This study also came across other people’s alerts, of course, and was picked up by a blog that tries to point out all the horrible things that people do when they breed purebred dogs. This resulted in a blog post called “Shocking new study: German Shepherds die because they can no longer stand up.” I am not going to link the blog, because I have no desire to give them even one click from my work. Google it if you want to read it.
The big problem is: That conclusion is completely wrong. German Shepherds don’t die because they can’t stand up, and the demographic study explicitly says so. But first…
Here is what you need to know:
The cause of death data is coming from a commercial software program called VetCompass. Practices in the UK that use VetCompass get all their practice data dumped into a big relational database that can then be accessed by researchers. This has led to a bunch of what I’d call quick-and-dirty demographic analyses, where connections are made between the various pieces of data the veterinarians or techs input. Virtually all of them are lead-written by one population epidemiologist, Dan O’Neill. He releases a new one every few weeks, which is why I say these are pretty quick and dirty. O’Neill isn’t an expert on GSDs or on musculoskeletal issues or on dogs standing up; he just looks at patterns of diagnosis data associated with breeds. There’s nothing wrong with doing quick epidemiological studies; they’re a great way to identify where serious research effort should go. But they shouldn’t be confused with serious research themselves.
The other important thing you need to know to understand these results is that the words used for the causes of death of these dogs are not words at all. They’re VeNom codes, which are the numerical codes assigned to diagnoses in the UK. Vets are not keying in “inability to stand”; they are looking for the closest description for the reason the dog is being euthanized, and choosing that code.
So what does the study actually say?
First, GSDs are actually a long-lived breed, especially for their size. The average lifespan across all GSDs was 10.3 years, which takes into account puppy deaths, injuries, and so on. Bitches actually had an average lifespan of 11.1 years, which (remember, that also counts puppies, car hits, and so on) is wonderful. Old dogs are dying at around age 12-13, which is a very normal lifespan for all dogs. As the study author himself says, “GSDs are not particularly short-lived given their large body-size.”
Second, and most important, as the study says, “The true underlying causes for inability to stand can only be speculated but are likely to be multi-factorial and to include combinations of musculoskeletal, neurological, neoplastic and other diverse conditions.”
So why is “inability to stand” so common as a reason to euthanize? Well, I’m not a vet in the UK, but I would make an educated guess that it will start to make sense once you consider how we, as owners, describe the reasons we make the ultimate and final choice for our dogs at the end of their lives. I know I’ve said it, and I am sure you have too – “He just couldn’t get up any more, and I knew it was time.” It is extremely normal for owners to continue to care for their dogs for the last weeks of their lives, even though they know the end is very near, as long as the dogs are relatively active and mobile. When the dog stops being able to stand up and move around, either because of weakness or pain, the dog is euthanized. “Couldn’t get up anymore” or “Too painful to stand and move” aren’t VeNom codes, but “Inability to stand” and the very vague “Musculoskeletal disorder” are.
So don’t read this study as “German Shepherds die because they can no longer stand up” – read it as “Old German Shepherds are euthanized when they can no longer stand up.”
Now go pet your dog, whether she’s a GSD or a Cardigan or any other breed or non-breed. That’s a lot more important than demographic data, after all.
It’s obvious that there is a lot of bad information out there – and a real lack of GOOD information – about breeding merles. What I am going to write is applicable to almost all merle breeds, but I am going to write here as a Cardigan breeder, knowing what I know about Cardigan pedigrees.
I want to get one thing out of the way immediately: I am, personally, very much pro-merle (as a color throughout dogdom) and I am not automatically against double-merle breedings. I think the best breeding rules are the ones that tell clubs to get the heck out of the way and let breeders do the best breedings they can.
Having said that, I believe that every breeder deserves to understand what’s going on so she can make her own decisions, not follow mine. And if genetic information is going to be shared, it has to be accurate.
I am marking this with the year in its title so that, if it is dug up in the years to come, somebody reminds me to come refresh it with the newest information. It is, however, current as of this day, this month, and this year.
What the heck IS merle?
Merle is a mutation in the SILV gene, called PMEL more accurately. PMEL is an important gene area for all kinds of colors in many animals; different mutations in PMEL create white chickens, silver horses, and silver dun cattle, among others.
Merle works by disrupting a certain stage in the formation of melanin. That’s how it changes pigment from its solid state to either white (if the mutation is present in its homozygous state, also called “double merle”), or to an intermediate color somewhere between white and the solid color on the dog. This intermediate state creates the “blue” of a blue merle or the creamy tan of a red/chocolate merle, and also lightens brindle and red/sable.
Every merle mutation carries with it a “tail,” a stretch of about 100 base pairs (a base pair is the linkage between T and A, or between C and G, that you learned about in junior high). That tail is fragile and often breaks. If it breaks shorter than about 65 base pairs, the cell it’s in doesn’t become merle; it stays fully colored.
Because this tail is so long, and it’s quite fragile, it breaks a LOT, and everywhere it breaks becomes a black patch. So when you see those black patches on your merle dog, they’re where, when the cell was first developing, way back when the puppy was an embryo, that tail broke off and the cell looks and acts non-merle.
What about double merle?
In a double merle dog, the action of the mutation is not affected by the non-merle gene, so you don’t see the intermediate state (the silver/grey in a black-based merle). You see a much more complete interruption of melanin formation = a mostly white dog. But the causative factor is the same; it’s an interruption of the way melanin is formed. It’s not, and never would be, a “bleaching” of existing melanin, a white “spot,” a destruction of cells, etc.
What’s the deal with deafness? Do white ears or white skin inside the ears on a merle or double merle mean the dog is deaf?
What creates deafness in merle and double merle dogs is NOT white skin! That’s like saying that spaghetti causes sauce. You have to go back into the “recipe” to understand where BOTH are coming from.
Melanin-producing cells don’t just create skin color. They also create certain aspects of the ear and the eye. In the ear in particular, they keep the cochlear hairs healthy. When they are malfunctioning, these hairs die and the dog is deaf.
“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 is not known, but appears to be associated with the absence of pigment producing cells (melanocytes) in the blood vessels. All of the function 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. “
You can have COMPLETELY WHITE SKIN, including surrounding and inside the ear, and entirely normal hearing – because hearing does not come from skin cells. It comes from the cells that feed the cochlear hairs, and those are not skin cells.
Conversely, you can have absolutely black ears, black hair and skin, and no hearing, because (again) hearing does not come from skin cells.
The fact that skin color is not the same as functional hearing is also why a small proportion of NORMAL merles (single merles, not double) have pigment-related hearing loss. If the merle gene affects enough of the cells that eventually become the ones that feed cochlear hairs, those hairs can be starved and die. Thankfully, it’s pretty rare. Single-merle-related deafness is pretty much invisible in a merle breed, because it’s almost always unilateral and so the dog functions normally. But we shouldn’t pretend that we never have deaf single merles; the evidence is entirely against us.
What creates heavily marked merles versus lightly marked ones?
This is not something that is known for sure, but the working hypothesis is that lightly marked merles have longer and/or more stable tails, and heavily marked merles have shorter and/or more unstable tails. The more often the tail breaks off below that magical 65 base pair length, the more spots the dog will have.
I would also hypothesize – and this is my personal belief, not backed up by research – that the timing of the tail breakage has something to do with it. The cells that will create the skin and hair of the dog start off smaller in number and then multiply, of course, as do all embryonic cells. If the tail breaks when there are relatively few cells, meaning that the broken-tail cell goes on to make many billions of eventual adult cells, that might create the very large patches we see. Tails that break later in the process would create small patches. But, again, that’s my personal guess.
What about cryptic merles?
Well, that depends on what cryptic means to you.
If cryptic means that the dog IS merle but it’s very heavily patched with black, so heavily that the merle is visible only on, say, a cheek or on a bit of one leg – that’s just an extremely heavily marked merle. So you’d go back to the above explanation, where a lot of those tails broke off during the development of the puppy.
There are two other, less commonly used by breeders, definitions of cryptic merle, which deserve to be explained. But you should not take my explaining them as a reason to think that they’re common or they’re going to happen to you. They are phenomena that you are very unlikely to see in your lifetime with Cardigans.
The genuine, real cryptic merle is called Mc (for merle, cryptic) is a normal merle gene minus much of its tail. It occurs spontaneously in multiple breeds when the tail breaks off the merle gene very, very early, even in the sperm or egg cell that eventually goes on to make the puppy. These dogs will be entirely solid, without a hint of merle, but still have the mutated PMEL that means they are merle.
Is Mc the “bogeyman” we’ve all been so afraid of, where using one will result in unforseen double merles? No. An Mc dog will produce like a non-merle in every way, including when bred to a regular merle. A M/Mc puppy may have some additional white, or its color may be a little funky, but often it’s completely normal looking. And M/Mc is not associated with deafness or other issues.
Can Mc revert to a long tail and become merle again? I’ve seen it mentioned in the literature as a possibility, but I think it is a guess by researchers. I don’t believe a reversion has ever been recorded in the literature (if you know of a case study please show me so I can fix this).
Why are some merles so brown and others are light powder blue?
There are a few things going on that can explain this well-known phenomenon.
First, a dog who would have been quite red if it was a non-merle – the tris that have extremely red undercoat and red shafts to their black hairs, or the brindle-pointed blacks that have a lot of brindle visible in the hair – will have very red-tinged merle. The red/yellow pigment – the phaemelanin – is not affected by merle as much as the black pigment. So red will survive the merleing process and look very obvious on the resulting merle dog.
Second, the merle gene itself – and here I am not talking about the tail alone – is an odd kind of mutation called a transposable element, or retrotransposon. It’s not a stolid, predictable, old mutation like “dominant black,” which always does the same thing. It’s a young, rebellious, unpredictable mutation that changes, mutating within itself, creating new and different versions all the time. Those different versions create various shades and effects of merle, from very heavy and muddy all the way to so light that the color between the black patches is actually gone and the dog is white and black instead of silver and black. Some secondary mutations create dogs that are simply grey, no black at all. Others place a patchwork of colors and white that is so striking that it gets its own name, tweed. So when you see a particularly odd merle, especially if it is visibly passed along from parent to puppy, you can often blame one of those secondary mutations.
(By the way, I have seen all of the above – the no-spot, white, and tweed merles – in Cardigans.)
What about “harlequins”?
There are two mechanisms that create harlequin, which is a merle with very little or no color between the black patches. Harlequins in Great Danes are created by the combination of a merle mutation and a completely separate mutation, called H for harlequin. When H is present in a non-merle, it’s invisible, but when it occurs in a merle it erases the color between the patches and creates a harlequin.
The second, and much more common (not in numbers of dogs, but in “how often it has happened in the history of merles”), mechanism is found in non-Dane breeds. In these breeds a mutation within the merle gene itself erases the intermediate form of the color and creates a white and black dog. There are multiple known mutations that do this, and there will likely be many more discovered.
In non-Danes, the mutated merle is passed along by the parent. So an oddly colored merle – whether harlequin or tweed or muddy or whatever – will generally create more of itself. These mutations can therefore be traced through pedigrees… at least until the merle gene mutates again!
Can merle be “carried”? Can it be hidden in a pedigree?
Most breeders use “carry” to mean that the dog is not a color, but has the ability to produce that color. We often say that our reds and brindles carry black, for example, or that our brindles carry red.
If that’s what you mean by carry, then no. Merle can never be carried. Every dog who has a merle gene IS merle. There is never any such thing as a dog who passes along merle to its children but is not merle itself.
The only way merle can hide in a pedigree is if the dog is both merle and ee red. Because merle affects black pigment but spares red/yellow pigment, and ee red dogs have no black hairs and only red/yellow hairs, they can BE merle without LOOKING merle. They are not carrying it; they are still very much merle. But they don’t have the big visible patches.
For this reason, if you have en ee red Cardigan who had one or more merle parents (including ee red merles), it would be smart to gene test it before breeding if you are considering breeding it to a merle. You want to know if your ee red is also a merle, in that case. If your ee red had non-merle, non-ee-red parents, then there is no way it can possibly be merle and you do not have to worry.
What does all that mean? The short story is that if you have bred two known non-merles, the likelihood that a puppy will be merle is INCREDIBLY SMALL. It approaches zero for most breeders.
My dog doesn’t look merle, but he’s got mottled ears. Are these spots on my Cardigan’s white ears, or these spots in his collar or on his face and feet, evidence of merle?
Most likely, no. If your puppy was born without those spots, ABSOLUTELY NO. Cardigans also have a type of marking called ticking, which is spotting that appears on white areas of the hair in the weeks and months after a puppy is born. Sometimes that ticking can be so heavy that it joins together and looks like a merle patch, but merle patches are there when the puppy is born. And, of course, if neither parent is merle, you don’t have to worry even if the spots look a little weird.
Was the Cardigan originally merle or did someone cross a sheltie or collie in?
The original color of the Cardigan was known to encompass “brindle, brown, gold, tri-color, merle,” according to Mrs. Bole, and “yellow,” “blue and grey merle,” and “most frequently a … golden brown merle” (a brindle or sable merle) according to Mr. Lloyd-Thomas. So merle is very definitely an original color of the breed, and was bred frequently in its sable and brindle forms as well as in its black-based “blue” forms.
As a note, isn’t it interesting to see “brown” and “grey” mentioned? From those narratives and from the existence of dogs like Farlsdale’s Silver Smoke, we know that chocolate and slate are also original colors and not evidence of crossbreeding either historic or modern.
Why do people say that merle disappeared and was rediscovered in Cardigans?
Merle never disappeared in the Cardigan, but the black-based blue merle did indeed go away, for about twenty years, from the 1930s to the 1950s.
Since by the 1930s the breed was only ten or twenty years out of the hills from whence it had come, it was very vulnerable to the preferences of the handful of people who had them. There were very few breeders at that time, and they were shouldering the task of keeping the breed going both in the UK and in the US. There was little or no market for show puppies, so generally if the breeders themselves did not keep the dogs for breeding they were never bred.
Mrs. Wylie, in the UK, had been committed to the merle color, and had many lovely dogs. But with her death, especially since she had not spread her dogs around, the black-based “blue” merle disappeared from view.
About twenty years later, the color “reappeared” from reds and brindles.
The key to understanding how this happened is to realize that lumped in with “red” were (and still are) what some breeders called “pale red” and Lloyd-Thomas had called “gold.” In other words, ee reds, which we colloquially call pink. As I said above, dogs who are ee red can also be merle, and still remain (visibly) red. And for those two decades they had indeed stayed red, and thus progressed through pedigrees for several generations.
But, interestingly, the breeders still knew what they were. Those interested in producing black-based merles again were told that these “reds with blue eyes” (ee red merles), when bred to other colors, would make blue merles. So even with the limited knowledge of color genetics of the time, there was no mystery about the fact that ee red and merle could coexist and be used to produce black-based blue merles. And, in fact, that’s exactly what happened.
I’ve heard that “pinks” are a terrible threat to the breed because they hide merle.
You may have a clue about what I am going to say based on the last paragraph – but to make it clear, NO. Pink (ee red) can make merle less visible, but knowledge is all that is needed. Whether you call it yellow, as Lloyd-Thomas did, gold as Mrs. Boles did, light red as is often recorded in pedigrees, or our current pink, ee red is a common and original color in the breed. And it was handled (and, I might add, valued), in concurrence with merle, by breeders without our current gift of easy color testing. Surely we can expect as much of ourselves, especially since we have gene testing at our fingertips.
If you have a pink you think might be merle, test it. If both parents are non-merle, you don’t have to worry.
I still have more questions. How do I get them answered?
Please put them in the comments. If I can answer them, I will. If I need to send you elsewhere, I’ll be happy to do that too.
If you don’t know the basic principles of linebreeding, or what it implies, start up here in this section. If you know all that stuff and want to get to the good part, start here.
One of the most common pieces of advice given to new and experienced dog breeders is to linebreed their dogs. The reason this advice – which is about 150 years old and is a holdover from the livestock breeding strategies of the Industrial Revolution – has survived is that linebreeding, over time, creates a situation where your breedings will be more predictable.
Imagine that you are pulling from a giant jar of M&Ms. The jar is opaque; what you have grabbed will not be seen until you’ve pulled your hand out. You HATE the green ones and you’re not too fond of light brown. You really want the red ones and you’re neutral about yellow. Your first handful brings up a whole bunch of reds, some yellows, a few light browns, and one green.
From here you have a choice – you can either go back in for your next handful, or you can put the handful you already pulled out into a second jar. That second one is a magic jar, and it’ll instantly fill up with thousands of M&Ms, but they’ll be in the exact proportion of colors that you put in.
This is not a trick question – OBVIOUSLY, to get closer to what you want, you choose the second jar. Once the second jar fills, almost every handful you pull out will be pleasing to you. Sometimes, by accident of chance, you’ll get a lot of greens and light browns, but on the whole you’ve created a great way to get the M&Ms you want.
This is exactly the way it works in dogs. By starting with something you like, and then creating many more dogs closely related to the thing you like, you are stacking the odds in your favor.
I hate to say it, but it’s going to be a VERY bad year for any tick-borne diseases and for heartworm. Because of our extraordinarily mild winter, the ticks were active all winter and we didn’t get a hard mosquito kill either. Snowless winters are also very bad for squirrels and other small furries, because they don’t have the snow cover they need to hide, and many have died. Compounding those problems, last year was a bust year for acorns, so a lot of mice and squirrels starved to death last fall. All of those factors mean the ticks have not had a blood meal in months, are going to be traveling further to find it, and they are in greater numbers than they’ve been in years.
I’ve already heard of one of our puppies from last year with a positive Lyme test. I am also sorry to say that (for the first time in my entire breeding life) I am not going to be surprised if one of your dogs comes back positive for heartworm. Sarah says they’ve already seen three positives this spring and it’s going to get worse.
PLEASE REQUEST the SNAP 4DX test! A negative for Lyme does not equal a negative for anaplasmosis or ehrlichia, which can be even worse.
If your puppy comes up positive for a tick-borne disease, a month of doxycyline should set him or her right. Please let me know, but don’t panic. If your puppy comes up positive for heartworm, contact me RIGHT AWAY. There are newer, safer, gentler protocols than the old immiticide (which many vets don’t have on hand anymore anyway, because it’s been short-shipping for months now) and I’d want your baby on those rather than the very harsh treatment. I’ll be happy to advocate for you with your vet if he or she doesn’t want to use the newer dosing.
This concludes your scary health alert of April – back to regularly scheduled puppy love :).
Here’s the background: For a very long time scientists have known that sperm production in mammals is actually pretty fragile. The structure of the testicles is a lot like a huge mall parking lot; in each of the parking spaces baby sperm grow. As they mature they back out of the parking spots and join others in the narrow aisles, moving out to the larger roads and then to the superhighway and then hopefully into the great dark world to make some puppies.
Because everything depends on those little tubes, if you damage them they can’t make the baby sperm. And it turns out it’s very easy to damage them with a mild caustic agent, something that’s not very harmful to anything but those fragile little cells.
Rsearchers figured out that a perfect solution was zinc gluconate. Inject zinc gluconate into a testicle and two things happen – sperm production is drastically reduced and the sperm that are produced have poor motility (which means they can’t fertilize eggs) AND – because testicle tissue also converts the hormones the pituitary gland sends out into testosterone – the testosterone production of the dog dropped by 40%-50%.
This is, honestly, a fantastic thing. The dog can’t make puppies, but he’s still producing 50%-60% of his vital testosterone. The drop in testosterone is why so many serious dog people keep dogs intact even if they have no intention of ever breeding them. It’s just simply healthier. If we can remove the possibility of puppies without removing all the testosterone, it’s a great thing.
The zinc injection that was discovered was put on the market as “Neutersol” in the early 2000s – and promptly taken off again.
Neutersol was taken off the market not because the product didn’t work but because (in their opinion) it was such a breakthrough method that people didn’t adopt it fast enough and (in my opinion) because it was stupidly marketed. Most owners in the US don’t worry about the health problems of neutering; they worry about the price. Most serious dog people don’t worry about the price; they worry about the health problems. Neutersol was positioned at the same price as a surgical neuter, which was ridiculous – they wanted to use it as a cash cow even though nothing about it justifies the price. It’s a zinc gluconate solution in a syringe; you don’t need to use anesthesia. And at that time it was positioned for use only in a very narrow age range of puppies. So vets didn’t offer it as a low-cost alternative and most owners never heard about it, and by the time show breeders and performance owners were ready to say that a male had proven that shouldn’t have puppies (typically over a year old) the product was unavailable.
Esterilsol, which is the same thing branded by a different company, has been promised to solve both problems. They say they’re positioning it at 1/5 the cost of a surgical neuter and that it’s no longer age-specific. If that’s the case – if they can make this work – it’s a process that show breeders and performance breeders should JUMP ALL OVER.
I am hoping their promises are true; if they are, this could be a huge game-changer.
By the way, I happen to have access to one of the (comparatively) few dogs that was Neutersol-castrated; when we pulled my sister’s dog Wilson from the Hartford Pound and had him groomed we discovered that he had been Neutersol-injected. So I can tell you from experience that it leaves dogs with small but intact testicles; there’s no way (because I can hear this question coming) that a judge would think he was normal, but they do still exist. And Wilson “feels” more like an intact male than a neutered one, both physically in muscle tone and width of chest and pelvis and behaviorally. He can (and has) breed and tie but is not enthusiastic (with the exception of Ginny who, in her one and only heat cycle with us, drove Wilson to feats of manliness that shocked even him) and obviously no puppies come of it.
I’ll be watching for more news, and hopefully updates in the fall.
They were all line-clear, so this is no great surprise, but the tests are back and the whole crew – Clue, her son and daughters, and Friday – are negative. Thanks and thanks and thanks again to VetNostic labs, who sponsored free testing for what ended up being about a hundred Cardigans.
3) Stop thinking of the visible colors as one thing.
We do this a lot – somebody will say that brindle is dominant to red or similar – and sometimes it’s loosely true. But if you try to make each color its own unit, you’re going to get hopelessly confused because the real statement is always something like “Brindle is dominant to red but sometimes red looks black” and sometimes it’s “Brindle is dominant to red but sometimes brindle looks white and red looks blue.” That’s how dog breeders can be shocked by litters where a white dog is bred to a blue dog and every single puppy is dark brindle. It was never really shocking at all if you understand how the color genes work, but that breeder is probably never going to do that kind of breeding again because things “went wrong.” That’s how we end up with fear-based breeding decisions, and that’s never the right way to breed dogs.
Here’s why colors are not just one thing:
The major divisions, and remember we can think of them like the face and number cards, are called “loci” (with one of them being a locus): Essentially, a locus is where on the chromosome the color instructions sit.
In junior high biology you probably drew punnet squares, where you figured out that brown eyes are dominant to blue and so on (and if a brown-eyed kid said “But my parents both have blue eyes!” your teacher looked startled and quickly said “Oh, well, there are lots of ways that could happen; remember that we’re just learning some simple rules here!” and then booked it to the teacher’s lounge to share a certain delicious fact with others). Punnet squares are still perfectly valid when it comes to simple genes, but gene loci that have to do with color can have more than two possibilities (though only two can appear at any one time).
The loci are named with letters that refer to their function, like “A” is Agouti. I’ll put them in alphabetical order for the sake of organization but please don’t think that therefore one is more important or one was discovered first or anything.
Here are the various divisions of color, as we understand them in 2011:
I) The “A” locus. A is for Agouti, and refers to the interaction of red pigment (called phaemelanin) and black pigment (called eumelanin). Every dog on earth has genes for both types of melanin, but dogs don’t necessarily show them in equal amounts (one or both pigments may be almost or completely turned off, turned off in certain locations, fight with each other, and so on).
Wild-type hair, designated as a^w (a with a little superscript w, which wordpress is not going to show properly so I need to use the carat. But imagine it superscripted). Wild-type hair is BANDED – the base is black, the middle is red, the top is black. Lots of hair colors have a light base and a dark tip, but only agouti has the three distinct areas. Agouti is seen in some of the primitive breeds and in dogs who are “wolf-sable.” Since the word sable also describes some of the other colors on the A locus, you need to know the difference – all banded/agouti dogs are sables but not all sables are banded/agouti. When in doubt, look for those three areas of color.
Fawn/red/sable, designated as a^y. This is the color that most color genetics nuts like me call “sable.” These are dogs with red coloring that shades to black at the tip of the hairs; the amount of black varies from almost none to a huge amount. All of them have some black on the hairs at birth, at least along the topline. Fawn pugs, red and sable Cardigans, sable collies, Belgian Malinois, fawn and apricot Mastiffs, orange Pomeranians, and red Akitas are all sables, and all identical genetically. Don’t skip that last phrase. They are all the SAME COLOR. In Cardigans it’s common to refer to sables and reds as though they are different colors, and I’ve seen many references to the “sable gene” as being different than the red one. This is just not true. We’re not sure what makes some sables very sooty and some very clear/red, but it’s likely to be a protein modifier of some sort and does not make the dogs different in terms of color genetics. They are the same thing
Black and tan, designated a^t. It’s VERY important to understand what black and tan is. People assume, and want to believe, that it’s a black dog with tan markings laid over it. This has led to all kinds of statements, and even AKC standards, that call for a black dog with certain additional tan markings. What is actually happening with those dogs, though, is that they are sables in which the red pigment – the phaeomelanin – is only on the edges of the body. Think of it as being a bit like dropping a bit of dish soap in the center of a bowl of oily water. The oil immediately leaves the middle of the water and leaps to the edge and builds up there. A black and tan dog is a sable/red dog on which the red is prevented from showing up in certain places, NOT a black dog with additional red. Sometimes the genetic action that shoves the red to the edges is very strong, and sometimes it’s weaker. A weak action leaves very large red borders (as in saddle-marked dogs, where the “points” take up most of the body) or removes the red poorly (as in black dogs with lots of cinnamon or red at the base when you part the hair). However, those dogs are still genetically black and tan; they are not “bad” black and tans. And, dispelling another myth, the amount of red in a black and tan coat does not show the dog’s parentage (those with one red/sable parent don’t have more red, etc.)
Recessive black, designated a. Recessive black is the all-over black of German Shepherds and Pulis and bi-black Shelties. Dogs have two flavors of all-over black – one is a dominant black (so a black dog can carry brindle or sable/red) and one is a recessive black (so in those breeds the brindles or the sable/reds carry black). Thankfully – at least as far as I know – there aren’t breeds that have both dominant black and recessive black. You just have to know which kind your breed has. Cardigans don’t have this gene, as far as we know.
II) The “B” locus (B is for black/brown)
All eumelanin on the dog is black, designated B. This is the normal and dominant gene, and allows the dog to make black pigment.
All eumelanin on the dog is brown, designated b. This changes all black pigment to brown pigment (NOT “red” or tan pigment, but chocolate brown). There are actually a bunch of b mutations but they all do the same thing and so most people just say “b.” All brown/liver/chocolate dogs are homozygous bb at this locus. Dogs who are bb cannot make any black pigment at all. All dogs with any black pigment at all, anywhere on their body, even if parts of their coat look kind of chocolaty, are either homozygous BB or heterozygous Bb. The bb chocolate mutation also changes the color of the nails and eye leather and nose leather, to either a pinkish chocolate color or what is sometimes called “self” coloration – a dark flesh color. (Interestingly, something very much like the “b” mutation occurs in humans, causing African American skin tones to turn lighter and redder.)
III) The “D” locus (D is for Dilution)
All melanin is fully saturated in small grains along the hair strand, designated D.
The melanin occurs in large clumps along the hair strand, designated d. This clumping makes the hair lighter in color, and so the dog looks “blue.” The d dilution changes black dogs to blue, chocolate dogs to a light brown/grey, and red dogs to a dusty red. It affects both types of melanin, though it seems to affect the eumelanin much more than the phaeomelanin.
IV) The “E” locus (E is for Eumelanin, which is black pigment)
Black pigment may cover the body, designated E. We used to think that this was “THE” black-dog gene. We now know that’s not the case, which is why there’s a “new” locus called K for blacK, but the E locus still functions in some dogs to make them black.
Black pigment may cover the face, designated E^m. This is the black mask that’s common in all but the hound breeds.
Black pigment may make an overlay on the body but leave lighter/creamier color on the belly, neck, legs, and face, designated E^g. The “g” is for grizzle, which is the color in Salukis that led to this gene being described. Grizzle is very similar to the “urajiro” in Shibas and the other spitz breeds (including, and this is interesting to corgi breeders, the Pems), and my personal bet is that we’ll find that these breeds are E^g as well. Right now we don’t know; research on this particular variation of color isn’t complete. Grizzle/urajiro can be confusing if you just look at it cosmetically, because on a black dog it “looks” like the dog is a wide black and tan (where the points are really big and soft instead of defined and small). On a sable dog it looks like the dog is trying to be a black and tan dog (I’ve seen people assume that these lighter areas on the underside mean that the dog carries tricolor, for example). But this is NOT the black and tan gene (a^t, above)
Black pigment may be entirely prevented from occurring on the body, designated e. Dogs that are ee are always a red, cream, or white color; they cannot have any black hairs anywhere. This is very common across the dog world; ee reds are found in a huge number of breeds. All Viszlas are ee reds, as are all Irish Setters, yellow Labs, Golden Retrievers, red/apricot/cream/white Poodles, and so on. “Pink” Cardigans are ee reds. As with the chocolate gene we looked at earlier, if even a single hair on the dog is black it is NOT an ee red.
V) The “G” locus (G is for Greying)
G is a postulated locus (we know it’s there but have not yet mapped it), designated G for graying. It’s the gene that turns silver poodles from black at birth to nearly white in age, and is also seen in Kerry Blues, a bunch of the terriers, and in many of the breeds that lighten progressively as they age (like Great Pyrenees and Lowchen). In other words, it’s probably a lot more common than we think. Greying seems to be dominant to non-greying, and it occurs no matter what other colors are present on the dog. Interestingly, if a dog has a black mask and the G gene, the rest of the dog will grey and the mask will stay black for years longer than the body.
VI) The “I” locus (I is for Intense)
I is another postulated locus (we’re pretty sure it’s there but are not exactly sure how it works) that has come to encapsulate what geneticists used to call “Chinchilla” or the C locus. It’s no longer called C because C is reserved for a type of severe dilution that causes genuine albino coloration, and it turns out that what we see in dogs is not a form of albinism but a form of diluting or washing out of the red pigment (phaeomelanin) but not the black pigment (eumelanin). The “Intensity” effect seems to be cumulative – that is, it may repeat itself and become stronger. If that turns out to be true, then one copy of the “I” gene changes a dog from, say, red to apricot, two copies will change a dog from red to cream and three copies will change a dog from red to white. The “I” effect is what creates most of the dog breeds who are white but retain black or dark nose leather, skin, and eyes. This includes white poodles, white German Shepherds, Samoyeds, and so on. I also dilutes red to apricot in Poodles and Vallhunds and Tervuren (“red” and “grey” Vallhunds and Tervs are actually sable and apricot sable). The I gene is very widespread and probably occurs relatively unnoticed in many breeds where the deepness of the red coloration is not paid much attention to.
VII) The “K” locus (K is for blacK). The K locus works with the A and E loci to result in various degrees of black and red pigment.
The dog is black all over, designated K. This is the “dominant black” present in Danes and Labs and in a huge number of other breeds. Because the black is dominant, the dog could be homozygous black (KK) or heterozygous black (Kk^br – black carrying brindle; or Kk^y – black carrying some sort of red/yellow like black and tan or fawn/sable).
The dog is brindle, designated k^br. The black is allowed to be expressed in a series of stripes or chevrons on the dog. The color of the coat under the striping depends on the E and A loci.
The dog is not black all over, designated k^y. What the dog actually ends up looking like depends at this point on the E and A loci; it could be fawn/sable, black and tan, etc. Because k^y is recessive to k^br, you can have a homozygous brindle or a brindle carrying k^y.
VIII) The “M” locus (M is for Merle)
The merle action is absent, designated mm. Whatever the dog is going to look like, he looks like.
The dog has a defect in its production of melanosomes that renders some of them ineffective, designated Mm. Where the defective melanosomes end up on the skin of the developing embryo, the dog’s eumelanin will be less visible. Where normal ones end up on the skin, the dog’s eumelanin will be normal looking. These patches of normal and defective melanosomes create the characteristic pattern of a merle dog.
The dog has a widespread destruction of its melanosome production, which leads to a coat that’s largely white – designated MM. Unfortunately, those same cells also are the ones that allow a dog to hear (the pigment cells in your inner ear are what tell your nerves to fire, which is what we interpret as sound) and also form some of the eye structures, so a dog with a drastically reduced number of healthy melanosomes is often deaf and may also have eye issues. The harm done to the dog seems to vary by breed, interestingly – Catahoula Leopard Dogs are often MM but are rarely deaf, while MM Danes are virtually always deaf and often blind. At least anecdotally, MM Cardigans are often deaf and may have eye issues but there are some individuals with neither problem.
To really address spotting would take a book in itself. The short story is that we used to think that all white spotting on dogs was part of the “S” locus, but now we know that there are multiple gene actions that produce spotted dogs and everybody is kind of back to the drawing table trying to figure out exactly which actions apply to which breeds and when.
You can’t tell just by looking at a dog which spotting gene is at work, because they all function the same way. Pigment cells travel over the developing embryonic body almost like frosting is drizzled over a bundt cake – beginning at the top of the head, down the topline, and then spreading down the body of the dog and ending at the feet and the chest and midline of the stomach.
Anything that stops the progression of those pigment cells creates a white spot, and because of the way the pigment cells move the spots always begin on the feet and chest and tailtip. Then as the action of whatever gene it is strengthens the dog becomes white around the neck, then has breaks in the body color, then begins to lose the body color entirely, then loses the head color.
The different spotting genes seem to have varying degrees of predictability, too – in some breeds, like Cardigans, you can “fix” a spotting pattern relatively easily and have most of your puppies with very similar white. In other breeds, like Boxers, the spotting pattern is created by a different genetic action and so their markings swing wildly from zero white to entirely white dogs in the same litter.
There isn’t a designation yet for the kind of white spotting we have in Cardigans and other herding dogs. We know it’s not a form of piebaldism and we know that it is common in herding dogs and not terribly common in the other groups. It’s predictable and breeds true. For lack of a better word, I call it “herding spotted.”
Cardigans ALSO have the piebald gene, which is what creates breaks in our blanket colors, gives a lot of tail white, and causes the white markings that go up high on back legs. We don’t know exactly how the piebald gene or gene group works, though, and how it combines with other spotting patterns, because in some breeds it seems that when two piebald carriers are bred you get dogs that have massive amounts of white (that’s the way collies work, where two dogs with stifle white can produce color-headed whites), where in other breeds piebald carriers produce only a little more white than before. In my own breeding, I paired two Cardigans with very high stifle white and big fat tailtips and I got some small breaks in the blankets and some white coming up the sides of the puppies (they were clearly showing the effects of the piebald genes meeting) but I got no splashes or spots. So we honestly just don’t know a ton about it in Cardigans.
Until we have a more encyclopedic knowledge of the spotting genes it’s difficult to use them to breed carefully, except for this (which all breeders should understand): Every puppy gets color that bundt-cake way. There are no exceptions. And sometimes things happen embryonically that prevent the color from migrating fully down over the body, leaving a solid-colored puppy with white toes and a small white chest spot. These puppies are NOT genetically spotted. They are genetically solid with a little glitch in the color migration. They are not evidence of cross-breeding with a spotted dog, they are not scary, and most of the time they won’t reproduce those spots.
Ticking has not yet been given a locus name, as far as I know, but it is very definitely a genetic phenomenon and is dominant to non-ticking (in other words, at least one parent must be ticked to produce a ticked puppy). Ticking is coloration that fills in as small spots or flecks within the white-spotted areas of a dog. It only appears within white spots. Heavy ticking is called roaning, and is found in English Cockers and Australian Cattle Dogs and others. Light ticking is found throughout the dog world. Some people think that ticking is always black, but that’s not true. The dog will tick in whatever color the white spot has deleted – so if the dog is tan or red, or the white spot covers a place that is cream or blue or whatever, the ticking will reveal that color and not black.
XI) Merle modifier: Harlequin
The dog is a black and mouse grey merle, designated hh.
The dog is a harlequin, designated Hh. The harlequin pattern is not really a gene but instead a particular protein encoder that tells the body to not fill in the areas that would be mouse-grey in a merle. As a result, the dog is white and black.
The dog is a homozygous harlequin, designated HH. No living HH dogs have been found, leading to a conclusion that H is an embryonic lethal.
Understanding coat color (and inheritance) in the Cardigan Welsh Corgi
Because the Cardigan has a history shared with a broad range of dog types – the teckel (primitive dachshund, accessing the hound genes), the herding dogs (accessing those genes, especially the recessive black), and even the spitz dogs (accessing certain dilution genes), we have the possibility of creating in our breed a whole bunch of colors. It’s like a playground for those who love color genetics, like I do, but unfortunately that possibility, and the associated “surprises” that sometimes pop up in litters, has made many breeders very afraid of what might happen when colors are bred together. There’s a feeling, which I think is quite incorrect, that the better breeders are the ones that do the very tightest range of breedings, and so to be a good breeder you need to stick within a very few possible breedings and possible colors lest you end up with what people call “bad” color.
My goal is not to tell you which breedings to do. It’s to show you that color breeding is one of the few things in dog breeding that we really can understand, get a grasp on, and control. It can feel very mysterious to a new breeder, and even to some experienced ones, but it’s actually very predictable and should never be scary.
Here are the things you need to know:
1) Colors are proteins, not paint.
Since the beginning of organized breeding, breeders have been tempted to think of coat color as though it can be mixed and swirled. Need a lighter color? Breed to a lighter dog. Need a darker one? Find yourself a black dog. This has led to all kinds of bizarre recommendations, old wives’ tales, and perfectly good dogs being discarded because they showed “evidence” of an unwanted color.
It’s completely wrong and we’ve got to stop. The color genes code for particular proteins that, when they work in concert with all the zillions of other proteins in the body, create a color on the outside of the dog.
The color genes are much more like a deck of cards than they are like paint. There are some major divisions (think of them like the face cards and number cards) and within each division there are a number of choices (think of the suits).
When all the cards are put together, they combine to form powerful units that tell the dog’s developing body where to put color cells and what proteins those color cells are allowed to produce.
But, in the same way that a full house usually beats a pair of twos, but make that pair into four of the same card and it beats the full house, the cards themselves don’t have the power. The combination does. And, in the same way that handing a two of clubs to one player may give him a straight flush, but handing the same card to another player gives her two of a kind, the contributions of each parent dog may result in a whole ton of different colors in the babies – sometimes dramatically different cosmetically than either parent.
2) Proteins are never just about color.
The genes that affect color are not just inkjet printers. That’s been the number-one discovery about color this century, and has turned a lot of color genetics on its head (and made things very exciting). As it turns out, the colors appear the way they do because the gene introduces defects into certain proteins. Most of the defective proteins don’t do anything bad to the dog, but a few of them are actually harmful – for example, it now seems relatively certain that the gene that turns Dalmatians from ticked dogs (with lots of little round specks) to Dalmatians (with a few big round dots) is the same gene that makes them unable to break down uric acid properly.
We’re also discovering that certain things we thought were simple are not so simple at all. I am sure you’ve heard that if you’ve got a big white blaze you run the risk of getting a blue eye. We want to intuitively understand this like it’s paint – paint white over the eye and it turns blue. But in fact it’s much more likely that the same proteins that prevent pigment from being expressed on the skin affect the way in which the eye develops. What we’re seeing is not causation – the white blaze doesn’t cause the blue eye – but correlation – same protein affects both skin and eye.
We’ve got to get our brains around this because the next few decades are going to see an explosion of new knowledge and we’re going to have to make ethical decisions based on that knowledge. What if we find that (and I’m just making this up, but it’s not far-fetched) chocolate-pigmented dogs are forty percent more likely to have thyroid problems than black-pigmented dogs? Or that (and this one I’m not making up) it may be that all merle dogs are at risk of hearing loss? We’re going to have to address that new information, and to do so we need to understand it.
A few weeks ago Doug and I offed seven young roosters (NOT a great experience – and no, not the one in the picture; I wouldn’t do that to you!) and gave them to the dogs as soon as we knew they were deceased. Feathers-on, everything exactly as in life except that they weren’t in life anymore.
I sort of thought there might be lots of hemming and hawing and nosing around and feather-pulling amongst the dogs. I couldn’t have been more wrong. They ate those birds like it was the best thing they’d ever been given; every single bit was eaten except a few of the biggest wing feathers.
It was all they ate for about four days and they’ve been snacking ever since on the frozen-and-buried portions they have stashed in the snow.
Because of this I am forced to come to the following conclusions:
1) I hate killing things.
2) The dogs look intensely amazing.
Seriously, where they’ve always had great coats, typical raw-fed dense gorgeous hair, now their coats are PACKED, from the skin out. Juno looks like a fur seal; I have to dig hard to touch Clue’s skin. And they’ve all put on hard flat muscle over the hard muscle that was already there. Bramble combined his rooster experience with a crash diet (meaning “If you steal food from people one more time I’m going to crash you”) and he lost all the typical dachshund heft and looks like a teenager again.
The casualty of the diet was poor Ginny, who was so appalled that she was being offered something that had feathers on it that she went on a hunger strike and refused to eat anything even resembling chicken. I caved today and bought her Bravo and Orijen because she was looking decidedly wan.
So, aside from Ginny, we now know we need to keep supplying whole birds to the other dogs. There are two or three more that are heading in that direction thanks to a sudden fondness for crowing, and after that I need to figure out whether I’m going to buy and raise meat chickens for the dogs or whether I can maintain enough of my own production to give each dog a whole one every couple of weeks and keep the pullets for myself. I also need to streamline the “process.” Ick.
More to come as we figure out how to do this the right way.