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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. While this site is primarily concerned with Shetland
Sheepdog colors and a long, working-type (double) coat, I will use
comparisons from other breeds and even other species whenever it seems
useful.
References, including other mammalian color genetics, are on a
separate page.
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 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. I've included a page which
defines some
of the terms used in genetics, as well as explaining dominant, recessive
and incompletely dominant genes. 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 As 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 ay dogs include Collies, fawn
Boxers and Great Danes, and some reds (Basenji red is thought to be
ay, for instance.) ay is recessive to As,
but incompletely dominant to at. 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 ay sable, but
other dominance relationships in the series need more investigation.
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 (As)
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 Ay 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:
- 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.
- 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 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 atatEmEm
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
co-dominant, 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 (ay-ee) were not viable and would be lost before
birth.
The dominance relationships in the Little proposal are not simple. He
assumes that Em and Ebr are co-dominant. In 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 EmEbr.
This assumption makes some predictions which should be readily testable:
- 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.
- 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.
- 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:
- 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.
- 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.
- 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.
- 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 (Newton
et al, 2000) 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 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 si 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 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 show-marked
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 (swsw),
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 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
Border Collie
on the front page of my site is ticked and probably sisw,
as well as having the gene(?) for half white head. The tick marks in her
ruff are not visible in the photo, but they are present (if difficult to
find) on the living dog.
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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