Panda German Shepherd

Let us begin with the fact that determines everything else on this page. The dogs called "pandas" are not a separate breed, not a designer hybrid, and not a Border Collie cross. They are German Shepherds that inherited a single change in the KIT gene — the gene of a receptor tyrosine kinase that governs the migration and maturation of melanocyte precursor cells. When that signal is weakened, some areas of skin simply receive no pigment cells, and the hair there grows white. So the white on a "panda" is not a different pigment and certainly not albinism: it marks the places the pigment cells never reached.

The mutation arose spontaneously — de novo, in one line of German Shepherds, in a dog whose parents carried no such pattern. Among owners, the founder is said to be a bitch named Lewcinka's Franka von Phenom, born in October 2000 in the United States; every later "panda" is traced back to her. That name lives in breed circles and in kennel presentations, and we give it with exactly that status — the version accepted within the community, not a line from a scientific paper.

What is genuinely recorded in the scientific literature is the mutation itself. The international database of inherited traits in animals, OMIA, gives it its own entry: OMIA:001737-9615, "Coat colour, white spotting, KIT-related" in the dog, gene KIT, chromosome CFA13. What is officially catalogued, therefore, is not a "panda breed" but the trait "white spotting, KIT-related", documented in two breeds — the German Shepherd and the Weimaraner.

There is a single primary source here, and it deserves to be quoted in full: Wong A. K., Ruhe A. L., Robertson K. R., Loew E. R., Williams D. C., Neff M. W., "A de novo mutation in KIT causes white spotting in a subpopulation of German Shepherd dogs", Animal Genetics, 2013, volume 44, issue 3, pp. 305–310 (published online on 8 November 2012). The first author worked at the Veterinary Genetics Laboratory of the University of California, Davis — the laboratory popular articles refer to as "UC Davis".

The approach was the classic one for mapping a trait. First a genome scan: 95 German Shepherds and 143 microsatellite markers. The signal converged on a single point — one locus on chromosome 13, the one that holds the KIT gene. Linkage strength: LOD = 15. To a geneticist that is not "this looks likely"; it is a question of location that is effectively closed.

Next the exons of KIT were sequenced, and the cause emerged: the insertion of a single nucleotide — an adenine — 70 bases from the start of the second exon. That one extra letter shifts the reading frame; premature stop codons appear soon after, and instead of a complete receptor of 974 amino acid residues the cell builds a fragment of 55 residues. This is loss of function in its purest form. In current nomenclature the variant is written c.140_141insA, p.(L48Vfs*10) (equivalently c.140dup); on the CanFam3.1 genome assembly it corresponds to g.47144513_47144514insA on chromosome 13. In OMIA it is variant no. 570.

The final step was verification across the whole sample. Genotyping showed a perfect match between the insertion and the pattern: 64 spotted dogs and 31 normally colored littermates, without a single exception in either direction. When a trait and a variant never separate across nearly a hundred animals, the "it must be something else" hypothesis exhausts itself.

There is one more point that is easy to miss and that is precisely what makes this work notable. Until then KIT was regarded as a gene "foreign" to canine spotting: in the pig, the cow, the horse, the cat and the human, white patches caused by KIT had long been described, but not in the dog. The authors state explicitly that they showed a loss-of-function mutation in KIT reproduces in the dog the same coat phenotypes observed in other species. The "panda", then, is not a curiosity: it is the first documented canine case of a mechanism well known elsewhere.

The suspicion is understandable: a white collar, a white blaze on the face, white feet — visually this really does suggest a herding dog from an entirely different corner of cynology. But genetics separates these cases more reliably than the eye does.

In dogs, "ordinary" white spotting belongs to the S locus, and a completely different gene is responsible for it: MITF. That gene produces Irish spotting, piebald and extreme white in dozens of breeds. Merle is a third gene again, PMEL. The "panda" belongs to none of these mechanisms: in its case it is KIT — a different chromosome, a different protein, a different kind of breakage. Had the white come from a Border Collie, it would have arrived with the "collie" variant and would have segregated together with a whole stretch of foreign genome. The study shows the opposite: one new insertion, absent from the preceding generations.

The second support is segregation. An infusion of another breed does not behave like a single dominant allele: it drags dozens of linked segments with it and produces a blurred variety of types. Here the trait behaves as a single locus: 64 spotted against 31 normal littermates, with a perfect match between genotype and phenotype.

The third support is the repeatability of the mechanism. Independently of the American work, a German group described an analogous case in another breed: Gerding W. M., Akkad D. A., Epplen J. T., "Spotted Weimaraner dog due to de novo KIT mutation", Animal Genetics, 2013, 44(5), pp. 605–606. KIT again, a newly arisen mutation again — only a different one: a deletion of three nucleotides in the thirteenth exon, p.(L646del), right inside the tyrosine kinase domain. Two independent episodes in two different breeds mean that KIT can "break" in the dog on its own, without any outside blood.

The question is legitimate: in dogs, white patches genuinely are sometimes linked to reduced hearing. The classic examples are the Dalmatian, the white Boxer and the merle breeds. The mechanism is the same as for color: the inner ear needs cells related to melanocytes, and where those are missing, hearing suffers.

But "spotting" is not one single thing. In dogs, pigment-associated deafness is traditionally tied to the piebald locus (gene MITF) and to merle (gene PMEL). The "panda" is neither.

What the literature says about these dogs specifically: the peer-reviewed review Strain G. M., "The Genetics of Deafness in Domestic Animals", Frontiers in Veterinary Science, 2015, vol. 2, article 29 describes a family of German Shepherds carrying a loss-of-function mutation in KIT that produced a white pattern on the face, the ventral abdomen, the feet and the tail tip, and states that all affected dogs had normal hearing on BAER testing — the recording of brainstem auditory evoked responses. BAER is not "the owner called and the dog came": it is an objective test that also catches unilateral deafness, which an owner may fail to notice for years.

That is the honest answer in full: in that family of dogs hearing was measured instrumentally and described as normal. The sensible position for an owner is not to treat the check as superfluous, but to have it done if the puppy is intended for work or sport: BAER is performed in neurology departments and does not take long.

This is where half the arguments online originate: people debate as if "recognition" were a single procedure. In reality there are at least two, and they run on different rules.

The first is the registry — entering a dog in the stud book as a representative of the breed. The second is conformation judging in the ring, where compliance with the standard is assessed. The clearest proof that these are not the same thing comes from the AKC itself: its list of registration color codes for the German Shepherd contains eleven entries — black (007), black and cream (010), black and red (014), black and silver (016), black and tan (018), gray (100), sable (164), white (199), liver (123), blue (037) and bi-color (454). White is on that list — even though the same AKC disqualifies a white dog in the breed standard. The registry records a fact; the ring judges conformity. They are parallel things.

There is no code of its own for the white-spotted pattern on that list: in registration papers the "panda" goes under one of the existing entries. And one more detail worth keeping in mind: nowhere is registration a statement about the quality of a dog. It says only that the parents are entered in the same book.

What follows for the owner. Working and sporting disciplines — obedience, tracking, agility, search — assess behavior and performance, not the drawing of the coat. The conformation ring assesses precisely the match with the breed description, and a color outside the list will always be a problem there. This is not a "conspiracy against pandas": it is the literal content of the document the judge works to.

Gastric dilatation-volvulus (GDV) is a condition that can kill a large, deep-chested dog within hours. A great deal of advice circulates about preventing it, and part of that advice contradicts the data, so it is better to rely on specific studies.

In a prospective cohort of large and giant breeds (Glickman L. T. et al., Journal of the American Veterinary Medical Association, 2000, 217(10), pp. 1492–1499) four things were significantly associated with the risk of torsion: increasing age, having a first-degree relative with a GDV episode, a fast rate of eating and — the most unexpected of them — a raised feeding bowl. The authors estimated that the raised bowl accounted for approximately 20 % of cases in large breeds and approximately 52 % in giant breeds. In other words, the widespread advice "feed from a stand so the stomach does not twist" has the opposite sign in this study, and we shall not repeat it.

A second paper by the same group (JAVMA, 2000, 216(1), pp. 40–45) gave the scale of the phenomenon: an incidence of 23 cases per 1,000 dog-years for large breeds and 26 for giant ones, a cumulative incidence of 5.7 % over the study period, and of the 105 dogs that developed torsion, 28.6 % died. A third (Raghavan M. et al., Journal of the American Animal Hospital Association, 2004, 40(3), pp. 192–203) concerned diet: risk was higher in dogs that consumed a larger volume of food per meal, regardless of the number of meals per day, and highest in those given that large volume once daily.

An important caveat about the reach of these data: the German Shepherd was not among the breeds studied — those were the Akita, Bloodhound, Collie, Great Dane, Irish Setter, Irish Wolfhound, Newfoundland, Rottweiler, Saint Bernard, Standard Poodle and Weimaraner. The correct formulation is therefore this: these are regularities established for large and giant breeds in general. The practical conclusion is simple — smaller portions more often, no raised bowl, slow down eating that is too fast, and know the signs of torsion by heart. The AKC breed reference describes it as a sudden, life-threatening swelling of the abdomen and advises owners to learn the symptoms and the plan of action in advance.

The context without which the "panda" hangs in mid-air. FCI Standard No. 166 sets out the history of the breed with reference to the official documents of the founding club — the Verein für Deutsche Schäferhunde (SV), based in Augsburg. The club was constituted at its first general meeting in Frankfurt am Main on 20 September 1899, on proposals by A. Meyer and Max von Stephanitz; it is the SV, as founding club, that is responsible for the breed standard.

The standard then states the design with remarkable frankness: the breed was built from the central and southern German herding dogs then in existence, "with the final aim of creating a working dog inclined towards high achievement", and it was for that aim that the description was drawn up, covering physical construction as well as traits and character. The German Shepherd, then, was never a companion breed with a working past: it is a working program set down in writing as a standard. That explains a good deal — both the restrictive character of the color section and the heat with which any deviation is debated within the breed.

• One letter of DNA. The whole difference between an ordinary shepherd and a "panda" is one extra adenine in the second exon of the KIT gene. Because of the frameshift, a receptor of 974 amino acids is reduced to 55.
• The first canine case of a known mechanism. Before this work, KIT-related white spotting had been described in the pig, the cow, the horse, the cat and the human — but not in the dog.
• Neither piebald nor merle. In dogs, piebald comes from the MITF gene and merle from PMEL. The "panda" belongs to neither of these loci.
• The mechanism repeated itself in another breed. In that same year, 2013, Animal Genetics described a white-spotted Weimaraner also carrying a new KIT mutation — but a different one: a deletion of three nucleotides in the thirteenth exon.
• Registry does not equal ring. In the AKC's list of registration color codes for the German Shepherd, white is present (code 199) — even though the standard of that same organization disqualifies a white dog.
• The standard puts a number on the format. The body length of a German Shepherd exceeds the height at the withers by roughly 10 to 17 %, and the head makes up about 40 % of the height at the withers.