Tag Archives: Gordon Setter

Grooming – Gordon Setter Videos

Oster ProfessionalOster  has offered many best selling grooming products for many years and are especially known for their animal clippers. Now they’re offering even more help and support for the self groomer via their website where they’ve posted very helpful video clips demonstrating how to groom several breeds. For us that includes the Gordon Setter. How wonderful is that? Here are all the links to their videos…happy tails to you all!

Sally Gift, Mesa AZ                                                                                  Photos by Ben Perez

14 Videos about grooming a Gordon Settter13173347_178245152575572_8841807142114207002_o

Face & Skull – Gordon Setter

Face & Muzzle – Gordon Setter

Face & Eye – Gordon Setter

Face & Ear – Gordon Setter

Body & Neck – Gordon Setter

Body – Gordon Setter

Body 2nd Time over – Gordon Setter

Body 3rd time over – Gordon Setterjuly

Front Leg & Legs – Gordon Setter

Legs & Front Foot – Gordon Setter

Rear leg – Gordon Setter

Rear Foot – Gordon Setter

Tail – Gordon Setter

 

Recap Complete – Gordon SetterJuly3

Nail Grinder – How to use

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Photo by Bob Segal

Why are European Dogs So Well Behaved?

Home

Why Are European Dogs So Well Behaved?

Dogs, Euro Style

By Kama Brown CPDT-KA, January 2017

Together we will build a resource

“Together we will build an interactive, searchable resource for the Gordon Setter Fancier” – Sally Gift

I have been asked by some GSCA members about the origins of the Gordon Setter Expert and, in talking to them, learned that there are many misconceptions about why I developed it. Gordon Setter Expert started because as chair of the GSCA Breeder Education committee, I heard from members expressing the need for a web based resource and communication tool for not only member owners and breeders, but all Gordon Setter fanciers. My intent, therefore, was to create a blog which was to be owned and hosted by the Gordon Setter Club of America, Inc. and managed by a team of GSCA member-expertsI called this blog Gordon Setter Expert because I envisioned the content would be contributed by the hundreds of Gordon Setter experts among GSCA ranks. I purposely used the word Expert as a word to draw non-GSCA members, to gain trust, to attract Gordon lovers to our resource and to the Gordon Setter Club of America. I hoped to illustrate, through our web presence, the value of being a member of the GSCA.

My proposed prototype for this blog was sent to the GSCA Board of Governors for approval in January of 2015, where that necessary approval stalemated. Understanding then that some on the Board at that time did not recognize the value for the breed as well as the club, as a labor of love for our Gordon Setter breed, I decided to launch this blog on my own, as a personal contribution to the breed and their owners. I believed then, and continue to believe today in this blog’s ability to promote, protect and advance the purebred Gordon Setter.

It will always be my hope to someday transfer this blog to the Gordon Setter Club of America, in the hope that my efforts will be accepted and GSCA will carry on the work that has begun here.

Today GSE visitors will find over 250 articles related to breeding, showing, field events, performance events, training and health. Gordon Setter Expert is followed by 2,372 people who receive the new articles by email and other web services. Followers come from all walks of life, from all around the world and include many of the current GSCA membership. I am pleased to see that so many individuals, breed clubs, and parent clubs link to Gordon Setter Expert in order to share this resource with their friends, members and visitors to their websites.

Gordon Setter Expert proposal sent to the GSCA  To read my first proposal to the 2015 GSCA Board to gain their approval and support to create this blog on their behalf click this link.

To learn more about me and GSE click here to read the “About” page

Sally Gift, Mesa AZSundance Logo

Sally at the beach

Please note that the views and opinions expressed on this blog are those of the authors and do not necessarily reflect the official policy or position of the Gordon Setter Club of America.

VACCINATION AGAINST CANINE CANCER STUDY

Thank you Barbara Manson, Stoughton WI for bringing this to our attention!

Attention all Gordon Setter owners – our breed is included among those being recruited for this study. If interested, follow the link below to submit your information online.

Sally Gift, Mesa AZ

VACCINATION AGAINST CANINE CANCER STUDY

UW Veterinary Care’s Oncology Service is recruiting dogs for the Vaccination Against Canine Cancer Study (VACCS trial), the largest clinical trial conducted to date for canine cancer.

The goal of the VACCS trial is to evaluate a new vaccine strategy for the prevention, rather than treatment of dogs with cancer. Healthy dogs of certain breeds, 6 to 10 years old, will be randomized to receive either a series of vaccines similar to other routine vaccines that are given to dogs currently, or placebo vaccines. Dogs will live at home and be checked 2-3 times yearly for 5 years after enrollment. A financial incentive will be offered to defray the cost associated with diagnostics and treatment of any cancers that dogs develop, regardless of whether they are receiving vaccine or placebo.

In addition to potentially providing a new strategy for cancer prevention in dogs, if successful, this study could provide important justification for eventually looking at a similar approach in humans.

TO QUALIFY, DOGS MUST MEET THE FOLLOWING CRITERIA:

  • Owners must live within 150 miles of one of the participating trial sites
    • University of Wisconsin–Madison · Madison, Wisconsin
    • Colorado State University · Fort Collins, Colorado
    • University of California–Davis · Davis, California
  • Age: 6 to 10 years old
  • Weight: 12 pounds (5 kg) or more
  • No history of previous cancer
  • No significant other illness that could result in a life span of less than 5 years
  • No history of previous autoimmune disease
  • No current treatment with oral or injectable immunosuppressive medications such as prednisone, cyclosporine, mycophenolate, or tacrolimus

THIS TRIAL IS NOW BEGINNING THE PATIENT ENROLLMENT PROCESS.

If you believe your pet meets the study criteria and would like to receive more information, please click the button below to enter your contact details and preliminary information about your dog.

A member of the Oncology team will contact you within a week of your entry to collect further information and schedule an appointment.

Questions? To learn more about this study, please email us: vaccs@vetmed.wisc.edu.

DOGS MUST BE ONE OF THE FOLLOWING BREEDS:

  • Mixed Breed
  • Afghan Hound
  • Airedale Terrier
  • Alaskan Malamute
  • Basset Hound
  • Beagle
  • Bernese Mountain Dog
  • Borzoi
  • Boston Terrier
  • Boxer
  • Briard
  • Bullmastiff
  • Cocker Spaniel
  • Corgi
  • Deerhound
  • English Setter
  • Field Spanie
  • Flat-coated Retriever
  • French Bulldog
  • German Shepherd
  • German Shorthaired Pointer
  • Giant Schnauzer
  • Golden Retriever
  • Gordon Setter
  • Great Pyrenees
  • Irish Setter
  • Irish Water Spaniel
  • Irish Wolfhound
  • Italian Spinone
  • Keeshond
  • Labrador Retriever
  • Leonberger
  • Newfoundland
  • Norwegian Elkhound
  • Nova Scotia Duck Tolling Retriever
  • Old English Sheepdog
  • Petit Basset Griffon Vendeen
  • Rhodesian Ridgeback
  • Rottweiler
  • Saluki
  • Scottish Terrier
  • Shetland Sheepdog
  • Siberian Husky
  • Springer Spaniel
  • Staffordshire Bull Terrier
  • Standard Poodle
  • Tibetan Terrier
  • Viszla
  • Welsh Terrier
  • West Highland White Terrier

FAR Better than Tomato Juice as a Skunk Rinse…

OMG!  SKUNK!

With the arrival of Fall comes bird season and the hunt, which reminded me that sometimes “stuff” just happens when you’re out having fun with your dog! For those unexpected encounters, Dr. Becker’s video and recipe could be the solution to your dilemma, just follow the link or the directions below.

Sally Gift, Mesa AZ

FAR Better than Tomato Juice as a Skunk Rinse…

By Dr. Becker

In this short video, Dr. Karen Becker shares the very effective method she uses to get rid of skunk smell on pets.

Today I want to give you my skunk rinse recipe, and here’s hoping you never have to use it!

If, heaven forbid, your dog or cat is ever sprayed by a skunk, you should have this recipe on hand. The sooner you apply the solution to your pet’s fur, the sooner he’ll get relief and smell better.

Skunk Rinse Recipe

Tomato juice isn’t nearly as effective as this recipe, and it’s easy to follow.

In a pail mix:

  • 1 quart hydrogen peroxide (the 3 percent hydrogen peroxide variety)
  • ¼ cup baking soda
  • 2 teaspoons dishwashing liquid

If you have a large breed dog, you may need to double, triple or even quadruple the mixture.

Wear dishwashing or other household gloves if you like during the whole de-skunking process.

Don’t wet down your pet. Apply the mixture to your pet’s dry coat from the collar back toward the tail. Don’t pour it near the eyes because the hydrogen peroxide solution can burn them.

Lather the mixture into your pet’s coat and skin. Rub the solution around for about five minutes or until the skunk smell starts to dissipate.

If the front of your pet is as stinky as the back, use a sponge to apply the solution to your pet’s chin, cheeks, forehead and ears, being very careful not to go near the eyes. When you rinse the head area, tilt your pet’s chin upward so the solution does not run down into the eyes, instead allow the water to run back off his neck.

Do a complete rinse once the smell starts to decrease, then repeat the entire process again.

You may need to repeat the lather and rinse process up to three times, but it’s a very effective method for removing the skunk smell from your pet.

Make sure to completely rinse the solution off your pet. Your final rinse should be very thorough.

You can’t prepare this solution ahead of time and store it – it won’t be effective when you need it. It must be made fresh, right before you apply it to your pet. So it pays to make sure you have all the ingredients ahead of time!

Good luck … and I hope you never have to use my skunk rinse recipe!

GSCA National Walking Gun Dog Championship

Couldn’t be more thrilled to share the news about about the

Gordon Setter Club of America, Inc.

National Walking Gun Dog Championship 

Monday, October 22, 2018

C&R Center on the Norman G Wilder Wildlife Area

Felton, Delaware

This is GSCA’s 3rd National event for 2018 and the newest addition to the GSCA lineup of spectacular events showcasing our talented and beautiful breed!

Premium List Link

Walking-field-trial (1)

Feature photo by Jim McWalter

Sally Gift, Mesa AZ

I promise to…

*Members are aware that since January 2017, I’ve served as Vice President and now President of the Gordon Setter Club of America, Inc. At times, GSCA financial matters, and Board controversy about these matters, have grabbed headline status in the newsletter, by email and during conversations at GSCA events.

What never changed or grabbed headlines was my dedication to the objectives of the GSCA and the reason we all belong – the dogs.

In September of 2015, well before I was elected to office in 2017, I wrote a blog that clearly states my personal dedication to our beautiful breed and my commitment to pursue and fulfill GSCA objectives. An excerpt from that article follows.**

“There is a call to action to be heard here, for those who want to protect and preserve the Gordon Setter, and that call goes out to all who own and love them. I am not advocating that we begin to mass produce Gordon Setters by indiscriminate breeding and one should never interpret this data, nor my words, to mean such action should take place. The AKC however, is taking appropriate action steps to improve the reputation and increase the interest in purebred dogs and we can follow their action plans and their lead. The AKC cannot be successful on their own though, it will take the support of everyone who loves a Gordon Setter and that includes pet owners, breeders and hunters alike. We each need to heed the call to act, to do our own small, yet vital part, to promote purebred dog ownership and the benefits of owning a purebred. We need to join and support our National club and regional specialty clubs to do any small part there that we can contribute. At the next level the breed’s parent club, the Gordon Setter Club of America, also needs to visit this call to action to ensure that we, as an organization, are doing our part on a larger scale to promote the breed, interest in the sport, the preservation of our breeders and the development of a future generation of breeders.”

It would be impossible not to recognize that GSCA events, activities and charitable donations could come to a grinding halt, if the club’s financial matters aren’t managed consistently and appropriately. And that attending to this task ensures the club can fulfill its objectives. One thing follows the other and vice versa. It is after all, about the dogs.

Sally Gift, Mesa AZ

*This is a personal message and is not intended to represent any official statement of or by the GSCA or the GSCA Board.

**excerpt from IS OUR BREED IN JEOPARDY?

 

Raw Chicken Linked to Paralysis in Dogs

Feature photo by Bob Segal

Raw Chicken Linked to Paralysis in Dogs

By Dr Nerissa Hannink, University of Melbourne

Chicken necks are a common treat for dogs, but pet owners are being warned they have been linked with a potentially fatal form of paralysis.

 

As pet ownership increases across the world, our furry (as well as feathered and scaly) friends have become firmly established members of the family.

Wanting the best for our pets, we often offer special treats, and chicken necks are a favourite in many families – often considered a ‘healthy’ option.

But vets are warning raw chicken, particularly chicken necks, can lead to a debilitating and potentially fatal form of paralysis in dogs.

new study, led by the University of Melbourne’s U-Vet Werribee Animal Hospital, found the consumption of raw chicken meat increases the risk of dogs developing a paralysing condition called acute polyradiculoneuritis (APN) by more than 70 times.

Dr Matthias le Chevoir, chief investigator on the project, says the cause of APN in dogs has baffled the veterinary community for a long time.

“It is a rare but very debilitating condition where the dog’s hind legs first become weak. It can then progress to affect the front legs, neck, head and face. Some dogs may die from the disease if their chest becomes paralysed,” he says.

“Most dogs eventually recover without treatment but it may take up to six months or more in some cases.

“In our clinic alone we see around 30 cases per year and around three in ten cases would not recover. Watching your pet suffer is obviously very distressing and it can be difficult for owners to nurse their pet if the condition can gradually improve.”

Paralysis results from the dog’s immune system becoming unregulated and attacking its own nerve roots, progressively worsening over several days.

APN is the canine counterpart of Guillain-Barré syndrome (GBS) in humans, a condition that also causes muscle weakness and may require ventilation if chest muscles are affected.

Dr le Chevoir says the bacteria Campylobacter is now considered a triggering agent in up to 40 per cent of GBS patients. It may be present in undercooked chicken, unpasteurised milk products and contaminated water.

“Our team at U-Vet Animal Hospital wanted to understand if consuming raw chicken could also be triggering APN in dogs. Many of us have previously worked overseas and know that a raw meat diet is less common there, so we were intrigued by this potential connection,” Dr le Chevoir says.

The team studied 27 dogs with symptoms of APN and 47 dogs without, examining physical symptoms and interviewing the owners about recent behaviours and diet; focusing on the consumption of raw chicken meat.

Faecal samples collected within seven days of the presentation of clinical signs (such as changes in voice, hind limb weakness or a choppy gait) showed the dogs with APN were 9.4 times more likely to have had a Campylobacter infection than the control group without the disease.

“The microbe Campylobacter is likely to be the reason for the dysregulation of the dogs’ immunity and the symptoms of paralysis,” lead author Dr Lorena Martinez-Antòn says.

“These bacteriological results were consistent with the hypothesis that the uncooked chicken meat was the source of the Campylobacter and as a result, triggered APN.”

In humans, scientists think Campylobacter, which is most commonly found in commercial poultry products, contains molecules similar in structure to part of the nerve cell. This similarity confuses the immune system, which attacks the body’s own nerves, resulting in paralysis.

Dr Martinez-Antòn and Dr le Chevoir say there appears to be a growing trend for feeding dogs raw meat diets, which is concerning given the risks.

“A significant association is also found between APN and smaller dog breeds. Based on our clinical experience this seems to be because smaller dogs are more likely to be fed smaller bones like chicken necks,” the doctors say in the research paper.

“We recommend owners choose regular dog food rather than chicken necks until we know more about this debilitating condition.”

E.D. This content was altered to remove the photos and video links supplied in the original publication. All other content of the article is retained in it’s entirity. 

Feeding Newborn Puppies

Sometimes tube feeding is the only way to save newborn puppies, however there are other options that can be tried first, and this article offers advice on that topic. By clicking on the title below”To Tube or Not to Tube” you will be taken to Mary Wakeman’s website where many other useful articles scan be found.  Enjoy!

Sally Gift, Mesa AZ

To Tube or Not To Tube

by Mary C. Wakeman, D.V.M Canine Fertility

March 16th, 117    The Best of Breed of Online Show Dog Magazines

The answer to this depends entirely upon whether you want your puppies to live or not. What! You say, tubing is the ONLY way to save puppies. And besides, it’s fast. Fast, yes, and deadly. It’s one of those things that sounds too good (easy) to be true; and if it sounds too good to be true it is; we know that it is in our most private thoughts.

Fast and deadly isn’t doing your part by the bitch or the puppies. You may be certain that you are getting the tube in the esophagus (which leads to the stomach) and not the trachea (which leads to the lungs). But, this isn’t the problem I’m referring to. Consider this: when we eat, the process of eating stimulates waves of contraction throughout our entire GI tract. You know very well that as puppies nurse they defecate. That reaction is due to these waves of contraction, which are called peristalsis.

OK. So, we have a sluggish or weak puppy. We put it on the bitch and it won’t nurse. What to do! TUBE. NO! If the puppy does not have a good sucking reflex, it will not have any peristalsis. This means the milk we force in through the tube will just sit there. When the tube is removed, it forces itself back up the esophagus, into the trachea, and ends up in the lungs. It does not travel down through the stomach into the intestine.

Now, how big is the stomach of a newborn puppy in your breed? 1/2 cc? Less? As much as 1cc? Probably not much more. That stomach is just a slightly wide spot on a narrow tube.

So; let’s stick 2 1/2 cc into it . Fast and Deadly. The stomach and esophagus will stretch a bit, then return to it’s original shape and size after the milk runs into the lungs. Not going to raise many puppies that way.

Well then, what do we do? Easy. We give them sub-cutaneous dextrose and saline. Sugar in salt water. The solution which is used for IV therapy. All puppies need 3 things. Warmth. Water. Sugar. That’ all they need right away and for an additional few days if necessary.  So, we take the weak puppy out of the whelping box. We drop a few drops of colostrum onto its tongue several times in the first few hours. Got that immunity taken care of. We keep it in a confined box with a heat source – a heating pad or light bulb, and we give subQ dextrose in saline to supply the sugar and water. We gently stimulate it to urinate and defecate. We’ve met all the puppies needs.

How much fluid do we give? We give enough to satisfy any current dehydration debt and to provide a cushion for an hour or two in the future. How much is that? It is enough so that when we refill the syringe with dextrose and saline, the last 10 cc injection we gave hasn’t already disappeared. And it will disappear, just that fast, if the puppy is already dehydrated.

So first, we need to satisfy the back log, and then we put in some more. We want to raise a good sized lump – say the size of a golf ball on a 12-16 oz puppy. We want that golf ball to stay there a while. If it does, we can safely leave the puppy for a couple of hours. As time goes by, the fluids in this reservoir will be absorbed and the lump will disappear. Also, gravity will take a hand in removing the lump, shifting any spare fluids down around the neck. We can keep this puppy going in this way for 2 to 4 days easily. There no danger here, if the area is clean when and where we inject, and as long as the needle is parallel to the body – not pointed down at the body. We don’t want to pith the puppy (look it up). With the needle parallel to the body, the worst we can do is squirt the wall. The wall can take it.

Fluids given intravenously, by contrast, would run the risk of drowning the puppy – excess fluids in the veins will force their way out through the lungs. This result is essentially the same as that of tubing. Not good. SubQ fluids are essentially outside the circulatory system – just in a repository under the skin. If a fluid defecit exists, they can be instantly drawn into the blood stream. Until then, they have no other effect on the body.

While we are satisfying the puppy’s needs in this way, we will also repeatedly present a nipple to the puppy, several minutes after we have placed a drop of Karo syrup on its tongue. The Karo give the puppy an energy boost, so that when we place it on the bitch, it will make as strong an attempt to nurse as it can muster. We will also present the puppy with a bottle, as it will be easier for it to get milk from the bottle’s nipple than from the bitch, most of the time, during the first couple of days.

One of the greatest deterrents to getting puppies started, after tubing, is the ‘Pet Nurser’ which is widely available. Few if any breeds will nurse off of this thing – maybe a couple of toy breeds I’ve never encountered. Rather, puppies from 4.5 oz to 2# and up will readily take a Playtex preemie, or Playtex 0-3 months nipple (slow flow), one which has a flat, button-like shape. ANY puppy which does want to suck, but is unable to get enough from the bitch, should be asked to take the Playtex nurser. And if they don’t learn to nurse from it within the first few minutes, as soon as an hour or two after birth, it’s your fault, because they like this nipple just fine.

Of course, you have to put the right stuff in it. The concept of using a formulated synthetic milk replacer seems a bit bizarre. Cow’s milk is good, it’s complete, it contains the same things as dog milk. It’s not quite as good as dog’s milk, however, because it’s too dilute. Cow’s milk is 1/2 as concentrated as dog milk. So, all we have to do is go to the store and buy evaporated milk. Nothing could be simpler; comes in a can, easy to store and have on hand, useful for other purposes. We use the evaporated cow’s milk, in the slow flow nipple (no modifications to the nipple, we want it to go in slowly, and to require some exercise from the puppy to make it work). We add a dollop of Karo syrup for energy and palatability, warm slightly, and that’s it; it’s perfect.

Some of us seem to have a need to make life more complicated than it has to be. If you think your puppies suffer from the rare human problem where the size of the cow butterfat globule is too large for comfort, you can search out a source for evaporated, canned goat’smilk. And you might wish to do that because it will make it seem as though your puppies have a special problem, not a routine, ordinary problem. However, goat’s milk has no special benefit for dogs. It also must be fed undiluted from the can, with some Karo.

Note: The only puppies I have ever seen which were nutritionally stunted – and didn’t recoup their early deficits when put on solid food – were 2 giant breed siblings which were fed fresh goat’s milk. To this day these two are ‘minis’. Fresh ruminant milk has 50% too much water in it. Evaporated ruminant milk is just fine as long as you don’t screw it up by adding water. If you are faced with total milk replacement due to the death of a bitch, you will eventually have to add an egg yolk (without the white) to a can of evaporated milk with Karo, in order to raise the protein level even more. But, there is no need for this when we’re simply supplementing.

These puppies which are eager to nurse, but just can’t get anything from the bitch’s nipples, will have good peristalsis. They will work at the nipple and develop their lungs and their body muscles, though only a fraction as well as they would if they were working on the bitch’s nipples. One caution when supplementing the large litter to lessen the stress on the bitch. You must be careful not to OVER feed. The idea is to take some load off her, so you should keep her out of the box for some time every day. We don’t want to supplement and then let them drink their fill from their mother as well, then we’ll only have fat and colicy puppies, not a mother in better shape.

The next question is, will their mother lick them and stimulate the urination and defecation reflexes? If she’s not yet into that, we also have to wash their tummies with a warm wet tissue. This will stimulate the elimination reflexes. We can’t skip this part either. If we do, they’ll all colic. Some bitches, even though they have milk and the puppies nurse with no problem, just don’t like to clean their puppies. If so, then it’s our job. We caused these puppies to be born, the buck stops with us; if they need to be cleaned we have to do the job. We have to be gentle, but we have to be just as certain that we’re successful in stimulating defecation and urination as we are that the puppies are getting enough to eat. What goes in must come out!

One good way to help you be certain you’re getting each one fed and cleaned is to place colorful yarn collars around their necks. This way we can identify each puppy at a glance, no waking them or dislodging them from a nipple in order to check markings. And later, when one puppy is repeatedly striking a pose we can see from a distance which one it is. Helps us identify that BIS Puppy.

Mary C. Wakeman, D.V.M Canine Fertility

Article
Photo by Dustin Hartje

Furnishings and the Three Genes That Account for Them

Thank you Silvia Timmermann for the various photographs used here to show the differences in the Gordon Setter furnishings.

From: National Purebred Dog Day

NPPD published this interesting article that explains how the furnishings on our Gordon Setter are inherited.

Furnishings, and Three Genes That Account for Them

“Furnishings” doesn’t refer just to furniture. The word itself is quite old and can be traced to back the 16th century and the Middle French word, “fournir,” which morphed into “fourniture”  to mean “a supply,” or the act of furnishing. In the dog world, “furnishings” refers to long hair on the extremities of certain breeds. In some wire-haired breeds, it can refer to a longer mustache, beard and eyebrows, while in setters, furnishings refers to the flowing hair coming off the dog’s body.

coat0Interestingly, variants in only three genes govern coat length, curl and furnishings. It was something discovered in 2009 by Edouard Cadieu and Elaine A. Ostrander of the National Human Genome Research Institute who looked at some 900 dogs representing 80 breeds. They were able to identify mutations at specific points, or loci, on three genes linked to fur length, curliness and growth pattern (what we call “furnishings”).  When they looked at the three loci on the genes of another 662 dogs representing 108 breeds — from Old English Sheepdogs to Pugs – they found that the presence of the mutations or not, in various combinations, accounted for the variation in coat in 95 percent of the breeds. Only a few breeds, including Afghan hounds, have coats that can’t be explained by these genes.

Here is the link to the study itself:

Coat Variation in the Domestic Dog Is Governed by Variants in Three Genes

Abstract

coat11Coat color and type are essential characteristics of domestic dog breeds. Although the genetic basis of coat color has been well characterized, relatively little is known about the genes influencing coat growth pattern, length, and curl. We performed genome-wide association studies of more than 1000 dogs from 80 domestic breeds to identify genes associated with canine fur phenotypes. Taking advantage of both inter- and intrabreed variability, we identified distinct mutations in three genes, RSPO2, FGF5, and KRT71 (encoding R-spondin–2, fibroblast growth factor–5, and keratin-71, respectively), that together account for most coat phenotypes in purebred dogs in the United States. Thus, an array of varied and seemingly complex phenotypes can be reduced to the combinatorial effects of only a few genes.

The tremendous phenotypic diversity of modern dog breeds represents the end point of a >15,000-year experiment in artificial and natural selection (1, 2). As has been demonstrated for traits such as body size (3) and coat color (4), marker-based associations with phenotypic traits can be explored within single breeds to initially identify regions of genetic association, and then expanded to multiple breeds for fine-mapping and mutation scanning (5, 6). Coat (pelage) phenotypes are particularly amenable to this strategy as they show a huge amount of variation across breeds but still allow for simple variation within single breeds (7). This offers a unique strategy for advancing the genetic understanding of a complex phenotype.

coat8We used the structured pattern of fur variation in dogs to localize the genetic basis of three characteristics of the canine coat: (i) the presence or absence of “furnishings,” the growth pattern marked by a moustache and eyebrows typically observed in wire-haired dogs; (ii) hair length; and (iii) the presence or absence of curl. To accomplish this, we generated three genome-wide single-nucleotide polymorphism (SNP) data sets using the Affymetrix version 2.0 canine SNP chip (8, 9). The first data set consisted of 96 dachshunds segregating three coat varieties: wire-haired with furnishings, smooth, and long-haired without furnishings. The second data set comprised 76 Portuguese water dogs (PWDs), segregating the curl phenotype. The final data set, termed CanMap, included 903 dogs from 80 breeds representing a wide variety of phenotypes. An additional data set used to map furnishings included a panel of microsatellite markers (10), genotyped on a 96-dachshund pedigree segregating all three coat varieties.

coat5The same strategy was used to map all three traits. First, a genome-wide association study (GWAS) within a breed segregating the phenotype was conducted to determine the most strongly associated locus. To rule out false-positives caused by population structure within the breeds (11), we did a second GWAS that used the CanMap data set divided into cases and controls based on the presence or absence of the phenotype in question. Fine-mapping of significant, concordant peaks was used to define the smallest shared haplotype, followed by sequencing to identify the putative causative mutations. Each mutation was validated in a large panel of at least 661 dogs from 108 breeds, including cases and controls for all phenotypes (table S1).

We initially mapped furnishings in the dachshund using smooth-coated and long-haired dogs as controls and wire-haired dogs as cases (Fig. 1A). Single-marker analysis of the dachshund GWAS data set and concurrent linkage analysis of the dachshund pedigree identified the same locus on canine chromosome 13 (CFA13) surrounding nucleotide 11,095,120 [P = 3.4 × 10−27, lod score (logarithm of the odds ratio for linkage) = 5.6; Fig. 1B]. We confirmed the association on CFA13 in the CanMap data set at nucleotide 11,659,792 (P = 10−241; Fig. 1C and table S2). A 718-kb homozygous haplotype in all dogs fixed with furnishings was located within both the original 3.4-Mb haplotype observed in the dachshund-only GWAS, and a 2.8-Mb haplotype identified in crossover analysis within the dachshund pedigree (Fig. 1D).

Fig. 1

GWAS and fine-mapping identify RSPO2 as the associated gene for moustache and eyebrow growth pattern (furnishings). (A) Three types of coat segregate in dachshunds: (from left to right) smooth-coated, long-haired, and wire-haired with furnishings. (B

Fine-mapping allowed us to reduce the homozygous region to 238 kb spanning only the R-spondin–2 (RSPO2) gene, excluding the 5′ untranslated region (5′UTR) and the first exon (Fig. 1D, fig. S1, and table S3). RSPO2 is an excellent candidate for a hair-growth phenotype as it synergizes with Wnt to activate β-catenin (12), and Wnt signaling is required for the establishment of the hair follicles (13, 14). Moreover, the Wnt-catenin pathway is involved in the development of hair-follicle tumors, or pilo-matricomas (15), which occur most frequently in breeds that have furnishings (16). Recent studies have shown that a mutation in the EDAR gene, also involved in the Wnt pathway, is responsible for a coarse East-Asian hair type found in humans (17), with some similarity to canine wirehair.

All exons and conserved regions of RSPO2 were sequenced in dogs from seven breeds (table S4). Only an insertion of 167 base pairs (bp) within the 3′UTR at position 11,634,766 was perfectly associated with the furnishings trait in dogs from both the case/control study and the extended pedigree (table S5). The result was further confirmed in a set of 704 dogs of varying phenotypes. In total, 297 of 298 dogs with furnishings were either homozygous (268) or heterozygous (29) for the insertion, and all 406 dogs lacking the trait were homozygous for the ancestral state, as is consistent with a dominant mode of inheritance (table S1).

This mutation does not affect the protein-coding region of the RSPO2 gene. However, because the 3′UTR frequently encodes elements that influence mRNA stability [reviewed in (18)], we examined whether the insertion was associated with a change in the expression level of the RSPO2 gene. We found a threefold increase in RSPO2 transcripts in muzzle skin biopsies of dogs with furnishings, consistent with a transcript effect (fig. S2).

We applied the same mapping strategy to hair length. Previously, mutations in the FGF5 gene were identified in Welsh corgis segregating an atypical “fluffy” or long-haired phenotype (19) and associated with excess hair growth in mice and cats (2022). Our study replicates these findings in an extended breed set. Indeed, association analyses in both the dachshund and CanMap data sets highlight the region on CFA32 containing FGF5 with P values of 3 × 10−27 and 9 × 10−44, respectively. After fine-mapping, a 67-kb homozygous region highlighted the FGF5 gene (Fig. 2A, fig. S3, and table S6). The strongest association was observed at position 7,473,337 (P = 1 × 10−157), in which a highly conserved Cys is changed to Phe (Cys95→Phe) in exon 1 of FGF5, consistent with the previous study (19). Sequencing within the homozygous haplotype revealed no SNPs with stronger association (table S7).

Fig. 2

Regions of homozygosity identify genes for pelage length and curl. (A) Homozygous region found on CFA32 defining the length locus. The red bar indicates the 520-kb associated haplotype from 29 long-haired dachshunds; the blue bar spans the 125-kb homozygous

This diagnostic SNP was typed in several hundred additional dogs of varying hair length. Within the dachshunds, all long-haired dogs had the TT genotype, whereas all short or wire-haired dogs had either the GT or GG genotypes, suggesting a recessive mode of inheritance, as predicted previously (23). Across all breeds, the T allele was found in 91% of the long-haired dogs, in only 3.9% of the short-haired dogs, and accounts for ~30% of genotypes found in medium-haired dogs. Three breeds with very long hair, including the Afghan hound, neither carry the Cys95→Phe variant nor show an association with CFA32, suggesting that additional loci exist that contribute to hair length in dogs (table S1).

To identify the gene that causes curly coat, we conducted a GWAS using PWDs (Fig. 2B) and identified a single associated SNP at position 5,444,030 on CFA27 (P = 4.5 × 10−7). A SNP in close proximity (5,466,995; P = 6.9 × 10−28) was associated with curly coat in the CanMap data set. Fine-mapping revealed a shared homozygous haplotype that included two keratin genes (Fig. 2C, fig. S4, and table S8). Sequence data covering 87% of the homozygous region identified one SNP at position 5,542,806 that segregated with the trait. Non–curly haired dogs carried the CC genotype; curly coated dogs had the TT genotype. In breeds where the trait segregates, such as PWDs, all three genotypes were observed. The relevant SNP is located in the KRT71 gene (previously called K6irs1, Kb34, and K71) and causes a nonsynonymous Arg151→Trp alteration (table S9). Genotyping an additional 661 samples at this SNP validated the association (P = 3 × 10−92) (table S1).

Keratins are obvious candidates for hair growth [reviewed in (24)], and mutations in KRT71 have been described in curly coated mice (25). The mutation described in our study is within the second exon of the gene and may affect either or both of two protein domains: a coiled-coil and a prefoldin domain (www.ensembl.org/Canis_familiaris/). Conceivably, sequence alterations in these domains could affect cellular targeting, receptor binding, or proper folding of the protein after translation [reviewed in (26)].

Notably, these three mutations in various combinations explain the observed pelage phenotype of 95% of dogs sampled, which include 108 of the ~160 American Kennel Club (AKC)–recognized breeds. A total of 622 dogs representing all identifiable coat phenotypes were genotyped at all three loci (table S10). By analyzing each of the three major traits both within and across multiple breeds, we show that combinations of these genotypes give rise to at least seven different coat types, encompassing most coat variation in modern domestic dogs (Fig. 3). Specifically, short-haired breeds display the ancestral state in all three genes. Wire-haired breeds, all of which have furnishings, carry the RSPO2 insertion. Dogs that carry both the RSPO2 and KRT71 mutations display “curly-wire” hair that is similar in texture to wire-hair but longer and curled or kinked rather than straight. Long-haired breeds carry the variant form of FGF5. Dogs carrying the FGF5 mutation, along with the RSPO2 insertion, have furnishings and long soft coats, rather than wiry ones. When dogs carry variants in both FGF5 and KRT71, the pelage is long and curly. Not surprisingly, coats must be of sufficient length to curl, and all curly haired dogs in our study were homozygous for the FGF5 mutation. Finally, if all three mutations are present, the phenotype is long and curly with furnishings.

Fig. 3

Combinations of alleles at three genes create seven different coat phenotypes. Plus (+) and minus signs (−) indicate the presence or absence of variant (nonancestral) genotype. A characteristic breed is represented for each of the seven combinations

None of the mutations we observed were found in three gray wolves or the short-haired dogs, indicating that short-haired dogs carry the ancestral alleles (table S1). Our finding of identical haplotypes surrounding the variants in all dogs displaying the same coat type suggests that a single mutation occurred for each trait and was transferred multiple times to different breeds through hybridization. Because most breeds likely originated within the past 200 years (27), our results demonstrate how a remarkable diversity of phenotypes can quickly be generated from simple genetic underpinnings. Consequently, in domesticated species, the appearance of phenotypic complexity can be created through combinations of genes of major effect, providing a pathway for rapid evolution that is unparalleled in natural systems. We propose that in the wake of artificial selection, other complex phenotypes in the domestic dog will have similar tractable architectures that will provide a window through which we can view the evolution of mammalian form and function.

Supplementary Material

Supplementary Data

Acknowledgments

We gratefully acknowledge support from NSF grants 0733033 (R.K.W.) and 516310 (C.D.B.), NIH grants 1RO1GM83606 (C.D.B.) and GM063056 (K.G.L. and K.C.), the Nestlé Purina company, the AKC Canine Health Foundation, the University of California–Davis Veterinary Genetics Laboratory, and the Intramural Program of the National Human Genome Research Institute. We thank L. Warren and S. Stafford for providing pictures. Finally, we thank the many dog owners who generously provided us with samples from their pets.

Footnotes

Supporting Online Material

www.sciencemag.org/cgi/content/full/1177808/DC1

Materials

Materials and Methods

Figs. S1 to S5

Tables S1 to S10

References

References and Notes

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