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.

• A^s 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 A^s 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.
• a^y 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 a^y 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 a^y, for instance.) a^y is recessive to A^s, but incompletely dominant to a^t. That is, an a^ya^t dog is on average darker (more black hairs) than an a^ya^y dog, but the difference is generally within the range of color for a^ya^y within the breed.
• a^t, 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.
• a^w 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," a^sa. It seems recessive to a^y 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 (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 (a^ta^tbb), 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 (bbc^chc^ch) 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.
• c^ch, 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 a^w, above) may also be due to a c^chc^ch genotype. Dogs with very light tan probably are c^chc^ch 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 bbc^chc^ch 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.
• c^e, 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 c^ec^eee. 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.
• c^h, 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.
• c^p, 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, c^ch which when homozygous lightens phaeomelanin (yellow) pigment to cream and more weakly affects liver and longhaired black. A second proposed allele, c^e 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 a^y 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 a^ya^ydd 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 E^d (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.

• E^m, 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 E^m. 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 E^m shows to its fullest extent on clear sable dogs (a^ya^y), but is visible on the tan points of black and tan dogs (a^ta^t) 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 a^ya^tE^mE^m parents producing an a^ta^tE^mE^m puppy. A similar but not quite as strong blackening of the head of a genetic black and tan occurs in German Shepherds.
• E^br, 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 E^br (or E^m), leaving no room for ee. Little implies that brindle and mask were co-dominant, with masked brindles being E^brE^m, 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 E^m and E^br.
• 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 a^ya^y 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 a^ya^y 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 E^br are co-dominant. In an a^ya^y dog, then, brindle without a mask could be E^brE^br, E^brE, or E^bre. A masked dog without brindling would be E^mE^m, E^mE or E^me. A masked brindle would have to have the genotype E^mE^br. 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 a^ya^yE- 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 a^ya^y 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 E^br 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 a^y background. This would leave E^m, E and e in the E series, giving a prediction that E^m- bred to ee could produce either 100% masks if the mask is E^mE^m, half masks and half sables without masks if the mask is E^mE, or half masks and half recessive reds if the mask is E^me. 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 E^br 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, K^d dominant black, K^br producing eumelanin stripes on any phaeomelanin (tan) pigment on the dog. The assumption is that K^d is dominant over K^br which in turn is dominant over k (more black dominant over less black.) The prediction would be that a dominant black (K^d-) bred to a clear sable would produce either all dominant blacks if the black is K^dK^d, a fifty fifty mix of dominant black and brindle if the black is K^dK^br, or a fifty fifty mix of dominant black and clear unmasked sable if the black is K^dk, but never a litter with all three colors. Unpublished studies on racing greyhound litters agree with this prediction.
3. E^m 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 a^ya^y, 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. 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.
• s^p, 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.
• s^w, 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 s^ws^w 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 s^w. 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^ws^w), 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, a^ya^yTT or a^ya^yTt, 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 sⁱs^w, 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.

http://bowlingsite.mcf.com/genetics/ColorGen.html#D