I was privileged to attend the 7th International Conference on Advances in Canine and Feline Genomics and Inherited Diseases this past week at the Broad Institute in Cambridge, Massachusetts. It wasn’t a large conference: about 150 dog and cat genetics researchers who get together every year and a half or so to catch each other up on what they’ve discovered recently, give each other suggestions about how to proceed or where to get good samples, and give their graduate students a chance to give some talks. I took notes on Twitter (#canfelgen) on my favorite talks (er, those of them that were not too technical; there were quite a few talks that I enjoyed hugely but that did not lend themselves to 140 character summaries). My apologies in advance if I got anything wrong; I was typing with my thumbs as fast as I could and may have made some mistakes.
Robert Wayne, Analysis of recent and ancient canine genomes suggest a new hypothesis for dog origins
Robert Wayne of UCLA talked about ancient canid genomes and “a new hypothesis for dog origins.” We are still not sure which gray wolf population was directly ancestral to modern dogs, and his work has shown that in fact no single population appears to fit the bill. Wayne believes that in addition to all the gene mixing between dog and wolves since domestication (which obviously muddies the picture), there was an ancient population of canids that gave rise to both dogs and wolves which we have not yet found samples from.
Wayne explained that ancient populations of wolves were much more diverse genetically than modern day populations, and we will really need to look to those ancient populations to solve the mystery of dog origins. About 10,000 years ago, populations of both wolves and dogs shrank dramatically in size, which explains why wolf populations are less diverse today than before that bottleneck. This was right around the time that domestication may have been happening, but we don’t know if the events are related.
So, based on this information, Wayne Lab embarked on a study of ancient canid DNA, comparing samples from dogs and wolves both from about 15,000-30,000 years ago. They found that the oldest dog populations were in Europe, not Asia. One interesting finding was in the black coat gene, which was relatively recently introduced from dogs into wolves and has swept through wolves. Apparently, being homozygous for black coat reduces fitness in wolves, but being heterozygous increases fitness. They don’t know why yet.
Wesley Warren, Genetic signatures of selection in the domestic cat lineage
Wesley Warren of the Washington University School of Medicine talked about using cats as models to study domestication. Comparing what we know about the behavior of cats to work in other species (dogs, horses, and chickens), he hypothesizes that cats aren’t actually undergoing significant domestication at all, because they are still very competent at living independently from humans and hunting their own prey. He talked about his work developing a SNP chip for cats, to aid in future genomic research in that species. A SNP chip is basically a library of known polymorphisms in the cat genome — single nucleotides that are known to differ between different individuals. Having all of these SNPs cataloged and available for use on a chip makes looking for correlations between these differences and things like behaviors or diseases much easier. At one point, his chip was used to discover the gene for curly coats in cats.
Warren talked about his recent work comparing the genomes of domesticated cats with their nearest wild relative. He found differences in RALY, a coat color gene. He found that cats have fewer receptors for smell than dogs do, but more for pheromones, and he wants to compare both olfactory and pheromone receptor genes in domesticated cats to big cats. He also talked about the 99Lives project, a project to get more cats sequenced (a theme which was returned to later in the conference).
Anna Kukekova, Simple behavioral pattern: is it simple?
Anna Kukekova of the University of Illinois talked about her work with tame foxes (if you don’t know about the Russian farm fox project, check out the excellent summary at the Thoughtful Animal). Kukekova opened by demonstrating the difference between the lines of foxes selected for tameness and the foxes selected for aggression with video in which a researcher performed a behavioral test on one fox from each line: first standing by a fox’s cage, then opening the door and reaching for the fox, then trying to pet the fox. The videos, shown side by side, were dramatically different: on the left, a clearly wild animal, both cowering from and menacing the human who stood near it. On the right, an animal reacting to human presence just as a dog in a shelter might, almost in a spasm of enthusiasm, wagging its tail, soliciting affection, rolling over to let the human pet its belly. Kukekova talked about analyzing the differences in behavior statistically, and how some of the most important behaviors they found for consistent differentiation between the populations were pricking ears forward, wagging tails, and approaching humans.
Kukekova investigated foxes which were second-generation crosses between tame and aggressive lines. The tame behavior was highly heritable, which was already known. Animals with heritage from both lines usually showed intermediate behavior, on the spectrum between tameness and aggression. What was interesting was that some of the crossed animals showed what she called “switching” behavior: the animals showed tame behavior at some points in the test, and aggressive behavior at others. For example, some of these animals were aggressive to humans who stood at their cage doors, but friendly when the door was opened. Others were friendly when the door was closed, but aggressive once it was opened.
Tara Baxter, Genomic approaches to identify putative canine behavior-associated genes
Tara Baxter of Cornell talked about her method of trying to track down some genes that are associated with different behaviors in dogs. This is a tough problem, as behaviors are usually influenced by multiple genes as well as by the environment, so tracking down a gene that influences aggression (for example) is a lot harder than tracking down a gene that is all by itself responsible for a disease. Baxter reviewed test results from owners who filled out a CBARQ (behavioral survey) about their dogs; she had access to a database of 19,000 surveys, so an impressive sample size. Using these tests, she averaged behaviors for each breed, getting a score of how likely animals of a particular breed were to display a particular behavior (for example, “begging”). Then she did an association study, using a canine SNP chip similar to the feline one discussed above. She used the chip to compare the SNPs found in individual dogs from various breeds, and looked for correlations between the average breed behaviors and the SNPs that she found in individuals of those breeds.
She had some interesting results which will benefit from more study. For example, for the behavior of urinating while left alone, she found an association in an area which is related to behavioral disorders in humans. Finding this association in an area which seems to affect behavior suggested to her that she might be on the right track, though of course a lot more work will need to be done. She mentioned some other interesting associations that she found as well. She also, of course, found associations that appear spurious, such as the association between a gene for long hair and chasing behavior. One amusing association she found was a relationship between the gene for short legs, such as you might see in a corgi, and a fear of stairs! She commented that sometimes physical traits explain behavior.
...And that is my smattering of summaries from the conference. Here’s hoping that I will manage to attend the next one, in eighteen months, in the other Cambridge — the one in the UK!
Poodles - running out of time
Poodles are so broke genetically that only a concerted international effort from those that love the breed will save it, warns the Institute of Canine Biology.
In a strongly-worded open letter to the Poodle Club of Canada, the ICB urges breeders to stop squabbling over cosmetic issues such as the banning of parti-colours or it will be too late for the breed.
"That breeders could even be seriously considering removing dogs from the gene pool of the breed because they have one copy too many of a recessive allele for a purely cosmetic trait is simply breathtaking. It reveals a profound and fundamental failure to appreciate the very dire genetic situation this breed is in."The letter in full:
22 September 2013
Mary Jane Weir
President
Poodle Club of Canada
An open letter to the Canadian Poodle clubs:
We are dismayed to learn that there is organized resistance to the effort in Canada to remove the disqualification of particolor Standard Poodles and their progeny.
The Standard Poodle has been the subject of extensive genetic research over the last few years. The data produced by this work are chilling.
The genetic diversity of the Standard Poodle has been reduced to the point where the immune system is seriously compromised. Without a competent immune system, dogs have no defense against the pathogens that we all encounter on a daily basis. Further, loss of the ability of the immune system to distinguish between an external pathogen and its own tissue is being manifested as skyrocketing rates of autoimmune disorders such as Addison's disease and sebaceous adenitis. These are horrible diseases for which there are no veterinary treatments adequate to restore an animal to normal health. Genetic research can increase our understanding of the underlying pathology of inherited diseases in dogs, but there is nothing geneticists can do to "fix" this problem. Many of the genes necessary for a functional immune system in Poodles have been lost from the breed's gene pool, and there is no modern technology that will restore it to proper function.
At this point, genetic salvation of this breed is going to require a concerted effort by breeders to reduce additional loss of genetic diversity to an absolute minimum. That breeders could even be seriously considering removing dogs from the gene pool of the breed because they have one copy too many of a recessive allele for a purely cosmetic trait is simply breathtaking. It reveals a profound and fundamental failure to appreciate the very dire genetic situation this breed is in.
There is no genetic technology that will restore the Standard Poodle breed to the good health that all dogs deserve. This can only be accomplished by breeders, who must recognize that time is very quickly running out for this breed. It is going to require a substantial realignment of priorities as well as an extraordinary level of cooperation among breeders around the world. Geneticists can provide guidance in this process and there are many that are ready and willing to help. But breeders need to know that it is possible to break something to the point where it cannot be fixed. The responsibility to get this right is solely yours.
Carol Beuchat, PhDScientific DirectorInstitute of Canine Biology, USA&Department of Molecular and Cell BiologyUniversity of California Berkeley, USA
Jonas Donner, PhDDirector of Research & DevelopmentMyDogDNA, Genoscoper Laboratories, Finland
Iwona Głażewska, PhDAssistant ProfessorDepartment of Plant Taxonomy and Nature ConservationUniversity of Gdansk, Poland
Claudia Melis, PhDResearch ScientistDepartment of BiologyNorwegian University of Science & Technology, Norway
Pieter Oliehoek PhD Conservation Biology & Canine Genetics Institute of Canine Biology, USA
CA SharpPresidentAustralian Shepherd Health & Genetics Institute, Incwww.ashgi.org
Finally, an organisation with two fully-descended testicles has stood up and called it as it is, rather than continue to pussyfoot round breeders with an appeasing grin and much hand-wringing about the need to keep everyone on board.
I am sure that Beuchat and her colleagues thought long and hard before writing a letter that so doesn't pull its punches. It should be hard to ignore given the quality of those signatures.
But there's no doubt that being this outspoken to dog breeders is a calculated risk. I know I won't be the only one holding my breath in the hope that it won't backfire.
That said...
The whole canine diversity movement was started by scientist and poodle lover , the late Dr John Armstrong. Thanks to his teaching (see The Poodle and the Chocolate Cake, written in 1998) and initiatives such as the Standard Poodle Project, the breed has been well-documented genetically. Indeed, Poodle breeders were among the first to embrace the need to reduce inbreeding - and the ICB's online course for Poodle breeders which started this week is, I hear, very well subscribed.
The ICB is also hosting an ambitious effort to create a global pedigree database for Standard Poodles - in fact being overseen by Mary Jane Weir, President of the Poodle Club of Canada (so one imagines she must be party to the above letter). I'm a huge admirer of Mary Jane. She knows her stuff and has already done so much to raise awareness about the impact dwindling genetic diversity has on the immune system.
I hope the ICB now throws its weight behind a world genetics congress for the breed.
If Poodle breeders could come together now in an international conservation effort to show the rest of world how it's done, it would be amazing. And a fitting tribute to John Armstrong, who cared so passionately about his Poodles and wanted the world to care, too.
Guessing at the mechanisms of dog aggression
I've been thinking a lot lately about how dog aggression works, since the recent dog fighting bust (second largest in history). Fighting dogs are bred for willingness to attack other dogs, but for docility with humans. You don’t want your fighting dog to turn on you in the training yard or in the ring! Willingness to attack another dog, and to continue to attack when the other dog retaliates, is called “gameness.” Despite intense selection on the part of the dog fighters, the dogs show a lot of variation in levels of gameness: some dogs are very game and some are less so, even with training. But it does seem to be true that gameness is heritable, something you can breed for.
So how do you get aggression which is so specific? And what are the fighting dog breeders actually selecting for? What’s different in the DNA of a game dog and a not-game dog? We don’t have any real idea. Recently I came up with one possibility (too new even to be called a theory). It opens more questions than answers, but here’s the story.
There is a well-studied phenomenon in rats and mice related to the position of the fetuses in the uterus. (I know, uterine position is probably not related to genetics, but bear with me for a minute.) If a female fetus is surrounded by two males, one on each side, she gets more than her usual dose of testosterone in the uterus. Because testosterone helps the developing fetus know what sex to develop into, this extra testosterone makes her develop some masculine characteristics which will stay with her throughout life: she will be what is referred to as a masculinized female. Among other things, her behavior will be affected. Her play style will change to a more rough and tumble style. And she will be more aggressive towards others of her species.
This phenomenon has been demonstrated in multiple species, including guinea pigs, rabbits, and marmots. It is suspected to be in effect in dogs as well: although there are no published papers reporting on it in dogs (at least none that I could find — please let me know if I’m wrong!) I have heard it discussed at dog training seminars as a possibility. And given the range of species it affects and the similarity of effects of reproductive hormones on development across species, it seems really likely to affect dogs.
The big question is: how could this be a genetic phenomenon? The genders of your neighbors in the uterus are random, right? Well, not completely: one of the differences between masculinized and non-masculinized females is that masculinized females have more male offspring. Really. We don't know how that works, though there are some theories about why it may be a useful adaptation to some environments.
Moreover, testosterone doesn't just come from other fetuses. It comes from the mother as well. Some amount of testosterone is normal in development. What if what dog fighters are breeding for, without knowing it, is mothers who produce more testosterone when they are pregnant? Or maybe fetuses which are worse at transforming testosterone into estrogen (as fetuses like to do)? Or fetuses which are more sensitive to testosterone (maybe have more numerous or more sensitive testosterone receptors)?
These questions lead to even more questions, of course, which is why I haven’t even called these ideas a theory yet. Do the more aggressive masculinized female rodents show more aggression to their own species than to humans (which is my initial question about the fighting dogs)? Do male rodents with more males beside them in the uterus show increased levels of aggression? Do we know anything at all about different levels of testosterone released by the dam, not just by uterine neighbors?
There is a lot known about intrauterine position. It is really well studied, partly because it might help us understand the effects of reproductive hormones on fetuses in general, such as possible effects of artificial hormones which are unintentionally introduced into our diets, like BPA. So as I continue to read about it, I hope I’ll start to figure out if this is an idea with legs or just a passing fancy. In the interests of keeping this post readable, I haven’t written about all the interesting facets that I’ve encountered in this phenomenon, so feel free to ask questions. And there are certainly holes in the idea beyond the ones I mentioned, so feel free to point those out, too!
Edited to add: I messed up in suggesting that intra-uterine position might affect dogs the way it has been shown to affect rats, humans, and cattle. Dog placentas are fundamentally different from rat and human placentas, and also different from cow placentas (which form a third category). In short, it would be pretty unlikely for two fetuses to share hormones in-utero in a dog the way they can in rats, humans, and cows. So while I still think it's an interesting idea that a dog fetus could be exposed to different amounts of testosterone in-utero (probably due to processing of hormones by the placenta) and that this could affect its adult behavior, I want to emphasize that it is actually not likely that these hormones could be from other fetuses in a dog. The hormones would be from some difference in the mother, not from a chance alignment of the offspring. So in summary: if your bitch gives birth to one female and two males, that's not a reason to worry about masculinization and temperament in the female.
References
So how do you get aggression which is so specific? And what are the fighting dog breeders actually selecting for? What’s different in the DNA of a game dog and a not-game dog? We don’t have any real idea. Recently I came up with one possibility (too new even to be called a theory). It opens more questions than answers, but here’s the story.
There is a well-studied phenomenon in rats and mice related to the position of the fetuses in the uterus. (I know, uterine position is probably not related to genetics, but bear with me for a minute.) If a female fetus is surrounded by two males, one on each side, she gets more than her usual dose of testosterone in the uterus. Because testosterone helps the developing fetus know what sex to develop into, this extra testosterone makes her develop some masculine characteristics which will stay with her throughout life: she will be what is referred to as a masculinized female. Among other things, her behavior will be affected. Her play style will change to a more rough and tumble style. And she will be more aggressive towards others of her species.
This phenomenon has been demonstrated in multiple species, including guinea pigs, rabbits, and marmots. It is suspected to be in effect in dogs as well: although there are no published papers reporting on it in dogs (at least none that I could find — please let me know if I’m wrong!) I have heard it discussed at dog training seminars as a possibility. And given the range of species it affects and the similarity of effects of reproductive hormones on development across species, it seems really likely to affect dogs.
The big question is: how could this be a genetic phenomenon? The genders of your neighbors in the uterus are random, right? Well, not completely: one of the differences between masculinized and non-masculinized females is that masculinized females have more male offspring. Really. We don't know how that works, though there are some theories about why it may be a useful adaptation to some environments.
Moreover, testosterone doesn't just come from other fetuses. It comes from the mother as well. Some amount of testosterone is normal in development. What if what dog fighters are breeding for, without knowing it, is mothers who produce more testosterone when they are pregnant? Or maybe fetuses which are worse at transforming testosterone into estrogen (as fetuses like to do)? Or fetuses which are more sensitive to testosterone (maybe have more numerous or more sensitive testosterone receptors)?
These questions lead to even more questions, of course, which is why I haven’t even called these ideas a theory yet. Do the more aggressive masculinized female rodents show more aggression to their own species than to humans (which is my initial question about the fighting dogs)? Do male rodents with more males beside them in the uterus show increased levels of aggression? Do we know anything at all about different levels of testosterone released by the dam, not just by uterine neighbors?
There is a lot known about intrauterine position. It is really well studied, partly because it might help us understand the effects of reproductive hormones on fetuses in general, such as possible effects of artificial hormones which are unintentionally introduced into our diets, like BPA. So as I continue to read about it, I hope I’ll start to figure out if this is an idea with legs or just a passing fancy. In the interests of keeping this post readable, I haven’t written about all the interesting facets that I’ve encountered in this phenomenon, so feel free to ask questions. And there are certainly holes in the idea beyond the ones I mentioned, so feel free to point those out, too!
Edited to add: I messed up in suggesting that intra-uterine position might affect dogs the way it has been shown to affect rats, humans, and cattle. Dog placentas are fundamentally different from rat and human placentas, and also different from cow placentas (which form a third category). In short, it would be pretty unlikely for two fetuses to share hormones in-utero in a dog the way they can in rats, humans, and cows. So while I still think it's an interesting idea that a dog fetus could be exposed to different amounts of testosterone in-utero (probably due to processing of hormones by the placenta) and that this could affect its adult behavior, I want to emphasize that it is actually not likely that these hormones could be from other fetuses in a dog. The hormones would be from some difference in the mother, not from a chance alignment of the offspring. So in summary: if your bitch gives birth to one female and two males, that's not a reason to worry about masculinization and temperament in the female.
References
- Ryan B.C. (2002). Intrauterine position effects, Neuroscience and Behavioral Reviews, 26 (6) 665-678. PMID: 12479841
- Monclus R., Cook T. & Blumstein D.T. (2012). Masculinized female yellow-bellied marmots initiate more social interactions, Biology Letters, 8 (2) 208-210. DOI: 10.1098/rsbl.2011.0754
- Hotchkiss A.K., Lambright C.S., Ostby J.S., Parks-Saldutti L., Vandenbergh J.G. & Gray L.E. (2006). Prenatal Testosterone Exposure Permanently Masculinizes Anogenital Distance, Nipple Development, and Reproductive Tract Morphology in Female Sprague-Dawley Rats, Toxicological Sciences, 96 (2) 335-345. DOI: 10.1093/toxsci/kfm002
- Bánszegi O., Altbäcker V. & Bilkó Á. (2009). Intrauterine position influences anatomy and behavior in domestic rabbits, Physiology & Behavior, 98 (3) 258-262. DOI: 10.1016/j.physbeh.2009.05.016
- Correa L.A., Frugone M.J. & Soto-Gamboa M. (2013). Social dominance and behavioral consequences of intrauterine position in female groups of the social rodent Octodon degus., Physiology & behavior, PMID: 23769692
AKC PR offensive - good luck with that...
The AKC has decided to hire Edelman PR ("the world's largest public relations firm") to improve the image of AKC breeders.
In an extraordinary article for this month's Canine Chronicle (read it here), AKC Chairman Alan Kalter lays the blame for the AKC's decline and dwindling reputation entirely on the AR movement.
He writes:
"Just 20 years ago, a purebred dog was the dog to have in your life. Twenty years ago, a responsible breeder was viewed as a respected resource. Twenty years ago there were virtually no important legislative efforts aimed at eradicating all dog breeding.
"What changed in those 20 years? The noble quest to give every dog a “forever” home was co-opted by the animal rights organizations as a method to raise funds for their mission to completely eliminate pet ownership."
There isn't even a nod to the fact that the AKC continues to embrace breeding practices that, if not modified, will lead to the genetic annihilation of all the breeds (or at least the AKC incarnation of them).
There's no mention of the fact that AKC shows continue to reward distortion, deformity and disease.
There's no acknowledgment at all of the responsibility the AKC needs to shoulder for chasing registration dollars rather than good health.
Kalter even goes so far as to say:
"As told by AR groups, purebred dogs have been wrongly defined as being plagued with genetic health and temperament problems caused by breeders."But who else is to blame for Cavaliers with brain cases too small for their brains, or Boston Terriers that can't breathe or breed; or Rough Collies with eyes so small that they verge on micropthalmia?
Neither, when I last looked, was PETA the ones responsible for producing Shar-pei riddled with Shar-pei Fever and entropion, or Flatcoats shot through with cancer - or the growing number breeds falling apart with immune-mediated problems.
And neither is it the HSUS's fault that, for instance, the AKC (English) Bulldog standard still demands a "massive head"- refusing, even to embrace the breed standard modifications introduced in the breed's country of origin.
And, last time I looked, it wasn't the ASPCA that continues to suggest that mating mothers to son/fathers to daughters and brothers to sisters might actually be a good thing. (See here.)
Instead, the AKC has resolutely stuck its heels in, resisted almost all reform, and fired off disparaging potshots at those KCs that have (partially) woken up and smelled the roses.
The AKC has built its house on sand and continues to stick its head into it. And yet Kalter maintains the concerns raised by critics are all "propaganda" and "fiction".
Sure, the anti-breeder camp overstates its case and blogs like mine tend to focus on the bad stuff.
And, sure, there are dedicated breeders that produce good dogs with love and care under the AKC umbrella.
But not to shoulder any responsibility at all for purebred dogs' falling star?
It is true that purebred dogs are in need of some good PR - and, actually, there's real potential to do a good job. Selectively-bred dogs produced by responsible breeders should be treasured and they do have some advantages over crossbreeds/mixed breeds.
But you don't do it by claiming that black is white.
How do you do it?
For a much smaller fee than Edelman PR, please feel free to ask. Although, gratis, I can tell you this: it requires change.
And it does not feature the sleight of brand involved in hiring a PR company to illuminate the good stuff while doing fuck-nothing about the bad stuff.
State of the Zombieverse
I finished my veterinary shelter medicine internship at the end of June. It was a crazy year. I learned so much, and I am so glad that I did it. I do feel that I did what I set out to do: learned a lot about the inner workings of animal shelters and made some very valuable contacts in the field.
I left the South and moved to the Midwest, where this fall I have started a PhD program. I'm working with a lab that focuses on the genetics of canid behavior and domestication (I know, right?). I'm so lucky that a place like this even exists. Sometimes I am frustrated that I found these interests in dog behavior and domestication so late in life, but then I remember that a few years ago, shelter medicine internships didn't exist, and there were no PhD programs studying canid behavior.
My life is very different right now compared to a few months ago. Instead of spending my days at chaotic shelters, I spend them alternating between lab work (so far, running PCRs) and lectures. Instead of having a highly organized schedule, everything is up to me: how many classes to take, how much to work in the lab, even what projects to work on in the lab.
So how will this blog's content change? I'm not sure yet. At a guess, I will write less about shelters, and more about the science behind behavior. I do hope to stay connected to the sheltering world in my Copious Free Time, though, so I may still write about that stuff. I'll see how my career here develops, and of course I am always open to requests from you guys!
I left the South and moved to the Midwest, where this fall I have started a PhD program. I'm working with a lab that focuses on the genetics of canid behavior and domestication (I know, right?). I'm so lucky that a place like this even exists. Sometimes I am frustrated that I found these interests in dog behavior and domestication so late in life, but then I remember that a few years ago, shelter medicine internships didn't exist, and there were no PhD programs studying canid behavior.
My life is very different right now compared to a few months ago. Instead of spending my days at chaotic shelters, I spend them alternating between lab work (so far, running PCRs) and lectures. Instead of having a highly organized schedule, everything is up to me: how many classes to take, how much to work in the lab, even what projects to work on in the lab.
So how will this blog's content change? I'm not sure yet. At a guess, I will write less about shelters, and more about the science behind behavior. I do hope to stay connected to the sheltering world in my Copious Free Time, though, so I may still write about that stuff. I'll see how my career here develops, and of course I am always open to requests from you guys!
Every breed... every test... every lab.. Today's useful link
 |
| Click to enlarge |
Want to check what DNA tests are available for your breed (or crossbreed) and which labs worldwide offer them?
You can now, here.
Thank you to PennGen at the University of Pennsylvania, the WSAVA and Waltham. I couldn't catch it out on a test-ride in terms of breed-specific tests offered - although I found the drop-down menus awkward to use and the info takes time to load on luddite internet connections.
But this is only a small niggle. It's a great resource.
Dogs - the elevator pitch
Last year, with little fuss, a bunch of smart dog and conservation people started the Institute of Canine Biology (ICB) - an essentially-online presence designed to act as a conduit between science and dog-breeders.
"The Institute of Canine Biology is an independent, international consortium of outstanding scientists that are working with the global network of dog breeders to manage and reduce the incidence of genetic disorders in dogs."It's doing that by disseminating research in an engaging way and by offering online courses to dog breeders - both general courses in population genetics, and courses designed for specific breeds.
One for Poodle breeders this month, for instance, includes the latest research into the breed's DLA diversity, a wonderful initiative funded by the Poodle Club of Canada in collaboration with Dr Lorna Kennedy at the University of Manchester.
(DLA analysis looks specifically at genes that code for immune function, of interest to any breed that suffers from immune-mediated conditions as it may provide a way to breed dogs with more robust immune systems.)
The ICB is also hosting The Global Pedigree Project which has the ambitious aim of creating a centralised, free database of the pedigree history of every purebred dog - an international effort that "will bring together pedigree information that is presently scattered among kennel clubs around the world and consolidate it so that the entire history of a breed will be traceable from founders to present day dogs."
The ICB is the brainchild of Carol Beuchat, a biologist and photographer with a lifelong passion for dogs, and she has brought to the party an impressive list of international names. These include Bob Lacy, a conservation guru who has revolutionised wild animal conservation with two key pieces of software - one that models genetic viability (Vortex); and the other a kind of match.com for managed species (PMx).
I spoke to Bob when we were researching the first Pedigree Dogs Exposed to ask if he might be interested in modelling dog populations. He was, but there was nothing that could be done in time for the film. Bob and Carol have already worked together on a paper looking at the genetic management of Basenjiis (link).
Other interesting names at the ICB include:
- French geneticist Grégoire Leroy, who has published several key papers on dog breeding, including several looking at vulnerable French breeds
- population geneticist Katariina Maki who works with the Finnish Kennel Club and is the author of key papers examining genetic diversity in Lancashire Heelers and Nova Scotia Duck Tolling Retrievers (the latter much discussed here).
- CA Sharp, a renowned lay expert on the genetics of Australian Shepherds who runs the fantastic ASHGI (Australian Shepherd Health and Genetics Institute) - a website offering much to breeders of other breeds, too. Sharp has been a tour-de-force in Aussies for several years.
The ICB has been up and running since spring 2012 and Carol has just written what she calls an "elevator pitch" on what dog breeders need to know (and what the ICB's population genetics courses cover).
Now it has to be said that it would have to be a very high building with a bloody slow elevator to qualify. But, in a nutshell, this is what it's all about:
1) All the useful genetic variation your breed will ever have was in the dogs that founded the breed. This genetic diversity is finite.
2) Every generation, alleles are lost by chance (genetic drift) and also by artificial selection by breeders, who select for dogs with the traits they like, and remove other dogs from the breeding population.
3) Because the stud book is closed, genes that are lost cannot be replaced.
4) So, from the moment a breed is founded and the stud book is closed, loss of genetic diversity over time is inevitable and relentless.
5) You cannot remove a single gene from a population. You must remove an entire dog, and all the genes it has.
6) You cannot select for or against a single gene, because genes tend to move in groups with other genes. If you select for (or against) one, you select for (or against) them all.
7) Breeding for homozygosity of some traits breeds for homozygosity of all traits. Homozygosity is the kiss of death to the immune system. And as genetic variability decreases, so does the ability of the breeder to improve a breed through selection, because selection it requires variability.
The consequences of inbreeding (in all animals) are insidious but obvious if you look - decreased fertility, difficulty whelping, smaller litters, higher puppy mortality, puppies that don't thrive, shorter lifespan, etc. Genetically healthy dogs should get pregnant if mated. They should have large litters of robust puppies, with low pup mortality. Animals that cannot produce viable offspring are removed by natural selection.
9) Mutations of dominant genes are removed from the population if they reduce fitness. Mutations of recessive alleles have no effect unless they are homozygous. So rare alleles are not removed, and every animal has them.
10) Create a bunch of puppies that have a (previously) rare mutation, and the frequency of that bad allele in the population increases, so the chance of homozygosity increases.
11) Genetic disorders caused by recessive alleles don't "suddenly appear" in a breed. The defective gene was probably there all along. Make a zillion copies, and you have a disease.
12) Using DNA testing to remove disease genes will not make dogs healthier (see 2, 5, and 6).
13) The breed will continue to lose genes (by chance or selection) until the gene pool of the breed no longer has the genes necessary to build a healthy dog.
14) At this point, the breed might look beautiful (because of selection for type), but will suffer from the ill effects of genetic impoverishment.
15) The only way to improve the health of a breed is to manage the health of the breed's gene pool.
16) The health of individual dogs cannot be improved without improving the genetic health of the population. Population genetics provides the tools for genetic management of populations of animals.
17) Breeders can improve the health of the dogs they breed if they understand and use the tools of population genetics.
.jpg)
The ICB has just launched on Facebook, too - find and like it here.
Subscribe to:
Posts (Atom)