PIEBALD ("ink spot" color pattern)

All topics pertaining to health and diseases that may affect your Tamaskan Dog, as well as treatment.
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PIEBALD ("ink spot" color pattern)

Post by Sylvaen » Sat Aug 11, 2012 4:10 pm

Lately more and more 'piebald' dogs - stemming from ancestors that also appear in Tamaskan bloodlines - are coming to light.

http://homepage.usask.ca/~schmutz/dogspots.html#Spotted

Since this color pattern (white spotting: sp/sp) is considered a serious 'fault' according to the Tamaskan breed standard it would be a good idea to share information about piebald dogs that have been produced, with at least one shared ancestor (Utonagan, Northern Inuit, CED, etc) in common with any Tamaskan bloodline so that we can track where these genes are coming from, and where they might next show up as a result of combining particular bloodlines.

Please post photos of individual dogs in this thread, along with known details (such as: call name, registered name, date of birth, sire and dam, etc)... by sharing this information we can put 'markers' on potential carriers (in the Tamaskan database) so that breeders can make informed decisions about which combinations might result in piebald puppies.

HEALTH ISSUES: extreme white piebald (in which the body is almost entirely white with just a couple of small color patches) can be associated with congenital deafness. So long as the area around the head/ears has patches of color, the dog should have normal hearing. If one side of the head (or the whole head) is white then the dog can be deaf on that side or on both sides... BAER hearing testing at 6-8 weeks old can determine if a puppy has normal hearing or not. [Note: recessive red (cream/white: ee) is not associated with congenital deafness.]
http://www.lsu.edu/deafness/Tufts.htm
http://www.lsu.edu/deafness/genetics.htm
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4672198/
http://www.doggenetics.co.uk/white.htm#extremewhite
http://www.animalabs.com/shop/dogs/pieb ... oat-color/
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Re: PIEBALD ("ink spot" color pattern)

Post by Tiantai » Sat Aug 11, 2012 5:41 pm

Hopefully this gene will get erased from the breed in the future as you continue to practice careful breedings.

I read somewhere online that some dachshund owners believe that the pied-bald gene in dogs might also carry other health risks (such as deafness in adolescent) but at the moment it has not been proven so I don't know if any of that is true. Although I do have great doubts about those informations! One way or another, I just hope that with more informations of those Utonagans and Northern Inuit used in the Tamaskan line that may have been carrying the gene are known so more future Tamaskan owners and breeders will become aware of the precautions to take when breeding from certain lines as Debby already said.
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Re: PIEBALD ("ink spot" color pattern)

Post by Sylvaen » Sat Aug 11, 2012 6:13 pm

PIEBALD DATABASE

Blustag Brightbear (Oran) - diagnosed with Addison's Disease
DOB: 17/09/2004
SEX: male
SIRE: Cougar [out of Amber X Thor]
DAM: Redkite Mitka at Blustag (Paloose) [out of Chanoni X Kiwani]
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Blustag Bluemoon (Obi-Wan-Kenobi) - died of Addison's Disease
DOB: 16/07/2004
SEX: male
SIRE: Redkite Loato at Blustag (Kyte) [out of Wahosi X Keisha]
DAM: Blustag Louba (Seagull) [out of Kyte X Paloose]
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Blustag Wolf Moon (Alfie)
DOB: 02/02/2004
SEX: male
SIRE: Redkite Loato at Blustag (Kyte) [out of Wahosi X Keisha]
DAM: Redkite Mitka at Blustag (Paloose) [out of Chanoni X Kiwani]
inkspot.alfie.JPG
Blustag Wolf XXX (Silver)
DOB: 02/02/2004
SEX: female
SIRE: Redkite Loato at Blustag (Kyte) [out of Wahosi X Keisha]
DAM: Redkite Mitka at Blustag (Paloose) [out of Chanoni X Kiwani]
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Silver Litter
DOB: 17/09/2003
SEX: ?
SIRE: Redkite Loato at Blustag (Kyte) [out of Wahosi X Keisha]
DAM: Redkite Wiyanna at Blustag (Sylka) [out of Shanaska X Keisha]
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Sulin Inca (Inca)
DOB: ?
SEX: female
SIRE: ToteTims Dreamcatcher (Timber) [out of Jarra X Tara]
DAM: Hanuka at Sulin (Hanuka) [out of Romana X Shana]
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Blustag XXX (Reaver)
DOB: ?
SEX: ?
SIRE:
DAM:
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Ta-Kari Abu (Riley)
DOB: 03/01/2010
SEX: male
SIRE: Alba Brun (Dakari) [out of Moonstone Make Me Pure at Alba (Odin) X Alba Sumarlidl (Kite)]
DAM: J&J Moonlight (Takeia) [out of Blustag River Rising at J&J (Lobo) X Blustag Menominee Owl @ J&J (Woulf)]
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Ta-Kari Eytukan
DOB: 02/07/2010
SEX: male
SIRE: Alba Brun (Dakari) [out of Moonstone Make Me Pure at Alba (Odin) X Alba Sumarlidl (Kite)]
DAM: J&J Moonlight (Takeia) [out of Blustag River Rising at J&J (Lobo) X Blustag Menominee Owl @ J&J (Woulf)]
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Ta-Kari Anise, Klorel and Skaara
DOB: 26/04/2012
SEX: male & female
SIRE: Alba Brun (Dakari) [out of Moonstone Make Me Pure at Alba (Odin) X Alba Sumarlidl (Kite)]
DAM: J&J Moonlight (Takeia) [out of Blustag River Rising at J&J (Lobo) X Blustag Menominee Owl @ J&J (Woulf)]
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Buck - early ancestor (Foundation Dog) for the breed
buck1.jpg
buck2.jpg
CED: Shepherdsway Snow Drifter at Blufawn (Riker) - relatively recent outcross for the UK bloodline
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sire of Blufawn Chives (Winni)

A new litter with 5 Piebald (extreme white) puppies:
DOB: ? May 2017
SIRE: Nanuq (Nanuq vom Münsterland) [out of Bobbi X Summer]
DAM: Cheyenne (Blustag Sunsprite) [out of Rann X Heidi]
piebald.jpg
[Please let me know if any of this information is missing or incorrect! Thank you!!]
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Re: PIEBALD ("ink spot" color pattern)

Post by pagan » Mon Aug 13, 2012 1:51 pm

Theres a bich called Inca (utonagan ) thats behind the tams.She is spotted to.Sulinn Inca.

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Re: PIEBALD ("ink spot" color pattern)

Post by Nino » Mon Aug 13, 2012 2:49 pm

pagan wrote:Theres a bich called Inca (utonagan ) thats behind the tams.She is spotted to.Sulinn Inca.
I know of this bitch - but I do not have any pictures with permission to use of her :?
>> Nino <<
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Re: PIEBALD ("ink spot" color pattern)

Post by Katlin » Mon Aug 13, 2012 5:46 pm

A lot more than I thought...good post though! *saves link*
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Re: PIEBALD ("ink spot" color pattern)

Post by TerriHolt » Mon Aug 13, 2012 5:55 pm

Katlin wrote:A lot more than I thought...good post though! *saves link*

More than i thought too (because i got told none existed with the exception of the CED)
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Re: PIEBALD ("ink spot" color pattern)

Post by pagan » Mon Aug 13, 2012 8:22 pm

I met Inca many years ago.

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Re: PIEBALD ("ink spot" color pattern)

Post by Tatzel » Mon Aug 13, 2012 11:57 pm

It's amazing how un-wolfy they look once the wolf mask and typical wolf markings/colors are off the dogs!
They're still all pretty cute and good looking :)

Hope the piebald gene can be get out off the lines though!
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Re: PIEBALD ("ink spot" color pattern)

Post by sky » Wed Aug 15, 2012 2:56 am

http://www.buckhorntamaskan.com/apps/ph ... d=73039088

Lyn B. of Sulin let me post this pic of Inca on my site.

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Re: PIEBALD ("ink spot" color pattern)

Post by Sylvaen » Thu Aug 23, 2012 1:55 pm

pagan wrote:Theres a bich called Inca (utonagan ) thats behind the tams.She is spotted to.Sulinn Inca.
Thanks, I added the info about Inca. :D
sky wrote:http://www.buckhorntamaskan.com/apps/ph ... d=73039088

Lyn B. of Sulin let me post this pic of Inca on my site.
Great, thanks! :)
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Re: PIEBALD ("ink spot" color pattern)

Post by BinBin » Thu Aug 23, 2012 3:01 pm

Just a correction, the Silver litter's sire is Kyte, not Anzara. :)
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Re: PIEBALD ("ink spot" color pattern)

Post by Sylvaen » Thu Aug 23, 2012 3:11 pm

Fixed it. Thanks! :)
Tiantai wrote:
Sat Aug 11, 2012 5:41 pm
I read somewhere online that some dachshund owners believe that the pied-bald gene in dogs might also carry other health risks (such as deafness in adolescent) but at the moment it has not been proven so I don't know if any of that is true. Although I do have great doubts about those informations!
Yes, the extreme white version of Piebald (where the whole body is almost all white) is associated with certain health issues, such as deafness...
Pigment Genes and Hereditary Congenital Sensorineural Deafness
An association between deafness and blue-eyed white cats was noted as early as 1828, and Darwin commented on it in his famous publication The Origin of Species in 1859. Blue-eyed Dalmatians were noted for having deafness as early as 1896. So, the existence of a relationship between white pigmentation and deafness in dogs and cats is not new, and there is an extensive bibliography on the subject (Refs 6-12), but the mechanism behind the relationship has only recently begun to be understood.
Melanocytes, which produce pigment granules in skin, hair, and elsewhere, originate embryologically in the neural crest, the source of all neural cells, explaining the linkage between pigment and a neurologic disorder. Melanocytes produce pigment granules - either eumelanin (black or brown) or phaeomelanin (yellow or red) - from the amino acid tyrosine. Albinism, in which melanocytes are present but one of the enzymes responsible for melanin production (tyrosinase) is absent or diminished, does not have an association with deafness. Otherwise, white color results from an absence of melanin, usually from an absence of melanocytes. Specific genes have been identified that produce white by suppressing melanocytes - either their migration from the neural crest, their maturation upon arrival at their final site, or their survival. Other genes are responsible for the pigment colors in the pigmented areas. In dogs the genes for white are the recessive alleles of the piebald gene (S) or the dominant allele of the merle gene (M) (Refs13,14). In cats the genes are the dominant allele of the white gene (W) and possibly the recessive piebald gene (S) (Ref 13). In turn, the effects of these genes can be modified by other, as yet unidentified, genes that can result in strong gene expression or weak gene expression (see below).
The S locus in dogs has at least four alleles. The dominant allele S is known as self or non-spotted, and produces a completely pigmented body surface, although minor areas of white may be present on the feet or thorax.

The si allele produces Irish spotting and presents with only a few white areas that are usually on locations such as the thorax, feet, face, or head.
The sp allele produces piebald spotting and produces significantly more white on the body surface than Irish spotting, including the limbs.
The sw or extreme-white piebald allele is associated with an even greater extent of white pigmentation, including the ears and base of the tail.
These alleles are listed in order of decreasing dominance. Although the specific allele responsible for white pigmentation is not known for many breeds, the Basenji and bloodhound are examples of homozygous Irish spotting, the beagle is an example that is usually homozygous piebald, and the Dalmatian and white bull terrier are examples of homozygous extreme-white piebald. Because these alleles are recessive they must be present in pairs to produce their white pattern, but it is possible for a dog to carry one copy each of two of the recessive alleles, as may occur with Boston terriers that are normally sisi but that may on occasion be sisp or sisw (Ref 13).
The alleles sp and sw are present in the great majority of breeds recognized to be subject to congenital deafness when the identity of pigmentation genes is known, but the white-producing allele is often not known. It is likely that additional genes regulate the expression of the three recessive S alleles. For example, strong expression of sw in Dalmatians results in blue irises from suppression of melanocytes in the eye, and weak expression of sw results in the large pigmented area on some Dalmatians known as a patch, which is present at birth when the rest of the puppy is still white.
A second canine pigmentation locus associated with deafness is merle (M). Homozygosity of the recessive allele (mm) produces uniform pigmentation, while the heterozygous merle (Mm) produces dappling or alternate body areas of fully pigmented coat and pale eumelanic or even white coat. Homozygous merles (MM) are usually nearly solid white, and in some breeds may be deaf, blind with microphthalmic eyes, and sterile. Dogs heterozygous for M are variable in their likelihood of deafness. The harlequin gene (HH) has been identified as a dominant modifier of the merle gene in Great Danes that is lethal when present in the homozygous state (Ref 15); harlequin Danes are at elevated risk for deafness, while other color variants are less likely to be affected. Great Dane dogs may carry M, m, HH, si, sp, or sw gene alleles in various combinations, as well as other potential modifier genes, which provides an indication of the complexity of pigmentation genetics in various dog breeds.
Other genes reported to produce white or light coat color in dogs - flecking, ticking, dilution with fawn - do not appear to be associated with deafness.
The W gene has been studied exclusively in domestic longhair and shorthair cats that were not from identifiable or identified breeds; there do not appear to have been deafness studies in any cat pure breed. The white pigment gene in cats is autosomal dominant over color (w), and is unrelated to albinism. Cats with this gene are not always solid white, often having a colored spot on the head that fades with age. Unlike homozygous merle dogs, homozygous W cats do not have clear-cut visual or reproductive deficits, although white cats had a higher mortality than colored cats (32% vs. 26%) during a 30-day quarantine period in one study (Ref 16) and embryo viability is lower in white than non-white cats (Ref 17). Homozygous white cats are more prone to blue eyes (and deafness), and the likelihood of deafness increases with the number of blue eyes (Ref 6). White cats carrying the underlying cs Siamese dilution pigment gene can have blue eyes without deafness, which is suggested as one reason why pure-breed white cats may be deaf less often than mixed-breed white cats (Ref 18); however, since there are no studies of the prevalence of deafness in pure-breed cats this assertion about differences in prevalence cannot be validated. Long-haired white cats were reported to have a higher prevalence of blue eyes and deafness than short-haired cats (Ref 7), but it is not certain whether this observation would stand up in a larger study.
A piebald gene (S) is also said to be found in various cat breeds (Refs 17,18) that produces white spotting, especially on the neck, feet, and belly, but its existence is not established. There is no report of deafness associated with its presence.
In dogs and cats with white-producing genes, deafness appears to result from strong expression of the gene. As stated above, melanocytes in the stria vascularis play a role in maintaining the ionic environment needed by the cochlear hair cells. When the piebald, merle, or white gene is strongly expressed, it suppresses melanocytes not only in the skin, but also in the iris (a blue eye is missing pigment granules, and the blue results for the same reason the sky is blue) and the stria. When the strial melanocytes are absent the stria degenerates, after which the hair cells die and the various cochlear structures collapse and the auditory nerve fibers start to degenerate. Not all blue-eyed animals are deaf, and all deaf animals don't have blue eyes, but there is a strong statistical correlation between the two (Refs 11,12). Conversely, weak expression of the gene is associated with a reduced likelihood of deafness. Dalmatians have a base color of black (dominant) or liver (recessive) covered up by the recessive extreme-white piebald gene (for which they are homozygous). The dominant ticking gene (T) "punches" through the white to show the black or liver. Dalmatians with blue eyes (strong piebald expression) are statistically more likely to be deaf. Dalmatians with a patch (weak piebald expression) are statistically less likely to be deaf. The same association between blue eyes and deafness holds in other dog breeds (Ref 11) and most white cat breeds. Efforts through breeding to reduce blue eyes in Norwegian Dalmatians reduced the prevalence of deafness (Ref 19). Blue eyes are allowed in the Dalmatian breed standard of the United States, but not in Europe; deafness prevalence rates in Europe are approximately 20% compared to the US rate of 30%.

The Dalmatian is sw, the English setter is usually sp, the English cocker spaniel (based on the American cocker spaniel) is usually sp, and the white bull terrier is sw while the colored bull terrier is si (Ref 13); the allele in the cattle dog is not known.
It is not necessarily the case that prevalence rates are lower in breeds other than these. Rather, it is often the case that breeds with deafness problems have not yet adequately addressed the problem. Few similar deafness studies have been reported for other breeds, except for the Norwegian dunkerhound, in which unilateral or bilateral deafness has been reported to occur in 75% of all white animals (Ref 20), and the dappled (merle) dachshund, where 18.2% were reported to be bilaterally deaf and 36.4% were unilaterally deaf (Ref 21). In both breeds the prevalence of deafness in colored or non-dappled dogs was not documented but is low.
Deafness prevalence in white cats has been studied by several investigators (summarized in Delack6), but the best data come from the breeding studies of Mair (Ref 7) and Bergsma and Brown (Ref 16) who examined crosses between white and non-white parents and between hearing and deaf parents. Prevalence rates among white kittens for deafness in one or both ears were 51.5% (N=66) and 42.6% (N=162) respectively. When kittens were homozygous for white (WW) the rates were 96.0% and 52.0% in the two studies; heterozygotes were 24.3% and 27.4%. In the Mair study at least one parent was always bilaterally deaf, while Bergsma and Brown included all possible hearing combinations in the parents, making it difficult to compare results between the studies. From these complex studies it is difficult to cite a single prevalence rate, but clearly the prevalence rates are high. The authors also found a clear relationship between blue eyes and deafness: deafness was 3-5 times more common in cats with two blue eyes than cats without blue eyes, and two times more common in cats with one blue eye. Pure cat breeds carrying the W gene, potentially susceptible to deafness, are listed in Table II.

Genetics of Deafness
The inheritance of the pigment genes described above does not provide a simple description of the inheritance of the deafness that is so often associated with white pigmentation. Hereditary deafness can potentially result from any of several mechanisms: autosomal dominant. autosomal recessive, X-linked, mitochondrial, or polygenic (or multifactorial). In most instances the mechanism is unknown. Incomplete penetrance, where not all aspects of a deafness syndrome are expressed in an affected individual, frequently complicates an understanding of the mode of inheritance. To complicate the topic even further, environmental factors may interact with genetic factors to trigger expression of a disease.
No known X-linked or mitochondrial deafness has been reported in dogs or cats. Although it has been a controversial subject (Ref 22), there appears to be no gender difference in deafness prevalence (Ref 11). Many literature citations report deafness in piebald-carrying breeds to be autosomal recessive, but this is incorrect: the associated pigment gene is recessive but the deafness is not. It is common to observe deaf offspring from two normal parents, ruling out an autosomal dominant mechanism. In a research breeding colony of deaf Dalmatians at LSU, bilaterally hearing puppies often resulted from breeding two bilaterally deaf parents, ruling out a simple autosomal recessive mechanism since the deaf parents should have been homozygous for the responsible gene. The result is unresolved possibilities of incomplete penetrance of a recessive gene, multiple genes, or modifier genes acting on a single recessive gene. As terminology has evolved in genetics, and a better understanding of the molecular bases for gene actions develops, it may turn out that incomplete penetrance, polygenes, and modifier genes prove to result from the same molecular mechanism. When working to identify the physical location of a gene on a chromosome, targets are referred to as loci (singular: locus) when an approximate location on a single chromosome has been found but the specific gene is not yet identified. Because a locus consists of many genes, several of which may be involved in inheritance of the disease, it is often difficult to unequivocally explain the mode of inheritance until a single gene is identified and sequenced. A recent study with Dalmatians (Ref 23) suggests that deafness is inherited as a single locus, but one that does not follow Mendelian genetics (see below). This finding appears to be supported by other studies (Refs 24,25). Nevertheless, except for the Doberman, the mechanism(s) of inheritance of deafness in dogs and cats is not yet known. It has been stated that white in the cat is a simple dominant gene with pleiotropic effects that include blue eyes and degeneration of the inner ear;6 it might also be said that the piebald alleles of S in dogs are simple recessive genes with pleiotropic effects that include blue eyes and degeneration of the inner ear (and likewise for merle), but neither statement provides a means to describe the inheritance of deafness.
The classic genetics of coat color in dogs is only now benefiting from molecular genetic studies, advancing toward a knowledge of which chromosome-based genes are responsible for the phenotype-based coat color genes S and M; studies in cats do not yet appear to be in progress. To date, several canine chromosomal genes have been excluded for S and M (Refs 26,27) but no promising candidates have been identified. By far, the great majority of the breeds affected by hereditary deafness are carriers of recessive alleles of the phenotype S gene, so identifying its location will be important.
Deafness in Dobermans, which do not carry the merle or piebald genes, results from direct loss of cochlear hair cells without any effects on the stria vascularis - primary sensorineural deafness (Ref 28). Vestibular system signs, including head tilt and circling, are seen, and the deafness has been reported to be transmitted by a simple autosomal recessive mechanism. A similar pathology has been described for the Shropshire Terrier.
Until a gene mutation is identified for pigment-associated deafness, and a DNA-based diagnostic test developed, breeders must base breeding decisions on the hearing background of potential mates if deafness prevalence is to be reduced. Since unilateral deafness is genetically the same as bilateral deafness (but just not completely expressed), unilaterally deaf animals should not be bred - and of course bilaterally deaf animals should not be bred. Even when both parents are normal, it is unwise to repeat a breeding that produced deaf animals, although in breeds with a high prevalence rates this may be difficult. Breeding to animals with a history of producing deaf should be avoided. Breeding to blue-eyed animals should be avoided in most breeds. If deafness has been identified as a problem in a breed, the hearing status of the animals to be bred should always be known in advance. Finally, breeding decisions should always take into consideration the overall good of the breed.
http://www.lsu.edu/deafness/Tufts.htm
Congenital deafness has been reported for more than 100 dog breeds, with the list growing at a regular rate (see list); it can potentially appear in any breed but especially in those with white pigmentation of skin and hair. Deafness may have been long-established in a breed but kept hidden from outsiders to protect reputations. The disorder is usually associated with pigmentation patterns, where the presence of white in the hair coat increases the likelihood of deafness. Two pigmentation genes in particular are often associated with deafness in dogs: the merle gene (seen in the collie, Shetland Sheepdog, Dappled Dachshund, Harlequin Great Dane, American Foxhound, Old English Sheepdog, and Norwegian Dunkerhound among others) and the piebald gene (Bull Terrier, Samoyed, Greyhound, Great Pyrenees, Sealyham Terrier, Beagle, Bulldog, Dalmatian, English Setter). However, not all breeds with these genes have been reported to be affected. The deafness, which usually develops in the first few weeks after birth while the ear canal is still closed, usually results from the degeneration of part of the blood supply to the cochlea (the stria vascularis). The sensory nerve cells of the cochlea subsequently die and permanent deafness results. The cause of the vascular degeneration is not known, but appears to be associated with the absence of pigment producing cells known as melanocytes in the stria. All of the functions of these cells are not known, but one role is to maintain high potassium concentrations in the fluid (endolymph) surrounding the hair cells of the cochlea; these pigment cells are critical for survival of the stria and the stria is critical for survival of the hair cells. A different form of congenital hereditary deafness is seen in the Doberman, which is also accompanied by vestibular (balance) disturbance; this deafness results from a different mechanism where hair cell death is not the result of degeneration of the stria but is instead the primary pathology. Deafness may also occur later in life in dogs from other causes such as toxicities, infections, injuries, or due to aging (presbycusis); most of these forms of deafness do not have a genetic cause in animals and thus do not present a concern in breeding decisions, but a newly-identified form of adult-onset hereditary deafness is now recognized in Border Collies and Rhodesian Ridgebacks.
http://www.lsu.edu/deafness/genetics.htm
Canine Congenital Deafness
Pigment-associated cochleo-saccular deafness
Many of the recognized forms of hereditary deafness in multiple species are associated with white pigmentation, where the pathology is CS. The recessive alleles of the piebald locus and the dominant allele of the merle locus are associated with congenital hereditary deafness in dogs, while the dominant allele of the white locus is associated with deafness in cats.

The white spotting locus S has four alleles: the dominant allele S produces solid color, determined by other loci, while the recessive alleles express increasing amounts of white in the coat: Irish spotting (si), piebald (sp), and extreme white piebald (sw) (Table ​(Table4).4). Because melanocytes must migrate from the neural crest during embryogenesis, the body regions most distant from the dorsal midline are the most likely to be unpigmented/white: the feet, chest, muzzle, and tail. Examples of breeds with Irish spotting are Basenji, Australian shepherd, border collie, and Bernese mountain dog. Examples of breeds with piebald are English springer spaniel, fox terrier, whippet, Bracco Italiano, and beagle. Examples of breeds with extreme white piebald are Dalmatian, bull terrier, Staffordshire terrier, and Samoyed. Because the alleles are recessive, white dogs must be homozygous for a recessive allele, but it is not known how often dog breeds mix two different recessive alleles. The boxer Tasha that was used to sequence the canine genome had a phenotype designated as flash (Ssw), which enabled construction of BACs (bacterial artificial chromosomes) for each allele from her DNA (74). Significant associations between deafness and the recessive piebald alleles have been demonstrated for Dalmatian, English setter, and English cocker spaniel (75), border collie (76, 77), Australian cattle dog (78), and Jack Russell terrier (79). It has also been shown that a strong relationship exists between deafness and the absence of pigment in the iris and tapetum lucidum, interpreted to be evidence of strong expression of the piebald locus (75). Likewise, a significant negative relationship has been shown between deafness and patch in Dalmatians (75) and double masks and body patches in Australian cattle dogs (78), interpreted to be evidence of weak expression of the piebald locus. Among breeds where data are available, the prevalence of deafness in dog breeds with the recessive piebald alleles is highest for the Dalmatian, where 8% of US dogs are bilaterally deaf and 22% are unilaterally deaf; prevalence rates are lower in countries that do not allow blue eyes in the breed standard (75). Other breeds with high prevalence rates include Australian cattle dog, bull terrier, English setter, English cocker spaniel, Catahoula leopard dog, Jack Russell terrier, Boston terrier, and Dogo Argentino (80).

White spotting is the result of an absence of melanocytes in skin and hair follicles from a failure of melanocyte migration, proliferation, or survival during development (73). The white spotting locus or piebald locus is colocalized with the MITF gene, located on canine chromosome 20 (CFA20) (OMIM entry 156845) (81–83). MITF regulates the differentiation, migration, and survival of neural crest-derived melanocytes during development, including melanocytes involved in coat color and melanocytes in the cochlear stria vascularis. MITF also regulates the gene tyrosinase (TYR, OMIM entry 606933), which encodes for the rate-limiting enzyme in the synthesis of melanin pigment. Two MITF mutations, located in a 3.5-kb region upstream of the M promoter region, were proposed by Karlsson et al. (82) in different combinations to explain the three recessive white spotting alleles. The first was a 198-bp short interspersed element (SINE) insertion located 3,167 bp before the start codon of exon 1M, and the second was a polymorphism in the gene promoter region. The SINE insertion was present in sp and sw dogs, but not in si or S dogs. The length polymorphism that was present in S dogs was longer and differed slightly in si, sp and sw dogs. The exception was the Dalmatian, where the polymorphism resembled that of solids.

Schmutz et al. (84) studied one of the six known isoforms of MITF specifically expressed in neural crest-derived cells, known as MITF-M (85). As had been reported by Karlsson et al. (82), none of the dogs from five breeds with Irish spotting had the SINE insertion in MITF-M, but dogs from 19 breeds with random white spotting (piebald or extreme white) were homozygous for the insertion. Most heterozygotes for the SINE were either solid or had minimal white markings, but some had white undersides with a white collar. In contrast to Karlsson et al. (82), Schmutz et al. (84) were unable to find evidence for either a specific sw allele at MITF-M or one for si. They also were unable to replicate the length polymorphism described by Karlsson et al. (82). A suggestion has been made that KITLG is a candidate gene for si (86), but there have been no further reports on this possibility.

Subsequent to the Karlsson et al. (82) study, a recent publication from the same lab (74) confirmed that the SINE insertion is present in sp and sw dogs but not in S and si dogs, and further concluded that the three recessive alleles were not due to independent mutations but instead to haplotype effects from combinations of different length polymorphisms. The authors stated that “MITF in dogs is another example of ‘evolution of alleles’ by consecutive accumulation of multiple causal mutations,” in this case in the length polymorphism in the MITF-M promoter. Findings in the Dalmatian were again different from other dogs with recessive alleles, with a length polymorphism shorter than those found in other spotted dogs but still longer than those in S dogs. The effects of the length polymorphism on the recessive alleles is to affect MITF-M transcription by alteration of the DNA helix to modify binding sites for LEF-1, SOX10, and PAX3 that are critical for MITF-M expression, and subsequent melanocyte function. PAX3 (paired box gene 3, OMIM entry 606597) is a paired box gene, formerly known as splotch, associated with eye, ear, and face development. SOX10 (sry-box 10, OMIM entry 602229) is a homeobox gene regulated by MITF that is involved in neural crest and peripheral nervous system development. Mutations of PAX3 and SOX10 are responsible for deafness in several forms of human Waardenburg syndrome. LEF-1 (lymphoid enhancer-binding factor 1, OMIM entry 153245) is involved in transcriptional self-activation of the MITF-M promoter, while PAX3 and SOX10 are transcription factors critical for MITF-M transcription. It was suggested that the SINE acted as a weak silencer element acting in addition to the length polymorphisms to reduce the MITF-M promoter activity associated with sp and sw (74).

The molecular genetics of the S alleles still require more elucidation. Commercially available DNA tests for “piebald” apparently only test for sp and sw dogs, based on the presence of the SINE insertion, but due to the lack of consensus on whether sw exists, the test may only demonstrate the presence of sp. Most commercial pigmentation tests evaluate other pigmentation loci (87).

No mutations in the SINE or length polymorphism have been demonstrated to co-segregate with deafness. These results, along with the positive association between deafness and blue eyes and the negative association between deafness and patches in Dalmatians, and double masks and body patches in Australian cattle dogs, suggest that a polygenic mechanism may explain deafness, with interactions between MITF-M and another modifying gene determining hearing status in white-spotted dogs. Interestingly, humans with blue eyes may be more susceptible to noise-induced hearing loss than people with darker eyes (88, 89).

Separate from the question of causative gene mutations responsible for deafness is the question of the mechanism of inheritance of pigment-associated deafness (90), knowledge that would be helpful in reducing disease prevalence. This is complicated by variable disease expression, since dogs can be deaf in either one or both ears and it is possible that dogs can be genotypically deaf but not exhibit the phenotype. Most attempts to establish an inheritance mechanism have utilized complex segregation analysis to analyze multigenerational hearing pedigrees to identify a major segregating locus with a large effect on the expression of deafness. In Dalmatians, Famula et al. (91) concluded that a single allele affected the prevalence of deafness but that one locus could not completely explain the inheritance. Muhle et al. (92) concluded that their data were best fit by a single locus with an incompletely penetrant recessive allele. Juraschko et al. (93) presented evidence for a monogenic–polygenic model with a recessive major gene, and Cargill et al. (94) reported that evidence was not persuasive for a single major gene affecting deafness. Analyses of Jack Russell terrier data found that a single locus model of inheritance was also not supported (95). Sommerlad et al. (96) reported that deafness in Australian stumpy-tail cattle dogs followed an AR pattern. Both Jack Russell terriers and Australian stumpy-tail cattle dogs carry recessive S alleles.

Studies have been conducted to identify loci of genetic mutations responsible for deafness using a variety of molecular genetic techniques. Rak et al. (97) mapped 20 candidate genes for deafness in the dog that have been identified in other species, but none were informative. Cargill (98) utilized the MSS1 set of 172 microsatellite markers for whole-genome screens of Dalmatian DNA (99). Maximum LOD scores for deafness were found with markers Cos15 on CFA17 (LOD = 1.69) and FH2585 on CFA28 (LOD = 1.34), but the LOD scores did not reach the significance level. One human deafness gene is located on the human marker HSA02, syntenic to CFA17. Within this region is the deafness locus for DFNB9, a non-syndromic deafness locus caused by a recessive mutation in the gene Otoferlin (OTOF, OMIM entry 603681) (100). However, with the possibility of a polygenic mechanism for deafness, a LOD score well above 3 would be necessary for significant association.

Stritzel et al. (101) performed an association study using a set of eight markers, two flanking and six internal to MITF in Dalmatians to identify associations between the markers, deafness, and blue irises. After genotyping, only four markers were polygenic in the Dalmatian subjects and therefore used for the association analysis. The authors concluded that MITF is involved in deafness in Dalmatians and that possible causative mutation or mutations might be in the non-coding sequence of MITF, but no actual gene mutation was identified or suggested to be a candidate.

Sommerlad et al. (96) performed whole-genome microsatellite studies of Australian stumpy-tail cattle dogs and found a significant linkage (LOD = 3.64) with a locus on CFA10. A candidate pigmentation and deafness gene located within the locus was Sox10; however, sequencing of the gene in six hearing, two unilaterally deaf, and two bilaterally deaf dogs did not demonstrate any deafness-associated Sox10 mutations.

Kluth and Distl (102) performed a genome-wide association study in Dalmatians using the Illumina canine bead chip, which contains 173,662 single nucleotide polymorphism markers (SNPs) spanning the canine genome, to identify quantitative trait loci (QTL) associated with deafness. Using a mixed linear model of DNA from all deaf dogs, significant loci were found on CFA2, 6, 14, 17, 27, 29, and 31. Affected dogs were also segregated by eye color since blue-eyed dogs are significantly more likely to be deaf than brown-eyed dogs. Six significant loci associated with deafness were identified in brown-eyed Dalmatians (CFA2, 6 (two), 14, 27, and 29) and four significant loci were found in blue-eyed Dalmatians (CFA6, 14, 27, 29, and 31), but only the locus on CFA27 overlapped both groups. The authors concluded that several loci contribute to pigment-associated hereditary deafness in Dalmatians. Overall, significant loci found on CFA6, 14, 27, 29, and 31 were located in close proximity to genes shown to be causative for hearing loss in humans or mice: COL11A1 (collagen type XI alpha 1) on CFA6, DFNA5 and HOXA1 (homeobox A1) on CFA14, GDAP1 (ganglioside-induced differentiation associated protein 1) on CFA29, and CLDN14 (claudin-14) on CFA31. These genes are involved in the development and maintenance of inner ear structures. Genes associated with melanocyte function were located in close proximity to four of the significant loci: ARHGAP12 (Rho GTPase activating protein 12) on CFA2, TWF1 [twinfilin, actin-binding protein, homolog 1 (Drosophila)] on CFA27, CDC42EP2 on CFA18, and AEBP2 (AE (adipocyte enhancer) binding protein 2) on CFA27. Two additional genes located in close proximity of significant loci may also have associations with auditory function: GIPC2 (GIPC PDZ domain containing family, member 2) on CFA6 and CRIM1 (cysteine rich transmembrane BMP regulator 1 (chordin-like)) on CFA17. See Kluth and Distl (102) for discussion of the functions of these genes. No significant loci were located within or near the genes MITF, SILV, SOX10, or KITLG, shown in other studies to be associated with deafness (82, 96, 101, 103–105). A marker near MITF previously shown to have an association with deafness in German Dalmatians (101) did not reach significance in this study.

In summary, a wide variety of candidate genes have been investigated as causative for deafness in S locus dogs, but no consensus gene or genes have yet been established.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4672198/
The extreme white pattern consists of a completely or predominantly white dog with just small amounts of colour on its head and sometimes base of tail. Small body patches may be present too. Sometimes the nose is pink or partly pink, and the eyes may be blue in some breeds due to lack of pigment.

So far all extreme white dogs that have undergone genetic testing have been shown to be homozygous for the piebald gene (spsp), just like the piebalds in the section above. However, as there is a fairly large difference between those dogs and the ones shown below, it is possible there is something else going on to cause the high white. In breeds with both true irish spotting and piebald the high white may simply be caused by the interaction between homozygous irish spotting and homozygous piebald (e.g. the Sheltie). In other breeds the cause is less obvious and has led some people to postulate a further S allele - sw. However, no evidence has yet been found for the existence of sw, on the S locus at least.

Extreme white can occasionally cause problems when it removes large amounts of pigment from the face and ears. The most common problem is deafness (due to lack of pigment in certain parts of the inner ear, which prevents it from functioning properly), but dogs with exposed unpigmented (pink) skin are also more prone to skin cancer than those with more pigment.
http://www.doggenetics.co.uk/white.htm#extremewhite
Piebald varies in display of white spotting from limited to extensive, with often colored head and patches on the body. Piebald phenotype is common in Beagle and Fox Terrier breed.

Characteristic of Irish spotting is modest white spotting dog coat color, most often present as white collar and a white belly and legs, present most often in Bernese Mountain dog and Basenji.

Genotype Ssw causes phenotype known as flash and it is similar to Irish spotting. For this reason it is often referred to as pseudo-Irish.

Among dogs with extremely white phenotype (swsw genotype) deafness has been recorded, where 2% of the dogs appeared with bilateral deafness and 18% are unilaterally deaf.

Until now, several mutations in MITF have been identified. Mutations in the MITF have an impact on development and function of melanocytes in the skin, eye and inner ear. Some mutations cause reduction of the eye, known as microphtalmia, and therefore, have an effect on vision. On other hand, some MITF mutations cause an early onset of hearing disorders.

A mutation in the MITF causing piebald coat color has been identified in more than 25 different dog breeds. Piebald gene is recessive to dominant S (non-white) gene. This means if two piebald carrier dogs are mated ( Ss genotype, non-white phenotype), there is a 25% chance of a piebald cub occurring in the litter, and 50% that the puppy will be a piebald carrier. Although allele S is dominant over allele s, in many breeds genotype Ss shows co-dominant expression, which results in limited white spotting. As previously mentioned, there are several other types of white spotting such as Irish white spotting, but their DNA variations are not known.
http://www.animalabs.com/shop/dogs/pieb ... oat-color/
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Re: PIEBALD ("ink spot" color pattern)

Post by Gaby » Fri Aug 31, 2012 3:03 am

Not piebald I believe, but two siblings from Mila from the dragon litter have white markings. A male and a female. The female is Kodi: viewtopic.php?f=20&t=1460 and the male is Finch (Blustag Norbert): viewtopic.php?f=20&t=2828 It sure looks very cute if you ask me. ;)

Date of birth: 13-02-2011
Sire: Dingo at Blustag
Dam: Blustag Diamonds are Forever (Dallas)

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Re: PIEBALD ("ink spot" color pattern)

Post by Tiantai » Fri Aug 31, 2012 3:51 am

Yeah I did mistaken Finch of being a pied-bald once when I first saw one of Laura's photos of him from a certain angle because he did looked white from the neck and has that white line going down the centre of his mask as well as the light areas on the sides after his nose. Of course, he's not really pied-bald, but because of that certain angle of the photo I made that mistake. I can't post the actual photo here though as I don't have Laura's permission to do that but it's basically that picture of Finch sleeping on the sofa on her cover photo on facebook.

Looking back at some of the pictures Debby posted above, if not for them being mentioned of having relations to some Tamaskan's line, I would have mistaken them as being Seppala Sleddogs or Alaskan Huskies as I have seen a lot of pied-bald Alaskan Huskies before.
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Re: PIEBALD ("ink spot" color pattern)

Post by arianwenarie » Fri Aug 31, 2012 3:56 am

@Gaby

Is Wheels also from the same litter as Mila (Dingo x Dallas)? I would say that he probably has more white on him than Finch and Kodi. Finch's masking looks like it evened out as he aged. Kodi, somewhat, but there's quite a bit of white on the tail still and on her shoulders. Judging from pictures, it looks like Wheels has the most white patches on him than either of the two - mask, shoulders and tail.

EDIT:
Perhaps we can dig around to see if we can find pictures of the dogs behind Dallas (Rann x Tumanra)? Though, it might also be worth trying to look into pictures of dogs behind Dingo - particularly the Huskies to see if/how much piebald was in the lines.

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Re: PIEBALD ("ink spot" color pattern)

Post by Gaby » Fri Aug 31, 2012 4:08 am

@ Arianwenarie, Wheels has been placed out and is renamed Finch, so it's the same dog. ;) And good idea about the pictures from the lines! Don't know if I can find the time though... :?

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Re: PIEBALD ("ink spot" color pattern)

Post by arianwenarie » Fri Aug 31, 2012 4:14 am

Gaby wrote:@ Arianwenarie, Wheels has been placed out and is renamed Finch, so it's the same dog. ;) And good idea about the pictures from the lines! Don't know if I can find the time though... :?
Ohhh...so Wheels = Finch, which is still Blustag Norbert? :P I was looking at the puppy picture (semi-pile) that you posted in this thread and I was trying to wrap my mind around this whole thing -- 2 dogs with incorrect masking, but 3 different dogs from apparently the same litter with the similar markings... I had a "whaaaaaat? o_O" moment. lol.

Thanks for clearing that up. :D

If we can get pedigrees of lines that have produced piebalds to include pictures of as many ancestors in the lines, then that'd be great. Unfortunately, I just don't have the time on my hands anymore either. :(

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Re: PIEBALD ("ink spot" color pattern)

Post by Gaby » Fri Aug 31, 2012 4:19 am

Yes, you are right, only two puppies with white markings. ;) I will try to find some time, would be nice to have a picture pedigree of my dog too.

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Re: PIEBALD ("ink spot" color pattern)

Post by arianwenarie » Fri Aug 31, 2012 4:21 am

Gaby wrote:Yes, you are right, only two puppies with white markings. ;) I will try to find some time, would be nice to have a picture pedigree of my dog too.
Riiight. Dilemma resolved and disaster averted. lol. I doubt you'd be able to post picture pedigrees publicly unless you get permission from all the dog owners... but there are pictures of some of the dogs behind Mila online. Mainly on the Tamaskan facebook page run by the Blus I think.

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Re: PIEBALD ("ink spot" color pattern)

Post by Gaby » Fri Aug 31, 2012 4:24 am

:lol:

Yes, I know, can't post them publicly. I already searched all the dogs in her pedigree up on the internet though. ;) Can't remember a piebald, but do remember some with white markings. But I don't know for sure any more.

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Re: PIEBALD ("ink spot" color pattern)

Post by arianwenarie » Fri Aug 31, 2012 4:37 am

Gaby wrote::lol:

Yes, I know, can't post them publicly. I already searched all the dogs in her pedigree up on the internet though. ;) Can't remember a piebald, but do remember some with white markings. But I don't know for sure any more.
If I remember correctly, Sulin Inca is a couple generations back in Dallas's pedigree. But so far, that's the only one I remember...

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Re: PIEBALD ("ink spot" color pattern)

Post by Nino » Fri Aug 31, 2012 6:02 pm

the lot of white on finch did strike me odd, but I doubt he is Pie bald.. I would rather suggest too much white spotting..
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Re: PIEBALD ("ink spot" color pattern)

Post by caninesrock » Mon Nov 05, 2012 1:56 am

Oh wow. Bluestag Brightbear is beauiful,but it's sad that he has a disease.

I noticed that Riker the CED is a piebald. And most of the piebald dogs are from Blustag. Is it confirmed through testing who those dogs parents definitely are? Because if not, could it be possible that all of the Blustag piebald dogs are actually offspring of Riker which was covered up?

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Re: PIEBALD ("ink spot" color pattern)

Post by arianwenarie » Mon Nov 05, 2012 2:33 am

caninesrock wrote:Oh wow. Bluestag Brightbear is beauiful,but it's sad that he has a disease.

I noticed that Riker the CED is a piebald. And most of the piebald dogs are from Blustag. Is it confirmed through testing who those dogs parents definitely are? Because if not, could it be possible that all of the Blustag piebald dogs are actually offspring of Riker which was covered up?
No, the piebalds produced by Blustag was from Utonagon lines and was before Riker joined their pack. ;) Riker, the CED, only produced two litters (that we know of): with Zuul, which produced Winni (Blufawn Chives) and one with the purebred CED, Rogue, also owned by Blufawn.

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Re: PIEBALD ("ink spot" color pattern)

Post by Nino » Mon Nov 05, 2012 2:40 am

Also winnie could with the wrong/right male she would produce piebalds too.. Piebald is a trait inherites from both parents before it is shown
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Re: PIEBALD ("ink spot" color pattern)

Post by caninesrock » Mon Nov 05, 2012 4:17 am

Oh. Ok. Thanks for the info.

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Re: PIEBALD ("ink spot" color pattern)

Post by Sylvaen » Tue May 09, 2017 4:41 pm

A new litter with 5 Piebald (extreme white) puppies:

DOB: ? May 2017
SIRE: Nanuq (Nanuq vom Münsterland) [out of Bobbi X Summer]
DAM: Cheyenne (Blustag Sunsprite) [out of Rann X Heidi]
piebald.jpg
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Re: PIEBALD ("ink spot" color pattern)

Post by Katlin » Wed May 10, 2017 3:07 pm

Oh man :(
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Re: PIEBALD ("ink spot" color pattern)

Post by Sylvaen » Wed May 10, 2017 9:51 pm

Since there are so many white puppies in the litter, more than you would normally expect based on genetic probability, another possible explanation is that some of the solid white pups without any dark color patches could be recessive red (ee) IF both Nanuq and Cheyenne are carriers (via Summer and Heidi). However, since recessive red (ee) - cream/white - can hide/mask piebald, it means that all the white pups need to be BAER hearing tested regardless. (Interesting fact: almost all Samoyeds are piebald, but they are also recessive red (ee) and so appear to be solid white.) If some of these solid white puppies turn out to be recessive red (ee) and not extreme white piebald (Sw) then their hearing will be fine as recessive red (ee) has normal skin pigment under the white fur. However, some of the pups in this litter clearly are extreme white piebald (Sw) as you can see from the small patches of color on their rear ends.

The main factor determining deafness in extreme white piebald (Sw) and double merle (MM) and double harlequin (HH) is whether or not there is pigment in the inner ear:
The deafness, which usually develops in the first few weeks after birth while the ear canal is still closed, usually results from the degeneration of part of the blood supply to the cochlea (the stria vascularis). The nerve cells of the cochlea subsequently die and permanent deafness results. The cause of the vascular degeneration... appears to be associated with the absence of pigment producing cells (melanocytes) in the blood vessels.
http://www.samoyedhealthfoundation.org/ ... 3-deafness
Breeding for or against particular color patterns based on aesthetics and personal preference is never a good idea... for instance: recessive red (ee) or recessive black (aa) or liver (bb). If it happens, it happens... but aiming TO produce these particular colors on purpose, or aiming NOT to produce these particular colors on purpose, unnecessarily limits the genepool... so it really doesn't matter if a Tam is white/cream (ee) or black (aa) or liver (bb). However, in the case of extreme white piebald (Sw), there is good reason to exercise caution: it's not about aesthetics but, rather, the real potential health issues that can result. The main thing to keep in mind is that merle (M) and harlequin (H) are dominant, so there is never an excuse to breed merle x merle or harlequin x harlequin. On the other hand, extreme white piebald (Sw) is recessive so it can pop up unexpectedly and unintentionally. However, both Nanuq and Cheyenne exhibit white facial markings (from the white spotting Sp gene) so this is a vital clue that breeders can use to their advantage in the future: not to breed two dogs with white facial markings together (Sp x Sp) thereby reducing the likelihood of producing extreme white piebald (Sw) offspring. It's also a good reason to get all breeding dogs DNA tested for coat colors (either MyDogDNA or Embark, for example). So long as breeders are open and honest and the new owners are informed of the potential risk of deafness, and the puppies are BAER hearing tested once they are 6-8 weeks old, that's the most important thing. Even if it's an undesired color pattern, they can still make great pets and I'll keep my fingers crossed that their hearing will be OK.
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Re: PIEBALD ("ink spot" color pattern)

Post by obisan » Sun Jun 25, 2017 4:29 pm

I was wondering. Are their any known Tamaskan's who are deaf and who are also piebald?

and by the way, to update your list Debby. In Germany is another litter born with Piebald pups. (DAM Tala x SIRE Chakay)

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Re: PIEBALD ("ink spot" color pattern)

Post by Sylvaen » Mon Jun 26, 2017 10:51 am

obisan wrote:
Sun Jun 25, 2017 4:29 pm
I was wondering. Are their any known Tamaskan's who are deaf and who are also piebald?
As far as I know, there are not yet deaf piebald Tamaskans. However, deafness associated with this color pattern can affect any breed (any piebald dog has a potential risk) as the lack of pigment in the inner ear is a random feature. During gestation, the skin of a piebald puppy develops random patches of pigment or non-pigment, so it's basically a matter of luck... a piebald dog has to be very unlucky to have no pigment in that very small relevant area (internal ear structure) which is about the size of a thumbprint. Generally speaking, if a piebald dog has a lot of pigment around the head area, it usually is safe to say that the hearing is OK but the inner ear pigment is not completely connected to the color pigment seen on the outside of the ear, so it isn't always the case. Basically, it's a random trait depending on how the skin pigment disperses when the fetus is being formed... if enough piebald Tamaskan puppies are born, then the potential of one of them being deaf increases due to statistical probability. To be certain, all piebald puppies should be hearing tested at around 6 weeks old.
obisan wrote:
Sun Jun 25, 2017 4:29 pm
and by the way, to update your list Debby. In Germany is another litter born with Piebald pups. (DAM Tala x SIRE Chakay)
Thanks Sandra. From the photo(s) I've seen so far, it looks like there are 2 white (recessive red/cream: ee) puppies and 3 colored (non-piebald) pups that have white spotting (Sp) on their tails and faces, which is considered a fault but not a disqualifying one (unlike true piebald). However, if those white spotted offspring are later bred to other Tamaskan Dogs with similar white spotting on their face and tail, then it is likely that combination would produce actual piebald puppies (50% white and 50% color patches spread out over the whole body) or even the extreme white version (90% white and 10% color patches spread out over the whole body).
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Re: PIEBALD ("ink spot" color pattern)

Post by obisan » Mon Jun 26, 2017 3:22 pm

Thanx debby for the information. :)

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Re: PIEBALD ("ink spot" color pattern)

Post by sauron » Tue Jun 27, 2017 8:47 am

Hey everyone. Research seems to be revealing that there is no such thing as "extreme white" in forms of a seperate allele besides the sp piebald one.

http://homepage.usask.ca/~schmutz/dogspots.html

As far as my english language skills go, it seems to be different expressions of the same piebald allele causing less or more piebald spots on the dog skin. The expression of this allele varys a lot between different breeds and also somethimes within the breed itself.
There were also studys about Irish Spotting and what it is caused by. First people thought of an allele si, then it seemed to be heterozygous piebald S/sp. But more likely ist a completely different gene in a different spot not yet detected... This was in a study with Great Danes, where a lot of S/S dogs showed Irish Spotting and even passed it on to their pups.

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Re: PIEBALD ("ink spot" color pattern)

Post by Sylvaen » Tue Jun 27, 2017 11:41 am

sauron wrote:
Tue Jun 27, 2017 8:47 am
Hey everyone. Research seems to be revealing that there is no such thing as "extreme white" in forms of a seperate allele besides the sp piebald one.

http://homepage.usask.ca/~schmutz/dogspots.html

As far as my english language skills go, it seems to be different expressions of the same piebald allele causing less or more piebald spots on the dog skin. The expression of this allele varys a lot between different breeds and also somethimes within the breed itself.
There were also studys about Irish Spotting and what it is caused by. First people thought of an allele si, then it seemed to be heterozygous piebald S/sp. But more likely ist a completely different gene in a different spot not yet detected... This was in a study with Great Danes, where a lot of S/S dogs showed Irish Spotting and even passed it on to their pups.
Good info. Yes, white spotting (sp), which causes the piebald and extreme white variations, is still one of the least understood color loci and there are definitely modifying factors that influence expression. For instance, in huskies and wolfdogs, you can also get solid color dogs without any white markings that have tested as Sp/Sp (genotypically they should be piebald but phenotypically they are not)... so there are certainly other factors involved. Since the gene markers are still not very comprehensive at this point in time, for now it's better to use visible phenotype as a guide (particularly puppy photos as the white markings can fade and blend in as the pup develops).
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The future lies before you, like a path of pure white snow...
Be careful how you tread it, for every step will show.

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