Jan 16, 2015 | Ailments, Breeding
The 5 Panel Genetic Test for AQHA registration
The AQHA offers its members a genetic test for a panel of 5 different genetic diseases affecting Quarter Horses. The panel tests for Hyperkalemic Periodic Paralysis (HYPP), Polysaccharide Storage Myopathy type 1 (PSSM 1), Malignant Hyperthermia (MH), Hereditary Epidermal Regional Dermal Asthenia (HERDA), and Glycogen Branching Enzyme Deficiency (GBED). All these diseases are genetic, and are caused by single mutations in DNA that are easy to test for. The University of California-Davis performs the testing for the AQHA, using mane or tail hair or blood samples.
The panel has been available for years, but just recently AQHA began requiring that results of the panel be on file for stallions before their foals could be registered. This applied at first only to stallions that were bred to more than 25 mares, but after January 1, 2015, ALL breeding stallions will need to have the 5 panel test results on file. This requirement doesn’t restrict the use of stallions that may test positive for one or more of the diseases, but it does give mare owners valuable information to consider when making breeding decisions. Although the requirements for the panel testing only apply to breeding stallions, owners may request testing of any horse if they are interested or have concerns.
HYPP
HYPP stands for Hyperkalemic Periodic Paralysis. This disease affects the electrical impulses within the body that control muscle contraction. The defective gene results in clinical signs of muscle tremors and fasciculations. In some severe cases, horses may be unable to stand, or even unable to breathe. Horses can show symptoms with only one copy of the defective gene, but symptoms are often more severe if they have two copies of the mutation. This disease affects mostly halter horses, and can be traced back to the prolific stallion ‘Impressive’. Since Impressive lines were also used in Paint and Appaloosa halter breeding programs, HYPP is found in those breeds as well. AQHA does not allow registration of foals that test positive for two copies of the defective gene (H/H), but will allow registration of foals that are H/N: one defective and one normal gene.
PSSM 1
PSSM stands for Polysaccharide Storage Myopathy. This disease causes changes in the way sugars are stored and used by the muscles. It causes frequent episodes of ‘tying up’ if not properly controlled by a special diet and regular low intensity exercise. There are two types of PSSM. Type 1 is caused by a genetically identified mutation, which is testable. Type 2 is suspected to be genetic, but that mutation has not yet been identified by researchers. Most Quarter Horses with PSSM have type 1. Horses will show symptoms of PSSM type 1 with one or two copies of the mutation. Like HYPP, PSSM type 1 is more common in halter QHs than in other lines. Some QHs have been shown to have mutations for both HYPP and PSSM.
HERDA
HERDA stands for Hereditary Epidermal Regional Dermal Asthenia. Horses with HERDA have defective collagen, an important protein that is part of skin, cartilage, muscles, and tendons. The major clinical sign is skin that is easily injured, torn, or even sloughed off. The skin is also very slow to heal. There is no treatment for the condition, and horses that have it are often euthanized. Horses will only show symptoms if they have two copies of the mutation for HERDA. Horses with only one copy of the mutation are clinically normal. These animals are called ‘carriers’. They can pass copies of the mutation to their foals, and if one carrier is bred to another carrier, the foal might inherit the mutation from both parents and be symptomatic. HERDA is limited mostly to horses with reining and cutting horse bloodlines.
GBED
GBED stands for Glycogen Branching Enzyme Deficiency. Like PSSM, this disease also affects how sugars are stored, but in a different and more severe way. It results in abortions, stillborn foals, and foals that are alive but weak at birth and die or are euthanized soon after. Like with HERDA, horses may be carriers for GBED – if a horse has only one copy of the mutation it will be clinically normal. Paints and Appaloosas can also carry the GBED mutation.
MH
MH stands for Malignant Hyperthermia. This disease changes the way muscle cells handle calcium, and thus the metabolism of the cell. Horses with MH will appear normal most of the time, but have specific occasions when they show symptoms. During an attack, horses will have a very high fever, profuse sweating, high and irregular heart rate, high blood pressure, and rigid muscles. Attacks are triggered by certain anesthetic agents or stress, and are sometimes fatal. MH is believed to be less common than either HYPP or PSSM, but the percentage of affected horses is not yet known. Several breeds including Quarter Horses and Paints can be affected. Horses may be positive for both PSSM and MH together, and these animals appear to suffer from more severe episodes of tying up than horses that have PSSM alone.
Dec 23, 2014 | Breeding, Uncategorized
White Horse
Is there really such a thing as a white horse? Many gray horses start out nicely dappled, but then fade to nearly white as they age, and are incorrectly called ‘white’ by non-horsey folks. However there are a handful of other colors, each genetically different, that can result in a horse that looks white.
Blue-Eyed Creams Blue-eyed creams, (cremellos and perlinos), are horses that inherit two copies of the ‘cream’ gene. This gene is a color dilution factor, and when a horse inherits two copies, the result is a horse with blue eyes and an off white or cream colored coat. In the summer when they are slick and shiny these horses can appear white. Cremellos and perlinos can be difficult to tell apart without a genetic test to detect the differences in their underlying coat color. Cremellos are genetically chestnuts with two cream genes, and perlinos are genetically bay with two cream genes.
Lethal White Lethal white is an inherited condition usually seen in paint horse foals. These foals are born either all white, or mostly white, and like the name implies, they heartbreakingly will all die or have to be euthanized shortly after birth. The all white coat color in these foals is associated with a genetic mutation that also produces a problem in the nerves to the gastrointestinal tract, which interferes with motility and causes severe colic. There is no treatment for the condition. Usually, but not always, these foals are a product of breeding two overo paint horses. There is a genetic test available to screen potential breeding animals as carriers for the condition, and all responsible paint breeders should know the status of their breeding stock.
Sabino White Sabino is a description for a collection of white markings, and the word is used by multiple breeds. Horses labeled as sabinos often have extensive roaning, belly spots or large face markings and high white on the legs. Geneticists believe that there are probably several different genes that produce sabino type markings, but one mutation in particular has been identified, and named Sabino1. The Sabino1 gene is found mostly in Tennessee Walkers and Miniature horses, but also in some Paints, Shetland Ponies, and Pony of America’s. One copy of the Sabino1 gene produces the typical roaning, belly spots, high leg white, and large face markings. However, horses with two copies of Sabino1 are at least 90% white, and are referred to as ‘Sabino-white.’ These horses usually have pink skin and dark eyes. Sabino-white foals can look identical to Lethal-white foals, but they will be completely healthy, so it is important not to assume that all white foals should be euthanized at birth.
Dominant White Dominant white is caused by a variety of genetic mutations that affects pigment cells in skin and hair follicles. These mutations produce a horse with pink skin, white hair, and usually dark eyes. One particular such mutation, from the QH stallion GQ Santana, has been identified, and there is now a test available for it. Since it is a ‘dominant’ trait, only one copy of the mutation is needed to produce a white coat color. So far no horses with two copies of the mutation have been identified, so it is not known if foals/fetuses with two copies would be ‘viable’.
Nov 10, 2014 | Breeding, Uncategorized
Welcome to part 2 of Equine Coat Color Genetics: Gray, Roan, and Dun
This blog builds on the information presented in the previous blog: Equine Coat Color Part 1. We recommend you read that post first to best understand this one.
The Gray Gene
We all know that gray horses aren’t born gray, but they are not all born black. A gray horse can start out any color at birth, and then they fade as they age, sometimes slowly, and sometimes rapidly. The ‘gray’ gene is simple. ‘G’ stands for ‘gray’, and ‘g’ for ‘NOT gray’.
GG = horse goes gray
Gg = horse goes gray
gg = horse stays whatever color it is at birth
The color that a gray horse is born with is determined by the other color genes. For example:
EE or Ee (black-based), with aa (unrestricted black), with GG or Gg (gray) = Horse born black, then goes gray.
EE or Ee, with AA or Aa (restricted black), with GG or Gg (gray) = Horse born bay, then goes gray.
ee (red-based) with GG or Gg (gray) = Horse born chestnut, then goes gray.
Roaning
The roan gene is a color modifier that causes an intermixing of white hairs with the base coat color, with more white over the neck and body and less white on the head and legs. Black based horses with roan have black and white hairs, and are called blue roans. Chestnut based horses with roan have red and white hairs, and are called red roans. Bay horses with roan have brown and white hairs, and are either called bay roans or strawberry roans.
The roan gene is a dominant trait, meaning that ‘Rn’ for ‘roan’ is dominant to ‘rn’ for ‘NOT roan’. The famous cutting horse mare Royal Blue Boon is an example of a blue roan, and her son, the famous sire Peptoboonsmal, is a red roan.
EE or Ee (black-based), with aa (unrestricted black), with RnRn or Rnrn = Blue Roan
EE or Ee (black-based), with AA or Aa (restricted black), with RnRn or Rnrn = Bay Roan
ee (red-based), with RnRn or Rnrn = Red Roan
Dun Dilution – Dun, Red Dun, and Grulla
The dun gene is a color dilution factor that causes a horse to have a diluted coat color, a dorsal stripe, and other ‘primitive’ markings, such as bars on the legs, and sometimes dark marks near the withers. The dun gene is responsible for grulla, dun, and red dun horses. Dun is a dominant trait. ‘D’ for ‘dun’ is dominant to ‘d’ for ‘NOT dun’. The other color genes determine what shade the base coat color is.
A grulla is a black horse with the dun dilution factor.
EE or Ee (black-based) with aa (unrestricted black) with dd (not dun) = Black.
EE or Ee (black-based) with aa (unrestricted black) with DD or Dd (dun) = Grulla.
A dun is a bay horse with the dun dilution factor.
EE or Ea (black-based), with AA or Aa (restricted black), with dd (not dun) = Bay.
EE or Ea (black-based), with AA or Aa (restricted black), with DD or Dd (dun) = Dun.
A red dun is a chestnut horse with the dun dilution factor.
ee (red-based), with dd (not dun) = Chestnut.
ee (red-based), with DD or Dd (dun) = Red Dun.
Look for the next installment of Equine Coat Color Genetics coming soon for info on Palomino, Buckskin, and Smokey Black!
Oct 7, 2014 | Ailments, Breeding
Cloning!
In 2008 the National Cutting Horse Association voted to allow cloned animals to compete in their aged events. There were at least 2 clones entered in the 2009 NCHA Futurity show for 3 year olds, but neither ended up competing in the event. Cutting horse trainer Phil Rapp trained both fillies – Playboys Ruby Too, a clone of Playboys Ruby, and what’s on Tap, a clone of Tap o Lena. Neither filly was ever on the top of his list for the Futurity, and he called their abilities “average”, even going on to say that What’s on Tap “did not progress as a cutting horse”, and that Playboys Ruby Too was the stronger filly, but “needed to do more than turn both ways”. The mediocre performances of these two clones confirms that genetics alone don’t make a superior athlete, and that cloning a world champion or Olympic medalist doesn’t ensure success in the top levels of competition.
In 2012 the FEI (International Equestrian Federation) made a statement that clones and/or their offspring would be allowed to compete in international events, including the Olympics. The decision came too late for it to effect the 2012 summer Games. Horses in Olympic disciplines like eventing, dressage, and show jumping are often considered ‘aged’ – older than 10 – before they are experienced enough for the international stage, so even if clones were being aimed at the Olympics, they probably wouldn’t have been ready yet. Maybe in 2016?
Polo may be the one exception where we should expect to see cloned horses competing on a regular basis. Polo ponies are being cloned at a faster rate than any other type of horse. By 2013, one owner alone, top polo player Adolfo Cambiaso, is reported to have cloned his top horses almost 100 times! Adolofo says that his goal is to one day complete an entire polo match riding only cloned animals. In 2013 he took a step toward this goal by riding one of his clones, a mare named Show Me, during the Championship match of the Argentine National Open, which his team won. He scored two goals while riding the mare, who is a clone of an American Thoroughbred, named Sage. Cambiaso currently has over 50 clones in training, and more will be coming of age for competition soon.
Registered Clones? Cloned racehorses?
You won’t be hearing about clones of Secretariat, Man O War, or First Down Dash any time soon. Why? Both The Jockey Club, which registers Thoroughbreds, and the American Quarter Horse Association (AQHA) have policies that ban the registration of clones or their offspring. Thoroughbreds have to be registered with the Jockey Club in order to race, and similarly, QH racehorses must be registered with the AQHA. For this reason, it doesn’t make sense to go to the effort to clone racehorses, at least not until the rules on registration change, and those changes may be coming soon.
The AQHA is in the midst of a long standing legal battle over clone registration. A group of cloned QH owners filed a lawsuit against the AQHA in April of 2012, arguing that clones (and therefore their offspring) should be allowed to be registered. The AQHA refused to give in, stating that over 85% of their members were against the registration of clones. In July of 2013 the court ruled against the AQHA, but the organization is appealing the decision, and opening arguments of the appeal begin this very week.
Oct 2, 2014 | Breeding, Uncategorized
Equine Coat Color Genetics, Part 1: Black, Chestnut, Bay
If I breed a gray mare to a bay stallion, what color will the foal be? If I bred two palominos, how did I end up with a chestnut foal? Equine coat colors actually follow some fairly straightforward rules – in fact, the same ones discovered by Mendel and his infamous peas that you may have learned about in biology. The first thing to understand is that each horse has two complete pairs of chromosomes – one that came from its sire, and the other from its dam. This means it has two copies of every gene, one from mom, and one from dad. The way the two copies of each gene interact with each other, as well as the interaction between separate genes, is the basis for all things genetic, including color.
We use letters to identify which types of each gene (which allele) the horse has inherited. Capital letters identify the dominant allele, and lower case letters stand for a recessive allele. Most of the time, recessive traits or characteristics are only observed if the horse inherits the recessive allele from both parents.
If for example there was a single gene for speed, (there’s not, but for example), then the letters we might use would be ‘F’ for fast, and ‘f’ for slow. If a horse was ‘FF’ (got ‘fast’ from both parents), it would be fast, and if it was ‘ff’, (got ‘slow’ from both parents) if would be slow. But if it was ‘Ff’ (got ‘fast’ from one parent and ‘slow’ from another, then it would still be fast, because ‘fast’, big ‘F’, is dominant to ‘slow’, little ‘f’. The dominant allele trumps the recessive one.
Another way to look at this:
FF = fast horse
Ff = fast horse
ff = slow horse
The ‘extension’ gene: Black, or Red.
The first gene you have to understand when talking about horse colors is the ‘Extension’ gene. Never mind its name, think of this gene as the “black or red” gene. The letters are ‘E’ for black, and ‘e’ for red (chestnut). Black, big ‘E’, is dominant to red, little ‘e’. All horses have this gene, (all horses have every gene), even ones that are colors other than black or chestnut. The other colors exist because of the way other genes interact with the extension gene.
EE = black-based
Ee = black-based
ee = red (chestnut)-based
You might be wondering, if black-based is dominant to red-based, why are there so few black horses compared to bays or chestnuts? Keep reading.
‘Aguti’ makes Bay.
The ‘Aguti’ gene controls black distribution across a horse’s body. Since red-based horses have no black, they will have two copies of this gene, but they won’t play in role in determining the horse’s color. On a black-based horse, the aguti gene determines whether the black will be all over the horse or only on certain parts (like the mane, tail, and legs). There are three alleles for this gene: ‘A’ restricts black distribution the most, (black main, tail and legs only), ‘At’ restricts black a little, and ‘a’ does not restrict black at all.
AA = black restricted to main, tail, legs
Aa = black restricted to main, tail, legs
AtAt = somewhat restricted black
Ata = somewhat restricted black
aa = black is unrestricted, black all over the body
So, combine this with what you know about the extension gene and you get:
EE or Ee (black based) with AA or Aa (restricted black) = Bay horse.
EE or Ee (black based) with AtAt or Ata (some black restriction) = Seal brown horse.
EE or Ee (black based) with aa (unrestricted black) = Black horse.
The reason for few truly black horses is that there are many black-based horses, but most of those turn out bay. Why? Because the big ‘A’, which restricts black, making bay, is dominant to the little ‘a’, and there happen to be a lot more big ‘A’s floating around in the horse population than little ‘a’s.
Remember, the aguti gene does not matter on red-based horses.
It only controls black. So:
ee (red-based) with AA, Aa, or aa (or any combination of aguti alleles) = Chestnut horse.
Sep 26, 2014 | Breeding, Uncategorized
Cloning!
Clones – Where are they now?
I overheard Dr. Bourke talking about cloned horses the other day. Seems like there are a quite a few of them out there now! I’m still not sure that cloning is a good idea, but it was interesting to learn what the cloned horses are up to.
The world’s first cloned horse was born in Italy way back in 2003 – a Haflinger mare that was named Prometea. What’s really interesting is that in this case, the mare that carried the pregnancy was also the mare they took the genetic material from – she gave birth to her own clone!
In 2005, Italy did it again, producing a clone of the famous endurance Arabian stallion Pierez. Then things really took off in 2006 when Texas A&M University announced the birth of FIVE clones of the cutting horse stallion Smart Little Lena. That same year the world’s first commercially cloned horses were born in Oklahoma – copies of top Quarter Horse cutting mares Royal Blue Boon, Tap O Lena, and Playboys Ruby. Since then, there have been handfuls of cloned horses born from several different equestrian disciplines. Examples include show jumping greats ET, Gem Twist, Calvaro V, and Sapphire, dressage stars Jazz and Rusty, international event horses Che Mr. Wiseguy and Tamarillo, barrel racer superstar Scamper, and several other well known cutters including Doc’s Serendipity and Jae Bar Fletch.
Clones Are Reproducing: Prometea is now 11 years old, and in 2008 she had her first foal, a colt, which was reportedly healthy. This was the first offspring of a cloned horse, but there have been several others since. The cloned stallions of Pierez, ET and Gem Twist all have foals on the ground. Pierez is even a grandsire. His first daughter gave birth to a colt in 2012.
Clones for Sale: The Smart Little Lena clones are now 8 years old. One of the five died at the age of 4 from bladder cancer. The remaining four stallions were sold by the syndicate that owned them at the 2009 NCHA World Finals sale. They went for $2400, $3000, $27,000 and $28,000. The highest selling stallion was exported to Australia and now stands at stud for a fee of $1500. One cloned polo pony mount from Argentina sold for a whopping $800,000 in 2010.
Clones in Competition: Because of the high costs involved with producing a clone (roughly $150,000 per horse) it is unlikely that very many will enter competition. The horses being cloned are all from the top ranks of their disciplines, so it would be difficult for the clones to perform as well as the original, let alone surpass or improve on their achievements. Clones have the genetics of superstars, so from a business and breeding standpoint, they have nothing to gain from competition, and everything to lose. For this reason, most clones will be used for breeding purposes.
However, several performance horse organizations have opened the door to allow for cloned animals in competition.
