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 American Pit Bull Terriers colors and a long,
working-type coat, I will use comparisons from other breeds and
even other species whenever it seems useful.
References,
including other mammalian color genetics.
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 a color which has become
very popular among contemporary pit-bull owners. 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.
1.
The as series
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.
2.
Ay in the absence 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.
3.
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.
4.
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 Doberman 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.
5.
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 Doberman
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:
1.
C
full
color, allows full expression of whatever pigment is prescribed by
other genes. Most dogs are CC.
2.
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.
3.
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.
4.
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.
5.
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.
6.
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.
7.
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.
1.
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.
2.
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.)
3.
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.
4.
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.)
5.
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:
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 (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. G for sure is the freak gene
that has caused a lot of negativity in the ADBA organization.
While at the same time the G has received wide acceptance and a
lot of popularity within the UKC organization. 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.
1.
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.
2.
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.
3.
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.
4.
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.
Oklahoma Bib Blue
Pits
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