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Standard Accepted Coat Color Genetics in Dogs
Below is an outline of the current understanding of coat color genetics in the domestic dog. As this was written specifically for the Great Dane breeder, the focus is on the needs of that breed, so comments are made to our needs, & the "Present in the Great Dane" portion of each secetion is the non-technical section meant for Dane breeders specifically. However the below has at least an outline of the real knowledge of coat color genetics in the dog generally (so many breeder websites are decades out of date) & all current research is noted.
For more on the latest on general information on coat color alleles in dogs, see Sheila Schmutz's Coat Color Alleles in Dogs. Also see the Canine Coat Color Genetics Info section at this website. Listed here are a few _ACCURATE_ articles for various breeds. Do be aware the majority of material presented on the Web is outdated and/or inaccurate, plus is often written by the inexpert, and can be motivated by personal bias as well.
Recommended reading: GENES AFFECTING COAT COLOR IN DOMESTIC DOGS: A REVIEW. SM Schmutz & TG Berryere. Animal Genetics, 2 August 2007: 38, 539-549.
To see a nice diagram of the pigmentation pathway, click here.
Most recent updates are noted in red.
1. BASIC COLORS
ASIP (LOCUS A=Agouti): A "pattern" locus that allows for the increasing
distribution of dark (black or brown, i.e eumelanin) pigment over yellow/red (phaeomelanin) in a recessive manner.
Contains 4 know alleles with general dominance established from yellow to black. (Note "Dominant Black"
has been removed to its own locus "K"--see below):
a^y = restricts dark pigment distribution; produces fawn/sable.
a^w = agouti "wild-type" allele: gives wolf-grey coloration. Also called a^g.
a^t = tan point allele: gives bicolored animal; dark body with tan points.
a^b=recessive black (present in some breeds).
All Danes are a^y homozygotes, regardless of coat color-- but for the rarely reported a^t animal--so the locus is essentially fixed in our breed. Recent work has established that there is a recessive black here and there is not a dominant black at this locus. (Hered 2003 Jan: 94(1):75-79 " Exclusion of Melanocortin-1 Receptor (Mc1r) and Agouti as Candidates for Dominant Black in Dogs." Kerns JA, Olivier M, Lust G, Barsh GS.) The notion of a saddle allele isn't established. For more on this topic, see Sue Bowling's site and Sheila Schmutz's website for the latest updates.
CBD103 (LOCUS K=Dominant BLACK): Dominant produces self-colored dog of eumelanin
pigment, recessives produce brindle and allows for fawn (& other ASIP alleles).
K(^bk) = dominant black (eumelanin) allele.
k^br=intermediate "brindle" allele.
k^f=recessive (phaeomelanin expression) allele.
All three alleles are present in Great Dane: All but fawn and brindle have at least one K dominant. All brindles have at least one k^br intermediate. All fawns are recessive homozgyotes: <k/k> ( i.e. the alleles at agouti and MC1R then direct the phenotype). Dominant black was formerly thought A' or A^s = a dominant at agouti that allowed for a self-colored dog (full body distribution of dark pigment). Fawn was considered "recessive" at agouti & brindle was thought to reside elsewhere (usually ascribed to the E locus). This is now clearly documented to NOT be the case. However fawn is still recessive to brindle (in fact just so), and brindle is recessive to black, but dominant over fawn. So no large practical change here for breeders, but this does mean that brindles can be homozygous for both brindling and masking, given mask is at "E" locus (MC1R) and brindle a recessive at DomBlk. Note fawns are fawns not because they are "fawn" at agouti, ALL Danes (with rare tan-point exceptions) have the same alleles (and are homozygous) at agouti.
The difference between a solid dark coat, and the patterns of brindle and fawn, resides here at the K locus. The gene involved here is a new one (see link for more info), and is a mutation from a gene normally involved in innate immunity, so interesting a mutation in dogs causing a coat color change. Recent publication: A beta-defensin mutation causes black coat color in domestic dogs. Candille, et al. Science 10-18-2007 (see at Science Express).
See Sheila Schumtz' very reader-friendly page on this gene specifically by clicking here.
MC1R (LOCUS E=Extension): restricts location of dark pigment.
Contains 3 alleles.
E^m =melanistic masking.
E = allows for self colored dog/action of alleles of A & K Loci.
e = restricts pigment to red/yellow (no dark pigment can form).
Most Danes have at least one E^m allele for masking. All Danes have either E or E^m: the recessive <e> doesn't appear to exist in the breed. Recent (2002) data has apparently confirmed the presence of masking at the E Locus. Brindling was once conjectured to be at this locus, however has been removed to the K locus. In 2003 Sheila Schmutz at U Saskatchewan offered evidence to place brindling at another locus (S. M. Schmutz, T. G. Berryere, N. M. Ellinwood, J. A. Kerns, and G. S. Barsh, MC1R Studies in Dogs With Melanistic Mask or Brindle Patterns J Hered 2003 94: 69-73.).
You can now test for the presence of all alleles at the E Locus. See Healthgene.
TYRP1 (LOCUS B: Brown recessive): allows for black & brown (also
called chocolate/liver) phenotypes.
Affects skin/eye color simultaneously. Contains 2 "functional" alleles (dominant/recessive pairing).
B = forms black pigment.
b = forms brown/liver/chocolate pigment (apparently new research indicates there are at least 3 <b> recessives
but all produce a brown that is phenotypically indistinquishable).
NOTE: Affects skin/hair color simultaneously (nose is brown).
Most all Great Danes are BB homozygotes. The rare <bb> brown (called chocolate) Dane is recorded, so some form of the brown recessive exists in some Danes/bloodlines. Dogs who are <bb> must have brown (not black) noses, eyerims & pads. Reduction in eye (iris) color intensity/depth is noted. These brown dogs are, quite literally, bleached in pigment at the molecular level ( as eumelanin is left unprotected from hydrogen peroxide). "Red" danes mentioned in early history/pedigrees/standards may have been this sort of bb "liver" red (called in the early stud books "rot"as opposed to fawn, which is called "gelb"). "Chocolate" (liver) danes have been noted both historically ("braun"?) & currently are occassionally still seen. See Jane Chopson's article of this title for more info on the topic, as well as the article on the Drapp Dane. Brown is a common color in dogs; some breeds are specifically and only brown in fact.
You can now test for the presence the recessive alleles. See Healthgene.
2. DILUTED COLORS
MLPH (LOCUS D=dilution): produces dilution of black to slate (blue/grey/maltese).
Affects skin/eye color simultaneously. Contains 2 "functional" alleles (dominant/recessive pairing).
D = allows for black pigment to form.
d = produces blue/slate/grey dilution (there are more than one form of mutation for this recessive, but, again,
the phenotype for all the recessive alleles appears the same, a dull sort of gunmetal gray called blue in the Great
Dane).
NOTE: Affects skin/hair color simultaneously (nose is slate).
Present in Great Danes: D = all animals with black pigment. d = all blues/animals with blue markings/without black pigment are recessive homozygous at this locus. All <dd> have non-black (gray, slate, etc.) nose, eye rims & pads. Reduction in eye (iris) color is also noted. Dr. Sheila Schmutz isolated the gene involved (MLPH) in the blue dilution. See her website for more information: http://skyway.usask.ca/~schmutz/dilutions.html
**bbdd-The Drapp-colored dane: This odd color, sometimes called "lilac" in Danes, occurs when both brown and blue recessives are simultaneously present it would seem. The color has many names: isabella, for example, and is called in Dobermans "fawn" & is the same color of all Wiemaraners. Perhaps more properly referred to as dilute chocolate, blue-liver or double dilute, this is the most likely candidate for the odd color referred to as "Drapp" in early discussions of the dane. The other likely explanation for this "drapp" ( a lilac color or cafe-au-lait brown with flesh-pink nose) is some other form of "double dilute."
You can now test for the presence of the Maltese or blue recessive alleles. See Healthgene.
OTHER DILUTES:
LOCUS C=Chinchilla: affects depth of red/yellow pigment especially--may dilute both melanins.
Contains 2 described alleles (dominant/recessive).
C = allows for full depth of red/yellow pigment.
c^ch = reduces depth of pigment: produces washy or pale yellow coats. Present in Great Danes: C = standard calls
for homozygosity. The recessive c^ch may be present in some fawns/brindles: "washy" coat color may be
explained by this locus (see "I" below for another possible explanation). Other alleles have been conjectured
for this locus, but any evidence to date is lacking.
LOCUS I: dilutes phaeomelanin (red/yelow becomes cream/white).
Contains 2 proposed alleles. I = dominant
for normal intensity of coat.
i = recessive results in reduced intensity of coat.
Present in Great Dane: unknown; this may be similar to the old idea of a "rufous" or "mahogany"
gene.
LOCUS P: dilutes both melanins.
Contains 2 proposed alleles. P = dominant
allows for normal density of pigment.
g = recessive results in paling of coat.
Present in Great Dane: unknown. The locus is likely irrelevant to Danes.
LOCUS G: produces incremental greying of eumelanin pigment
as animal ages.
Contains 2 alleles. G = dominant greying/paling
allele
g = recessive allows for normal pigmentation to be maintained (no greying). Present in Great Dane: unknown, but
the phenomenon of "Kerry Blue" greying doesn't appear in the breed. The locus is likely irrelevant to
Danes.
3. WHITE MARKINGS
2007 UPDATE: MITF (S LOCUS: Random Spotting): Extensive white markings produced by the recessive found here. Traditional thought has placed four alleles together at the S locus, with solid and more heavily pigmented dogs dominant over those with more white; incomplete/codominance appears to occur between alleles. "Modifiers" independently inherited from the main locus are traditionally thought to explain the variations between distinct alleles, but currently the evidence demonstrates a dominant that allows for body pigment and a recessive gene that results in a predominantly white dog with a random spotting pattern are all that exist here (note the heterozygote appearing from "mismarked black" to Mantle (boston) in breed parlance presents a third phenotype & is a "hybrid" sort of show mark at times). So it appears that the "spotting locus," Little S locus, is actually a simple codominant, meaning one gene with two alleles produces three distinct phenotypes: solid, colored with white trim, and predominately white with some patches of color.
To read about new updates on advances in MITF, click here.
S = allows for self-colored dog with no more than 10% body white confined to the toes and chest when full extension
of white.
s = "piebald pattern" or "random spotting: produces a wide range of variation in color percentage
& location of pigmented areas.
NOTE THERE ARE THREE DISTINCT PHENOTYPES PRODUCED BY THESE 2 GENES because the heterozygote is different than either homozygote: (1) SOLID (self-colored) DOGS are <SS> dominant homozygotes, (2) PIEBALD (mostly white) DOGS are <ss> recessive homozygotes, and (3) the heterozygote <Ss> dog presents in pattern as a Mantle and is Little's "PSEUDO-IRISH" dog.
Homozygous <SS> self-colored dogs are our normal fawn, brindle, blue & black dogs. If there is any white on them, that white will be limited to very small markings on the chest and toes. (There will NOT be extensive white in the throat and belly area, or on the head and actual feet.) SS dogs can range from solid with no white to these small white markings **SO THERE IS NO DIFFERENCE** in their spotting inheritance. It is considered a random event, NOT controlled by genes, as to how much white is left on a solid dog. It's worth noting that pigment continues to fill in (spread) in puppies until at least 3 month, so the amount of white seen at birth is likely to decrease.
Heterozygous <Ss> dogs will have more white that the solid <SS> dog but less than the <ss> homozygous recessive: they will appear to Dane people as a solid dog with white markings--in black from what is called by Americans now "mismarked black" ("harlequin black) to the Boston or Mantle pattern.
Homozygous <ss> (random spotting) dogs appear as pinto, piebald, particolored or color-headed. Heterozygotes are strongly pigmented with restricted white markings & cannot always be visually distinguished from dogs who have white trim (i.e. the Mantle pattern) via another gene. Random (piebald) spotting is reported to be less symmetrical than Tuxedo/Trim (true Mantle pattern). Piebald heterozygotes were called by Little "pseudo-Irish" dogs. Piebald or random spotting in the Great Dane contributes to the loss of show marked puppies and can increase the number of deaf puppies, so has undesirable consequences potentially for our breed. MITF or Microphthalmia Transcription Factor is a late acting gene in the pigmentation pathway that modifies the expression of genes in the tyrosinase cascade. For more on this issue see the references here.
Present in the Great Dane: In all but dogs from a Harlequin/Mantle family background, this gene is irrelevant. In Harlequins and Mantles only SOME families and only SOME dogs bear the recessive here for piebald or random spotting. For despite the still commonly held idea (from the old "Little" system), that the "S locus" was reported to contain 4 alleles (that "blended" together in various ways), for some time ongoing research has clearly shown that only one recessive is here, and this is for *random spotting*--what is typically called the "piebald gene". Only this "piebald gene" (& only one piebald allele) actually exists here as a recessive to allow for white markings on the dog. And, again, the only way a dog can be correctly marked when this gene is present is in the Ss heterozygote, and that sort of "Mantle" (or Harl) can never breed true, and will continue to produce a large number of mismarked offspring. And the piebald recessive can increase also the number of defective pups (which is NOT to say the average "boston head" is obviously deaf to the owner, but that this gene is generally associated with the massive loss of pigment that produces deafness in any & all breeds with which it's associated, and in Danes it's normally the merlikins and harl-heads that consequently suffer). And unless and until claims that piebalds are "normal" are substantiated in our breed with actual proof (using CERF & BAER) we anyway have to assume our breed, like all other breeds that share this gene, have a lot of otherwise undetected abnormal dogs, many of which pass on their defects in sometimes even more major aspects. After all, every breed testing has found that "undetected" deafness, for example, increases the actual rate of defect 2-4 fold. So the take home message is this is an undesirable recessive in our breed.
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The gene that consistently produces the pattern called "irish" (our Mantle or Boston--where there is a "tuxedo" like set of markings, with white undersides or white "trim" on a dog consistently seen), is apparently produced by a completely seperate gene at a different location (i.e. independently sorting: on another chromosome).This is already proven as some fully collared Mantle Danes do NOT have the piebald gene. This is the gene Mantle and Harlequin breeds wish to cultivate, as it is the one that produces consistently a line of dogs that are always colored with white trim (i.e. boston-marked, "show" marked typically). But since the two alleles (solid and piebald) here at MITF are codominant, the SINE heterozgyote can appear as a Mantle in phenotype (as with "flashy" Boxers), thus causing some well-documented confusion between how a dog looks and how a dog breeds. For those for whom this is hard to digest, THE POINT HERE is to move on from using piebalds to the correctly marked offspring that are only piebald carriers, and from there to avoid breeding carriers to each other whenever possible, to move away from a gene that detracts from fully achieving the breed standard. To read about piebaldism in Danes, click here. To see more of this gene, look to the many links in every breed from Dalmatian to White Bull Terrier and Colored-Head Collies and so forth that are posted at the two sections devoted to coat color at the ChromaLinx.
TO See Diagrams & Descriptions of Various Harlequin Family Dogs, CLICK HERE.
Locus W/H: (Bagala 1966/Sponenberg 1985) Proposed dominant white/harl locus that produces the harl pattern when the M allele is present: "takes the mid-range (grey) pigment to white." Merles would not carry this allele and would therefore be unable to produce Harlequins without an "H-factored" partner: Harlequins would be MmHh and merle Mmhh. Conjectured to be lethal in all iterations when homozygotic while producing only a change in base coat in the heterozygote. See Neil O'Sullivan's notes and Jane Chopson's diagrams for more on the "Sponenberg Hypothesis." Other theories could account for the variation from Harlequin to merle. Little suggested harls and merles are both Mm dogs and the variation from "clean" to "grey" background is simply phenotypic variation and/or results from the action of S Locus modifiers/synergy (Little 1955). Other authors have suggested there is more than one merle gene and the interactions thus produce the Harlequin (see Willis 1989). If "modifiers" of some sort interact with the M Locus, as has been proposed for the S locus, these could account for the variations seen in harl & merle coloration (Yousha 1995). Currently there is no molecular data available and several theories to account for the phenonemon seen. However it appears that it _IS_ the case that Harlequin is a modification of merle, and the convention of treating the Harlequin as a "double heterozygote" (HhMm dog) seems an effective rule to use when breeding. Research is ongoing to find this gene. See below for more discussion; will be<G>less when more in known!
Click here for the preliminary paper on the harlequin gene was published
in summer of 2008: Research is ongoing.
THIS GENE IS HISTORICALLY CONSIDERED UNIQUE TO THE GREAT DANE & IS ONLY FOUND IN THE HARLEQUIN COLOR FAMILY: Since merles are routinely produced from Harlequins, theories predicated on notions of merles being one heterozygote and Harlequins another (i.e. Mm vs. M^hm) would seem to founder. So some sort of "multi-gene" theory seems in order to explain the Harlequin as a merle variant. The problem of explanation is two-fold: first to explain the variation from Harlequin to merle, then to explain the variance in pattern seen within each variant. A notion of "modifier" or multiple gene interaction has been used to explain both phenomenon simultaneously. The Sponenberg Hypothesis takes the approach that the Harlequin is a dual heterozygote with one single gene altering the merle to a Harlequin. This theory resulted from work within the breed and seems the currently prevailing notion and has the advantage of being easy to work to outline and work with and even if more genes are involved could act as a sort of short-hand to understanding the merle-harl continuum. Note this hyopthesis conjectures that HH is uniform lethal which requires a minimal reduction in litter size of 25%, regardless of the phenotype of the Dane involved (i.e. a mantle, black or even fawn, blue, etc.--any Dane--when carrying H would produce embrionic lethals when bred to another H carrier). Where merle itself is involved (with or without Harlequin present), data to date does suggest some losses in embryo in all merle-related breedings.Note this also implies that blacks and mantles (arguably any Dane but a merle) could contribute to the production of Harlequin. Thus "harlequin blacks" could contribute unequally to the production of harlequins: i.e. a mmHh blacks COULD produce harls off a Mmhh merle, in theory, for example, as well as increase the production of harls (MmHh x mmHh) over that of a mmhh (non "Harl-factored") boston-black. More specifics will likely require a molecular approach to the problem of merle/harl coloration.
TO See Diagrams & Descriptions of Various Harlequin Family Dogs, CLICK HERE.
SILV=PMEL17 (LOCUS M=merle): the so-called "merle" or "dominant white" locus which causes a reduction in allowed pigment. Merle is a pleiotrophic gene, meaning it affects more than one trait simultaneously. So not only does merle reduce the pigment in haircoat, skin, eyes, etc. it also typically (adversely) affects sensory organs, other neurological function and apparenly reproductive capacities at times as well. So in its effects at least it is related to other such dominant white spotting loci common in mammals (e.g. von Waardenburg's Syndrome) that cause deafness and other deformatives. Merle is a codominant, meaning this one gene with two alleles produces three distinct phenotypes: non-merle, normal merle (the heterozygote) and white merle (the homozygote which is commonly defective). The merle gene produces a characteristic increase in white areas & in areas of reduced pigment, with patches of mid-tone and full pigment in the heterozygote typically, with the homozygote usually being mostly white (at least in the Great Dane breed). Most all white merles are deaf and many have MOD (merle ocular dysgenesis)--various eye defects. An increase in fetal death rate for the MM (homozygous) dogs has been reported to reach even 50%, and the surviving pups generally do suffer from sensory & other anomalies. The gene is found in only a small handful of breeds therefore (most breeds have discriminated against it strongly), and the breeds where it is present attempt to control the breeding of it to reduce/avoid defects. Merle produces dogs called dapples, blue & red merles, leopards, etc. and it is now understood that merle is necessary to produce Harlequins. Harlequins essentially are a "dominant modification" of normal (Mm) merle, in that the Harlequin gene acts on the merle gene to produce the Harlequin coat pattern, so the Harlequin, in Neil O'Sullivan's eloquent phrase is a "double heterozygote (HhMm)."
Contains 2 alleles.
M = merling/dappling/patching with increase in white/mid-tone areas.
m = non-merling allele.
NOTE THERE ARE THREE DISTINCT PHENOTYPES PRODUCED BY THESE 2 GENES because the heterozygote is different than either homozygote: (1) SOLID (non-merle) DOGS are <mm> recessive homozygotes, (2) MERLIKIN OR WHITE (double-dilute) DOGS are <MM> dominant homozygotes, and (3) the heterozygote <Mms> merle dog presents as a dog with a largely diluted coat (typically a mouse (greyish-brown) in the Dane) that appears as a patched or dappled pattern when the Harlequin gene is absent, and as the Harlequin phenotype when the Harlequin gene is present.
You can now test for the presence of the merle gene: Click on this link for more information on the details of PMEL17.
Present in Great Danes: M & m--the gene is codominant with the heterozgote having an intermediary phenotype. The merle allele is only present typically in the Harlequin family; all normal Harlequins & Merles are heteroygous (Mm);"whites" (including merlikin & some "lightly marked" harlequins) are MM homozygotes (white in the coat predominates). MM homozygotes are usually deaf, and may have eye & reproductive (other) anomalies. Some (>50%?) MM embryos may be non viable. Note MM "white" Danes may be difficult to distinguish at times (phenotypically) from piebald dogs (including "harl-heads). Merle is a dominant gene of this pair & typically produces a phenotype obvious to the eye. The m (non-merle) recessive is exclusively present in all but certain Harlequin family Danes. Fawns, brindles, blues, blacks are all homozygous recessive (blacks include Mantles ("bostons"), piebalds, boston-heads, head-n-tail spot dogs (i.e. colour-headed dog) from harl/merle breedings. Merles (normal merles) and normal Harlequins are Mm heterozygotes. Predominately white dogs, especially those lacking head color are typically MM homozygotes; some Hh "Harlequins" are actually homozygous merles ("whites" in breeder terms) that carry also a Harl gene. This same phenomenon appears in piebald recessive homozygotes, where the "Harlequin" is an animal with the harl gene, but is not typically an animal with the Harlequin pattern as described under the standard.
In both cases such animals are excessively white according to the breed requirements and obviously also carry an increased risk of having and producing sensory defects. The so-called "merlikin" is a dog ironically without a harl gene usually, being either a piebald merle <Mmhhss> or a white (homozygous) merle <MMhh>. Animals that are excessively white (more than 70-75%) would benefit from being tested for the presence of the merle gene. And it is worth noting that some MM white merles can have up to 50% pigmentation, so testing for merle homozygosity might be wise in all cases where the animal is predominantely gray and white in at least a 50/50 ratio. Harlequins do NOT suffer from merle defects unless combined with piebald genes. Note that many dogs described as harlequins are not genetic harlequins (i.e. "lightly marked" harlequins that are genetic piebalds and/or white merle homozygotes), so for the mostly white Dane it has to be assumed the dog is at high risk for having and producing defects. BUT normal "gray" merles and harlequins with extensive black patches are not going to have defects associated with loss of pigment and merling.
TO See Diagrams & Descriptions of Various Harlequin Family Dogs, CLICK HERE.
LOCUS T: Pattern locus. "ticking locus" produces pigment spots on areas of white coat color.
Contains 2 alleles.
T = dominant Ticking allele
t = recessive non-ticking
Present in Great Danes: only recessive t reported.
Ticking appears in the first week of life: typical breeds are the Dalmation (swswTT) & the ACD (sp/swTT). The
"ticking" or rather salt-and-pepper background on harls that is less prefered to a pure white base coat
is not likely caused by the ticking allele. Perhaps it is simply a product of pigment cell migration & so possibly
an after effect of the documented instability of color in merle & harl dogs? It certainly doesn't follow the
typical phenomena documented for ticking in any case.
Locus R: proposed roaning locus with possible dominant action.
2 alleles. Not reported in Great Danes.
Roaning is reported as separated from ticking as it seems to increase pigment slowly over the life of the dog,
"filling in" areas of white with pigmented hairs. If it's action were to be considered as recessive,
(or ?), it could possibly be employed to explain the phenomena of increased pigmentation that is characteristic
of members of the harl family but it's not reported in the breed. See ticking & T Locus above.
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EXAMPLES OF GENOTYPES OF STANDARD COLORS:
(dashes - represent unknown second allele, as dominant allele is present & the animal may be homo- or heterozygous
at this locus--this uses standard accepted theory and ignores potential problem areas simply for clarity. Parenthesis
indicate significant alleles in genotype as to breed's basic breeding phenotypes.
Fawn: A-B-C-D-E^m-(k^f/k^f)ggmmppSSttww
Brindle: A-B-C-D-E^m-(k^br-k^br)mmppSSttww
Black: A-B-C-D-E-K-mmppSSttww
Blue: A-B-C-(dd) E-K-mmppSSttww
Variations in genotype are possible, where recessives such as b=blue are carried by heterozygotes & will only
be expressed in phenotype as a result of a hetero x hetero mating which will produce, statistically 25% offspring
with the recessive phenotype. For example: Black (A-B-C-DdEEmmppSStt) x Black (same) produce 25% dd= blue offspring;
the same applies to blacks producing chocolates, irish/piebalds, fawns & brindles, and fawns/brindles producing
blue/chocolate masks/stripes and irish/piebalds. Note Black can "hide" all the other acceptable, as well
as some unacceptable colors & appear solid black.
TO See Diagrams & Descriptions of Various Harlequin
Family Dogs, CLICK HERE.
Harlequin: A-B-C-D-E-K-MmS/- (Mantle gene?)ttHh
Merle: A-B-C-D-E-K-MmS/- (Mantle gene?)tthh
Mantle: A-B-C-D-E-K-mmS/-(Mantle gene?)H/or/h?
White: "double-merle/dominant white/white merle" = A-B-C-D-E-K-MMS/-(Mantle gene?)-(hh or Hh). Dominant-whites which are "harl-factored" could produce harls; dogs that carry a different set of modifiers and no would be unable to produce harls. Phenotype, however, would appear (nearly?) identical, however the "harl-factored" white is less likely to survive.
White: "hybrid white" or "piebald harlequin" = A-B-C-D-E-K-Mmss(Hh). This is essentially an undermarked (overly white) harlequin, just as the piebald white described below is an undermarked Mantle. Such animals will contribute to the production of mismarked (i.e. white bodied, colour-headed dogs).
White: "piebald/recessive-white/colored-headed white" = A-B-C-D-E-Kmmsswhh. These whites cannot
contribute to the production of harl/merle offspring; but will contribute, recessively, to the extension of white
and the lack of body markings.
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EXAMPLES OF 'TYPICAL HARL-TYPE BREEDINGS:
(Black includes all black and black & white offspring: mismark/Mantle=boston/piebald/boston-
head=extreme piebalds) (White progeny is restricted to MM "double-merle/dominant" whites).
harl x harl = 16.6% merle(Mm), 25% black(mm), 25% white(MM) & 33.3% harl(MmHh)
(as whites have reduced viability, some of these embryos die, giving a smaller percentage of whites born).
harl x black = 16.6% merle, 50% black, 33.3% harl (no MM whites are possible).
white (MM) x black (mm) - all merles &/or harls (assuming white is fertile)
harl x merle = 25% of each four colors: white, merle, black, harl.
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PROBLEMS ASSOCIATED WITH HARLEQUIN BREEDING: (problems that do not generally afflict the other colors in the
Great Dane breed)
1. Harlequins, being heterozygotes, cannot breed true; i.e. cannot reproduce themselves consistency in either
phenotype or genotype.
2. There is a loss of possible progeny due to MM and/or HH reduced viability.
3. There is considerable difficulty in controlling the color patterning & the amount of pigment even when correctly
marked individuals are consistently bred to each other; so multiple incorrectly marked puppies therefore are born
in most all litters, resulting in a reduced number of show/breed stock to select otherwise correct/superior individuals;
high number of pets-by-markings produced..
4. Remaining well-marked animals may lack for breed type, conformation & soundness, so breeding choices and
even quality can be starkly reduced when trying to assemble suitable breeding stock.
5. The genotype of the various near-white individuals cannot be determined necessarily on phenotype; test breedings
may have to be performed to determine genotype, (if these animals are kept for potential breeding stock, rather
than culled): which requires raising & rearing mismarks which may prove useless for breed improvement.
6. All near-white & white individuals should be checked for hearing & eye anomalies if not euthanized at
birth as defects are to be expected in the majority of animals. Also animals with such defects may contribute to
a rise in defective offspring.
7. Modifiers/other undefined genes inherited independently of recessive spotting (S locus) and dominant spotting
(M/H loci) may affect the resulting phenotype and may prove hard to control. Currently it's considered that all
these white spotting loci are incompletely dominant and may well interact, leading to unpredictable pattern variations
in offspring & mismarks born routinely to even correctly marked stock.
8. All stud contract/co-ownerships must be carefully read & agreement of which color-type individuals will
be euthanized at birth/how all mis-marks must be handled (e.g. how culled, euthanized, limited registration, spay/neuter
contracts) must be settled between attendant parties given the ethical dilemmas inherent in this situation.
9. It is not uncommon for litters to include only 1 or 2 correctly marked Harlequin offspring. Further, many of
the (now acceptable) Mantle offspring may be poorly marked or poorly made for consideration as breeding stock.
Successive litters therefor may contain no correctly marked offspring,or the correctly marked offspring present
may be the least adequate in all other breed features. The sex desired in also often unavailable in the desired
color pattern.The result is few animals of breeding quality being available. So breeding appropriately becomes
a certain challenge indeed. Since the serious fancier can easily find the opportunity (such as with fawns producing
~8 pups to choose from in every litter) to more reliably select and breed suitable Great Dane breeding stock, there
is little long-term, educated and sustained interest in breeding Harlequins, given the constraints.
10. After careful consideration, most breeders interested in consistently producing quality stock turn to one of
the other acceptable colors in Great Danes, where this is more likely to be a reality. This, combined with the
low number of animals acceptable as breeding stock means there is a reduced gene-pool in the harlequin family.
The color unfortunately attracts many novices who are unable/unwilling(?) to learn enough about the breed &
the harl variant to produce correct specimens, or simply abandon the color after some poor breeding results. Given
the internal constraints of breeding Harlequins also there is a supply and demand problem naturally met by many
rather unsavory or simply opportunity-motivated individuals who exploit the novelty of the color and it's "rarity"
to produce entire lines specifically for sale to a ready market. An added burden for the Harlequinn breeder who
must judiciously (even zealously) screen to avoid homes who are more interested in owning "the spots"
than the breed And limited registrations/spay and neuter options must be rigorously enforced to avoid "spawning"
situations where more poor-quality 'spotted' Danes are ultimately bred. Ultimately a few knowledgeable, dedicated
individuals with a flair for genetics, a good eye for a dog & a gambler's heart carry the Harlequin variant
through history. (Many more who are mating harl-bred routinely and profitably selling these dogs know only enough
about the variant to be dangerous to the breed IMO.)
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This message prepared by JP YOUSHA (1995; updated 2001, 2003, 2005,6,7) for educational purposes & permission
is given to disseminate this message for that purpose & that purpose only. All copyrights & authors' rights
are to be respected. For further information contact: jpy@chromadane.com
