Editor’s note: This very timely piece is one of the last articles I received from Dr Cattanach, and was published in the May 2019 Boxer Digest along with some wonderful photos from his website of Dr Cattanach with Ch Steynmere Nightrider.
When my ex-husband and I started out in Boxers in 1973, we quickly learned not to question (at least not openly) the American Boxer Club’s proscription against white Boxers: to wit, “reputable” breeders were not to register, sell or even “place” the white puppies that appeared with great frequency in flashy x flashy litters…despite that backyard breeders were free to sell “rare white boxers” for many times the price of a plain brindle puppy from a champion-sired litter. The rationale for that proscription was the alleged poor health and genetic inferiority that accompanied white coat color.
The ABC has come a long way since then, bowing to the lobbying of many of its members, especially new members, who wanted to be able to acknowledge their white puppies and place them in loving homes, along with the fawn and brindle “pet” puppies in their litters. The relatively new AKC Limited Registration policy greatly facilitated the ABC’s official enlightenment on the subject.
Now, some breeders are discussing the possibility of being able to use white boxers in their breeding programs. The following is a letter sent by UK geneticist and Boxer breeder Dr. Bruce Cattanach to a group of Italian Boxer fanciers,
29th March 2019
Breeding from white Boxers
Dr. Bruce M. Cattanach
I have been asked to comment, as a professional research geneticist and experienced UK Boxer breeder and judge, on the belief of some breeders that white Boxers are prone to health problems, and that breeding from them therefore poses risks to the genetic health of the breed.
My short answer is that there is no basis whatever for this idea.
The rationale for my response lies primarily with the fact that the white spotting gene responsible for the white ‘colouration’ in Boxers (s^w) is the same as that for the white coats in dogs of a number of breeds (Bull Terriers, Sealyhams, Dalmatians etc) and in none of these breeds have serious abnormalities been found. There is however a variably minor incidence of deafness in these white dogs, but this is well known and understood.
The validity of the above statement is confirmed by studies at the DNA level which have shown the same gene locus is involved in these ‘white spotting’ breeds. That there are other breeds, such as Collies and Dachshunds, which have dogs with white markings that ARE associated with serious abnormalities, is irrelevant, as the gene, Merle (M), responsible for white markings in these breeds, is different from that in Boxers (s^w). M functions in a different way from s^w, it is located on a different chromosome, and also has a different mode of inheritance. The white Boxer is not at risk of any defects other than, as said, the low risk of deafness.
How large is the risk of deafness?
I know of no scientific study on deafness directly in Boxers. A best guess for incidence of deafness would be that it will be similar to that in White Bull Terriers, a breed in which the incidence has been found to be less than 2%. This is a breed in which, like Boxers, there has been no selective breeding for the presence/absence of pigmented patches in whites. The incidence of deafness is higher in Dalmatians (5% to 12%) but this higher incidence has been attributed to the heavy selection for totally white dogs in this breed (excluding the spotting which derives from a different mechanism); pigmented patches are not wanted in Dalmatians, only spots. And deafness correlates with pigmentation seen in the coat.
It may help understanding of whites and deafness if the mechanisms involved are explained. Basically, the primary effect of the responsible s^w gene involves pigment cell migration. Before birth, pigment cells in the foetus are confined to paired sites along the back near the spine, from head to tail. There may be three such sites on the head (around the eyes, the ears, and the occiput), perhaps six on the body, and several on the tail (numbers are based on my own studies). Pigmentation, as we observe it, is achieved by migration of the pigment cells from their starting sites to spread down the sides of the body with most of the migration ceasing prior to birth. It often incomplete such that more distant regions (between the eyes, and on the chest, neck, belly and lower legs) may not be reached and therefore remain white. The ending of this migration is best seen on the head where it continues for several days after birth (the white blaze gets smaller and the nose becomes pigmented). The pigment cells also spread internally where they give colour to the eyes and have a role in the maintenance of the auditory hair cells of the inner ear. If they do not reach the eyes, the eyes are blue rather than brown. If they do not reach the ears, the auditory hair cells die within a few weeks of birth, when hearing is then lost (about 6 weeks). The migration is not uniform; left and right forelegs, for example, may have different amounts of white. Likewise, the eyes can be of different colours (brown and blue) and, with the ears, deafness can affect one or both. There is a correlation between extent of white in the coat and incidences of blue eyes and deafness. This is best documented in Dalmatians: dogs with the most white in the coats are more likely to have blue eyes and become deaf. The extent of the migration is loosely inherited.
As I have indicated, the white spotting gene (s^w) is primarily responsible for whites in Boxers but there are a number of versions (alleles) of this gene in other white marked breeds. Only two of the versions now seem to exist in present-day Boxers:
- the normal full-colour version (S) gives, in the double dose (S/S), solid Boxer which may still have a white chest spot and maybe white toes (the pigment cell migration is near complete).
- the extreme version (s^w) gives, in the double dose (s^w/s^w), the near all-white dog, which may have occasional pigmented patches which are most often located around the eyes and/or ears on the head and more rarely elsewhere on the body.
But the combination of the two versions (S and s^w) gives the intermediate, flashy Boxer that is generally favoured for show purposes. The white marking indicates the limitation of the spread of pigment cells. In S/s^w dogs, the spread is less (more white) than in S/S dogs, and obviously far more than in near all-white s^w/s^w dogs. Generally, the amount of white in the S/s^w dogs is less than one-third of the total, as actually required by the Breed Standard.
In summary, genetic studies indicate that white Boxers differ from flashy Boxers only by the more restricted level of pigment cell migration, and they are not at greater risk of major inherited disease that would validate their exclusion from breeding and showing. They are, in any case, knowingly produced by the regular use of flashy animals for breeding. Thus,
flashy x flashy produces - 25% solid, 50% flashy and 25% white
But the Breed Standard does not disqualify the flashy white-producing dogs. However, disqualifying whites from showing may be acceptable, but only for cosmetic reasons. But to ban them for breeding based on imagined abnormality has no scientific justification.
If I may add my own view as a former Boxer breeder: I believe few serious breeders would want to produce high frequencies of whites, so matings of whites to flashy dogs would seldom be considered. Likewise, matings between whites would also be avoided. But if whites could be exclusively mated to solids, this could be seen as an acceptable breeding option and it would not ultimately cause any increase in the numbers of whites or damage the breed in any way. Indeed, as all puppies (100%) from white x solid matings would be of the favoured flashy appearance, thus
white (s^w/s^w) x solid (S/S) can only produce flashy (S/s^w)
and these would breed exactly as flashy dogs from routine flashy x flashy matings. It would leave open a further breeding option for show Boxer breeding.
I have bred from a number of white Boxers for experimental reasons, and always they bred exactly as expected, and none produced abnormalities of any kind.
Bruce M Cattanach BSc PhD DSc FRS
(Retired as Acting Director of the Medical Research Council Mammalian Genetics Unit)