong blackening
of the head of a genetic black and tan occurs in German Shepherds.
Ebr, brindle. This gene probably got into the E series by mistaken homology with Japanese brindle, which
behaves quite differently from brindle in the dog. In Japanese brindle, the patchy color is believed to be due to
two alleles of the E series side by side on the same chromosome. Only one can be expressed, and different
parts of the animal will show the expression of different genes. The result is a coat made up of random small
patches of tan and black pigment, rather like a tortoiseshell cat. If a Japanese brindle animal also has the
genes for extensive white spotting, the tan and black pigmented areas tend to become larger and more
compact, similar to what one sees in a calico cat (genetically, a tortoiseshell with white markings.) There is a
canid which might be Japanese brindle with white spotting, the Cape hunting dog, Lycaon pictus. This animal
has a coat which is a rather random patchwork of black, yellow and white. The color has very little similarity to
brindle in the dog.
Brindle in dogs consists of black, vertical stripes on a sable/fawn background, usually rather soft-edged, but
much more regular that a typical Japanese brindle, and showing no tendency for the tan and black patches to
become more distinct in the presense of white spotting genes. Genes that affect eumelanin will affect the dark
stripes, so a bb brindle, for instance, will have brown rather than black stripes. Brindle on a black and tan will
show only in the tan areas, while brindle on a black cannot be distinguished at all. If in fact recessive red (ee)
is in the same series with brindle, it is not possible for brindle (or mask) to occur on an ee dog as one of the E
genes would have to be Ebr (or Em), leaving no room for ee. Little implies that brindle and mask were codominant, with masked brindles being EbrEm, in which case masked brindle could not breed true.
E, normal extension of black, allows the A-series alleles to show through with no masking or brindling. It is
apparently recessive to both Em and Ebr.
e, recessive red, overrides whatever gene is present at the A locus to produce a dog which shows only
phaeomelanin pigment in the coat. Skin and eye color show apparently normal eumelanin, although some ee
dogs appear to show reduced pigment on the nose, especially in winter (snow nose.) A number of breeds
show recessive red as a normal or even breed-wide characteristic - Irish Setters, Golden Retrievers, yellow
Labradors. In a few breeds such as the Cocker Spaniel "reds" may be either ayay or ee, and crossing the two
can produce unexpected blacks. I believe there may be a key in the color of the whiskers, which on my
observations seem to be black in ayay breeds and straw to cream (dilute red) in ee breeds, always assuming
the whisker base sprouts from a pigmented area. Little hypothesized that dogs with both forms of red (a y-ee)
were not viable and would be lost before birth.
The dominance relationships in the Little proposal are not simple. He assumes that E m and Ebr are co-dominant. In

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an ayay dog, then, brindle without a mask could be EbrEbr, EbrE, or Ebre. A masked dog without brindling would be
EmEm, EmE or Eme. A masked brindle would have to have the genotype E mEbr. This assumption makes some
predictions which should be readily testable:
1. Two masked brindles, mated together, should produce appoximately a 1:2:1 ratio of masked fawn to masked
brindle to brindle without masking. In other words, masked brindle should not breed true.
2. A masked brindle could not carry E or e. Thus a masked brindle, bred to sable ayayE- would pass either mask
or brindle. The expectation would be a litter of brindles without masks and masked sables (fawns) without
brindling, but no sables without either mask or brindle and no masked brindles.
3. If a masked brindle is bred to an ee red, the results would depend on the A series genes in the ee red, but
there would be neither ee nor ayay reds with neither masking nor brindling. Some blacks might occur, but if
the puppy had areas of tan pigment, the tan would be either masked or brindled, but never both and never tan
without either mask or brindle.
My impression in talking to breeders of masked brindles is that these predictions are not fulfilled. Possible revisions
of the E series include:
1. Remove Ebr from the E series, instead recognising that in many ways it is closer to tabby (Ta) in the cat
family. This is the gene series responsible for the various stripes, ticking, spots and rosettes seen in both wild
and domestic cats. Granted, the pattern is not the same (striped cats normally have stripes ringing the legs),
but brindle is also a black striping gene which is visible primarily on an ay background. This would leave Em,
E and e in the E series, giving a prediction that Em- bred to ee could produce either 100% masks if the mask
is EmEm, half masks and half sables without masks if the mask is EmE, or half masks and half recessive reds
if the mask is Eme. The one outcome that would be missing is that a masked to recessive red breeding could
produce unmasked sables and unmasked recessive reds in the same litter. Given the difficulty in
distinguishing sables from recessive reds, this might prove difficult.
2. Remove Ebr from the E series, possibly putting it in the same series with dominant black (currently in the A
series.) The new series (here called K - the last letter of black - for convenience) would have three genes, Kd
dominant black, Kbr producing eumelanin stripes on any phaeomelanin (tan) pigment on the dog. The
assumption is that Kd is dominant over Kbr which in turn is dominant over k (more black dominant over less
black.) The prediction would be that a dominant black (Kd-) bred to a clear sable would produce either all
dominant blacks if the black is KdKd, a fifty fifty mix of dominant black and brindle if the black is KdKbr, or a
fifty fifty mix of dominant black and clear unmasked sable if the black is Kdk, but never a litter with all three
colors. Unpublished studies on racing greyhound litters agree with this prediction.
3. Em might still be in the E series, but this should be tested. The test breeding would be difficult, because of the
difficulty in being sure whether a "red" dog is ee or ayay, but the test is whether a masked dog, bred to
another mask or to a recessive red ee, produces both ee red and fully expressed, unmasked tan-point or
sable in the same litter. Probably some cross breeding would be required to be sure of the genotypes of
parents and offspring.
4. If both removals hold up, this would leave the E series with just two alleles, normal expression of the A series
(E -dominant) and recessive red (e - recessive.) It has now been reported in the scientific literature that the
genetic sequence of canine e/E correponds to the E-locus (specifically recessive red) in several other
species (fox, cow, human and mouse.)
G, the graying series. Although only two genes were recognised in this series by Little, this may be a more complex
locus, or genes that affect graying may reside at more than one locus. The effect of G, in single or double dose, is

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the replacement of colored by uncolored hairs as the animal ages, very much like premature graying in human
beings. This gene should be suspected in any breed where a dark puppy pales and washes out with age, and the
paling is due to interspersed white hairs. The gene is almost certainly present in some Poodles, Old English
Sheepdogs, and terriers. The fading may start immediately after birth or after a period of weeks to months has
elapsed, and may go as far as it is going to by the first adult coat or may continue through the animal's lifetime. G
may or may not be the gene involved in the graying of muzzle and over the eyes in aged dogs, or in the lightening of
black to steel blue without interspersed white hairs. This is a series that definitely needs more work.
M, merle. This is another dilution gene, but instead of diluting the whole coat it causes a patchy dilution, with a black
coat becoming gray patched with black. Liver becomes dilute red patched with liver, while sable merles can be
distinguished from sables with varying amounts of difficulty. The merling is reportedly clearly visible at birth, but may
fade to little more than a possible slight mottling of ear tips as an adult. Merling on the tan points of a merled black
and tan is not immediately obvious, either, though it does show if mask factor is present, and may be discernable
under a microscope. Eyes of an Mm dog are sometimes blue or merled (brown and blue segments in the eye.)
Although merle is generally treated as a dominant gene, it is in fact an incomplete dominant or a gene with
intermediate expression. An mm dog is normal color (no merling). A Mm dog is merled. But an MM dog has much
more white than is normal for the breed (almost all white in Shelties) and may have hearing loss, vision problems
including small or missing eyes, and possible infertility (Little). The health effects seem worse if a gene for white
markings is also present. Thus the dachsund, which is normally lacking white markings, has dapples (Mm) and
double dapples (MM) the latter often having considerable white, but according to Little other effects are limited to
smaller than normal eyes. In Shelties, Collies, Border Collies, and Australian Shepherds, all of which normally have
fairly extensive white markings, the MM white has a strong probability of being deaf or blind. The same is probably
true with double merle Foxhounds and double merles from Harlequin Great Danes with the desired white chest. A
few double merles of good quality have been kept and bred from, as a MM double merle to mm black breeding is
the only one that will produce 100% merles.
It is possible that merle is a "fragile" gene, with M having a relatively high probability of mutating back to m. The
observed pattern would then be the result of some clones of melanocytes having suffered such a back mutaion to
mm while they are migrating to their final site in the skin, producing the black patches, while others remained Mm.
This hypothesis also explains why a double merle to black breeding occasionally produces a black puppy, the
proposed back mutation in this case occurring in a germ cell. On the other hand, the observed blacks from this ype
of breeding may actually be cryptic merles - genetically Mm, but with the random black patches covering virtually all
of the coat.
Merle is a part of the pattern of ragged black spots seen in the harlequin Great Dane. There appears to be an
additional gene which removes the dilute pigment, leaving the "blue" area clear white. The fact that harlequins
continue to produce merles argues that animals pure for this proposed extra factor may not exist, and one possibility
is that a homozygote for this whitening factor is an embryonic lethal. Interestingly, there are recent reports of
Shelties born with a harlequin pattern, but in this case the "blue" area actually develops color with time, winding up a
light silvery blue. These dogs appear to have larger than normal black areas, at the extreme being so-called cryptic
merles, that is, no blue is visible without an extensive search. Other shelties born harlequin or "domino" retain the
white body color.
Although Danes are usually solid color, the harlequin color description includes a preference for a white neck and
front. Since the black patching is as apt to be on neck and front as anywhere else, this requires incorporation of a
gene for white spotting (probably irish spotting, si si). Given that SS double merles seem to fare better than their s i si
counterparts, I would expect that double merles from harlequin Danes with patched fronts and necks might be
healthier than from those that fit the standard better. The harlequin description also faults black hairs in the white
area. The harlequin - silver blue pattern in Shelties could be an extreme case of black hairs in the white area. Both
harlequins and the silver-blue merle Shelties have occasional patches of gray (merle?) as well as black, though this

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is not considered desirable.

R, roan. This may or may not be a true series. Both Little and Searle suggest that roan may simply be a very fine
ticking, with dark hairs growing in an initially white area of the coat. A second type of roan, in which white hairs
develop in an initially dark coat, could be due to gray or could be a type of roaning different from the progressive
development of dark hair in a light area. In any event, roan (R) appears to be dominant to non-roan (rr). It is not clear
whether this is full dominance or incomplete dominance. I will here treat roan as being at the ticking locus.
S, white spotting. This is another somewhat unsatisfactory series, and one in which modifying genes appear to have
a very large effect. Certainly there are genes for solid color, for a more regular white spotting, and for basically white
with some colored markings. But the variability within each type makes it unclear how many alleles actually occur at
this locus. In general dominance is incomplete, with more color being dominant over less color. Heterozygotes
commonly resemble the more-pigmented homozygote, but with somewhat more white.
S, solid color. This is the normal gene in breeds without white markings. An SS dog can completely lack
white, but it can also express very minor white markings - white toes, white tail tip, or a star or streak on the
chest. SS breeds generally fault these markings.
si, irish spotting. Irish spotting is generally confined to the neck, the chest, the underbody, the legs and the tail
tip. White does not cross the back between the withers and the tail, though it may appear on the back of the
neck. Breeds with "Collie markings" which breed true for the markings are generally si si.
sp, piebald. This is a more difficult gene to identify. Certainly some breeds, such as parti-color Cockers, seem
to breed true for piebald. Crosses of parti-color and solid in Cockers, however, often have minor white
marking. Piebald and irish spotting seem to overlap in phenotype in one direction, while piebald and extreme
white overlap in the other. In general, it seems a piebald has more than 50% white, white often crosses the
back, and the pattern gives the impression of fairly large colored spots on a white ground.
sw, extreme white piebald. Extreme white piebalds range from the color-headed whites (Collies, Shelties)
which may also have a few colored spots on the body, especially near the tail, through dogs with color
confined to the area around the ear or eye (Sealyham, White Bull Terrier, Great Pynenees) to some pure
whites (Dalmation ideal). There is some anecdotal evidence that swsw dogs without color on or near the ear
have a higher probability of deafness than dogs with color on the ears, but this varies with breed and it is not
known whether a separate allele of S might be involved. In Boxers, some whites are produced from showmarked parents. Little believed that the Boxer lacked the gene for si, the irish-type spotting desired in the
show ring being produced by heterozygosity for S and sw. Since the Boxer club is adamantly opposed to any
breeding of whites, even test breeding, this has not been independantly confirmed.
All of the spotting genes are assumed to be affected by the action of modifiers, with + (plus) modifiers being
generally understood to increase the amount of pigment (decrease white) while - (minus) modifiers being assumed
to decrease the amount of pigment (increase white.) Merle appears to act as a minus modifier, in addition to its
effects on coat color.
It is not clear to what extent the S series affects head pigment. Color-headed white shelties, for instance (s wsw), can
have completely colored heads - not even a forehead star or white nose. On the other hand, relatively conservatively
marked dogs can appear with half white or all white heads. There is probably at least one other gene series that
affects head markings. It is at least possible that the plus and minus modifiers affect head and body markings
simultaneously.
T, ticking. Some dogs develop flecks of color in areas left white by genes in the S series. The clearest and most
obvious ticking is seen in Dalmations, where additional modifier genes have enlarged and rounded the ticks. A large
number of irish, piebald and extreme white breeds also have variable ticking, though not often as obvious as the

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Dalmation. The color of the ticking seems to be the color the coat would be in that area if the white spotting genes
were not present. Thus a genetically black and tan Dalmation (a fault) will have tan spots where a black and tan
would have tan markings. A ticked sable, ayayTT or ayayTt, may not have obvious ticking, becasue there is not much
contrast between the tan and the white. Careful examination, however, will often show tan flecks on the legs. Ticking
on a long-haired dog is also difficult to discern.
The usual dominance relationship given is that T (ticking) is dominant over t (lack of ticking.) Some breed-specific
sources suggest that ticking acts as a recessive. I am inclined to suspect incomplete dominance of T. In Border
Collies, for instance, a color called blue mottle is in fact a very heavily ticked piebald. The dam of the Border Collie
mentioned above was such a blue mottle, presumably TT, while Dot is apparently Tt.
Ticking is also very much affected by genes which modify the size, shape and density of tick marks. In fact roan,
which can develop by the gradual growth of pigmented hair in white areas of the coat, may simply be a form of
ticking.

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