Many factors come into play to determine the conformation, temperament, and color of a horse.
When breeding horses, the mating matchups determine the quality of the offspring. You need to have knowledge of genetics to predict what traits the foal will inherit from his parents. You are shooting in the dark if you look only at the individuals when selecting the mare and stallion to be mated; you must also know something about their genetic inheritance. Some recessive traits are not evident in the parents but may appear in offspring if the foal inherits a recessive gene from each parent. Some perfectly normal and outstanding horses are carriers of undesirable genes and may produce an abnormal foal; therefore, it is important to know as much as possible about the genetics of the horses you wish to mate.
An individual’s characteristics are determined by genes and chromosomes. Genes are chemical codes that transmit various traits. They are located on chromosomes, which are strands of genetic material carried in every cell of the body. Chromosomes occur in pairs. As cells divide, half the genetic material goes with the new cell; it is a perfect replica of the old one (except when chromosomes become twisted, damaged, or misplaced, resulting in mutations).
Each cell contains chromosome pairs that carry the code of inheritance. Egg and sperm cells have only one chromosome from each pair, so when they unite, the newly formed pairs are a joining of one from the male and one from the female — the offspring gets half his genetic material from each parent. Because there’s such a variety of genetic material in the many genes and chromosomes, the possibilities for different matchups are great. No two foals (even full brothers or sisters) are exactly alike unless they are identical twins.
Most characteristics are determined by several sets of genes. It’s impossible to predict what the foal will be like, except in traits affected by only one pair of genes. Some genes are dominant and others are recessive. When chromosomes join to form the new individual, two genes (one from each chromosome — one from each parent) control the trait. If one is dominant, the trait it expresses will appear in the foal. The trait represented by the recessive gene won’t be expressed with the dominant gene present but might be expressed in future offspring if the gene is not masked by a dominant gene in that next union.
In some instances, genes work in tandem to express combined traits. There are also “dilution factors” involving some of the color expressions, which make things more complicated than simple dominants or recessives. These genes are usually incompletely dominant, so you can often tell the differences between two copies of the other, or one copy of each gene.
Dominant and recessive genes can be combined in three different ways:
Color is a less important trait than conformation, athletic ability, soundness, disposition, or intelligence; however, understanding the genetics of color makes it easier to understand the inheritance of other traits because the expressions of color genes are so visible. If you’re raising horses in a “color” breed such as Appaloosa or Paint, or for customers who want a certain color in their favorite breed, then having a working knowledge of color genetics is extremely important.
Traits controlled by dominant and recessive genes, such as those for color, are readily seen. An example of color inheritance can help explain how traits are passed from parent to offspring. For instance, let’s say “G” is the gene for gray and “g” is the one for nongray. The only time a horse can be a color other than gray is when a “gg” combination (two recessives) exists in the gene matchup because gray is the dominant trait. The foal may inherit from one parent a recessive chestnut gene or a bay gene (which is dominant over chestnut) but will always turn gray if he inherits the “G” gene for gray.
This dark foal will likely turn gray like his mother as he grows up.
Gray, bay, and chestnut are easy to predict because they are controlled by fairly simple dominants and recessives. Of these three colors, gray is always dominant. A gray horse is born bay or chestnut and becomes gray later because of the dominance of the graying gene. The gray horse must have at least one gray parent; gray can never skip a generation as can chestnut.
Bay is dominant over chestnut but still recessive to gray. Chestnut is always recessive; a chestnut bred to a chestnut can produce no other color but chestnut. Chestnut may appear from a mating of two bays or two grays, or a bay and a gray, if each parent carries a recessive chestnut gene.
In the first cross (below), the “pure” dominant parent will decide the color of the foal when mated to a recessive. The foal will then carry a recessive color gene that can be passed on to its offspring.
A gray horse who carries a bay gene will produce mostly gray foals but can still produce a bay foal. When mated with another gray horse who carries a chestnut gene, the foal has these four possibilities (right): pure gray, gray but carrying a chestnut gene, gray but carrying a bay gene, and bay carrying a chestnut gene.
If a gray horse who carries a recessive chestnut gene is mated to a bay horse who carries one also, the foal has these four color possibilities (right): gray carrying a bay gene, gray carrying a chestnut gene, bay carrying a chestnut gene, and chestnut — if he inherits both recessive genes.
Color Inheritance: Gray. A pure gray mated to an impure gray (carrying a bay gene) will produce nothing but gray foals, but some of them may carry a bay gene and pass the bay color to their offspring if mated with another horse who carries a bay gene. A pure gray mated to a bay carrying a chestnut gene will produce nothing but gray foals, but some will carry bay genes and some will carry chestnut genes. Two gray horses carrying bay genes can produce a bay foal, but the chances are one in four.
Color Inheritance: Bay and Chestnut. A pure bay mated with a bay who carries a chestnut gene will produce bay foals, but some of the foals may carry the recessive chestnut gene. Two bay horses carrying a chestnut gene can produce a chestnut foal.
Color Inheritance: Gray, Chestnut, and Bay. Gray is dominant and chestnut is recessive, but two gray parents can produce a chestnut foal if each carries a recessive chestnut gene.
Chestnut to chestnut always produces chestnut.
Chestnut to any other color (provided the other color doesn’t carry a chestnut gene) will always produce the other color or its genetic possibilities. In this case, a chestnut was bred to a gray who carried a bay gene. The foal will be either gray or bay and will carry a chestnut gene.
Note: Gray = dominant over all colors; bay = dominant over chestnut; chestnut = recessive; capital letters denote dominant gene; lowercase letters denote recessive gene. These general rules are relatively consistent, although somewhat oversimplified. Because these genes appear at different loci (locations on the chromosome), the results may occasionally be skewed.
Breeding for black, palomino, dun, Paint, or Appaloosa colors is more complicated. Roan is dominant over all colors except gray and white. Some colors appear because of recessive factors that “dilute” another color gene. There are several dilutions, each genetically different. When one of these factors (sometimes called “cream”) is present, bay dilutes to buckskin, brown becomes red dun, and chestnut becomes palomino. When both recessive dilution factors are present, each color is diluted to some shade of cream with blue eyes. Bay becomes perlino (nearly white, with rust-colored mane and tail), and chestnut becomes cremello (creamy white with light mane and tail and blue eyes). Another dilution factor involves dun, which dilutes in one dose or two. This can produce grulla from black or brown, change bay to dun, or chestnut to red dun.
To get a desired color in a foal, you have to know whether that color is dominant, recessive, or heterozygous (mixed) or dependent on dilution factors. You also must know the mare’s and stallion’s genotypes. This is easy if they have already produced offspring because you can see the color of their foals. Checking the colors of ancestors (in their pedigrees) also gives clues as to the presence of recessive genes.
Dominant colors are bay, gray, tobiano paint, blanket Appaloosa, roan, and line-backed dun. Black must have multiple traits present; it can occur without black parents. Recessive colors are chestnut, perlino, and cremello. Mixed (heterozygous) colors are white, buckskin, and palomino. Breeding for these is complicated because heterozygous colors cannot breed true; there is a 50–50 chance of producing the same color as the parent. Pure white at birth exists only in heterozygous form because these genes are lethal to the embryo when doubled up (homozygous) in dominant form (See Lethal Genes).
There are several genetic “tools” that a breeder can use to reach certain goals and produce outstanding individuals. A good knowledge of genetics helps a breeder use these techniques properly.
Inbreeding involves the mating of closely related individuals and it should be avoided, except in special cases, because it increases the chance of doubling up undesirable recessive traits or genetic defects that are hidden in the parents. Most undesirable traits are recessive homozygous; therefore, breeding closely related animals (ones who may carry the same recessive trait) brings them out. Inbred animals are also generally less hardy; inbreeding decreases the genetic variations within a bloodline. If undesirable or lethal genes are present, inbreeding presents a greater chance of birth defects and problems. Inbreeding concentrates the genes available, both good and bad.
Many breeders use inbreeding as a tool to intensify and “fix” certain good traits in a family line. If a horse is outstanding and has no known faulty genes, a breeder may double up the good genes by mating sons and daughters (half siblings) of the outstanding horse. This offers the chance that the offspring will be exceptional, especially in genetics that can be passed on. Inbreeding is always risky, but with luck, a horse who is a product of inbreeding from outstanding parents will carry only doubled-up, good attributes in his genetic makeup. He’ll be genetically pure for these characteristics, serving as an outstanding sire (or dam) and passing on those traits consistently to the foals.
Linebreeding, a form of inbreeding, involves the mating of relatives (the descendants of one particular outstanding horse) in an effort to double up and “fix” the traits of a superior ancestor so the animals will breed true and pass on the traits of that ancestor. Because the total number of gene combinations in a linebred animal are limited (owing to less outcrossing to bring in different genes), the linebred (or inbred) animal is fairly predictable in traits it will pass to offspring. Linebreeding, like inbreeding, must be done cautiously, with careful examination of all known traits of the bloodline to make sure there are no undesirable traits that might be doubled up as well. Some of the devastating genetic defects described later in the chapter, such as SCID, HYPP, HERDA, WFFS, and GBED, that have cropped up in various breeds during the past several decades are the result of linebreeding to a popular ancestor who carried a defective recessive gene. The defect appeared in later descendants when these genes were doubled up by linebreeding.
Outbreeding refers to the mating of unrelated individuals within a breed. This often produces superior offspring, but their genetic makeup is more varied than that of the inbred or linebred horse, and there may be more variance among their offspring.
Crossbreeding involves breeding individuals of different breeds to obtain offspring with characteristics of both breeds. Crossbred animals also may have certain traits superior to those of both parents through hybrid vigor (heterosis). When the best characteristics of each parent are combined, the foals have more versatility and hardiness. The key to successful crossbreeding is to choose animals with traits you want; outstanding parents usually produce a crossbred foal that is exceptional — partly because of hybrid vigor and partly from combining the traits you desired from each breed.
Most of the breeds in existence today were originally created by crossbreeding. For example, many of the non-draft-horse breeds have some Arabian blood in their background. In earlier times, the “breeds” of certain locales were improved by crossing with Arabians. Selective crossbreeding can produce versatile athletes. For example, crossing a Thoroughbred with a Quarter Horse or warmblood may produce a superior jumper. Crossing an Arabian with another breed will often produce a good all-around athlete with more endurance.
If your goal is a specialized sport like racing, however, you are usually better off sticking with breeds that have been selectively bred for speed — such as the Thoroughbred for fastest speed at a mile or a Quarter Horse for the fastest burst of speed in a short sprint. If your goal is exceptional endurance, the Arabian (or an Arabian derivative such as the Spanish Mustang) is best. For certain gaits, choose the gaited breed that has been bred for that specialty. Crossbreeding, however, often works well to create a more all-around athletic horse.
Some individuals and family lines carry genetic defects; be wary about using these horses for breeding. The most common inheritance pattern involves a simple recessive trait; the defective foal inherits a recessive gene from both sire and dam — individuals who are otherwise completely normal. A few defects are caused by genes with incomplete dominance, and some are caused by two or more sets of genes, but the most common problems are caused by simple recessives.
Defects run in families; therefore, inbreeding or mating closely related animals is risky unless you know there are no bad genes in that family to cause a defect when doubled up. For example, the parents of a defective foal often have at least one ancestor in common. Today, with the availability of DNA (genetic material) testing, there are tests for some of the most common devastating genetic defects, and you can make sure that individuals are free of these defects before you breed them.
A few genes, when doubled up, cause death of the fetus before or shortly after birth. Some of these genes, when doubled up as an expressed trait, result in a fetus whose organs are improperly formed (such as lack of an anus, absence of eye sockets, or water on the brain). A common lethal gene is the one that creates a white coat. It is inherited as a dominant trait and is only lethal to the embryo when appearing on both chromosomes.
White hair or coat, which results from lack of hair pigment, can lead to foal mortalities. Lethal whites die soon after conception, and lethal overo whites (a white foal produced by breeding two overos, a type of pinto) die soon after birth because of faulty intestinal tracts; the foal looks normal at birth but cannot survive without a functioning gut. Not every white horse carries the lethal genes for early fetal death, and not every overo-patterned Paint or Pinto produces white foals who die young. The lethal situation occurs when two horses carrying the gene are mated.
True White. These horses are usually entirely white with pink skin and brown eyes. Albino coloring, with pink eyes, does not exist in equines. In other mammals, albino individuals lack all pigmentation due to impairment of tyrosinase production through defects in the Color (C) gene. They have pink skin, white hair, reddish eyes, and vision impairment. No mutations of the tyrosinase or C gene are known in horses, however.
Lethal white is a dominant gene; but because all true whites are heterozygous, they produce 50 percent white and 50 percent colored offspring when mated with colored horses. When true whites are bred to other true whites, the result is 25 percent colored foals, who inherit the recessive color gene; 50 percent heterozygous true whites; and 25 percent homozygous whites, who do not survive.
Lethal Overo (Lethal White Foal Syndrome). Paint breeders have learned to beware of mating frame-type overos to each other unless they have been tested and found negative for LWFS. A frame overo is basically another color (like chestnut) with jagged-edged splashes of white over the body.
Horses with one copy of the gene are normal and healthy, with the single gene producing the frame overo pattern. Solid-colored horses can carry that gene without expressing it. An owner might think the horse doesn’t carry the defect because the horse doesn’t have a paint pattern. If you are breeding that solid-colored horse to a frame overo, you’d need to test the solid-colored horse as well as the frame overo, to make sure it doesn’t carry that gene.
A rare few white horses from overo breedings survive, but these are usually sabinos and not frame overos. Sabino-white horses are pink-skinned with all-white or nearly-white coats and dark eyes. They are homozygous for the dominant SB1 allele at the Sabino 1 locus. Without a DNA test, sabino-white horses are indistinguishable from dominant white horses.
Foals with two copies of the frame overo gene are white and have nonfunctioning guts as a result of failure of nerve development to the digestive tract. These foals may seem normal at birth, and may get up and nurse, but nothing can move on through the digestive tract and they soon die.
SCID is a fatal disorder of Arabian foals (and sometimes part Arabians if both parents have the defective gene); it is a defect of the immune system inherited from two carriers who otherwise appear normal. SCID foals are normal at birth, but a portion of their immune system fails to develop. As soon as their temporary protection from maternal antibodies in colostrum begins to wane (a few months after birth), they die from infections.
When two SCID carrier horses are mated, there is a 25 percent chance that the foal will inherit the recessive gene from each parent and be affected with SCID, a 50 percent chance the foal will be normal but carry the recessive gene, and a 25 percent chance of not inheriting the gene at all. If a carrier horse is bred to a noncarrier, none of the offspring will develop SCID but half will be carriers.
There is no treatment for SCID; the only way to avoid this problem is not to breed two horses who are known carriers. You can test for this defect in a horse’s DNA through an oral swab plus a blood or hair sample. Hair samples consist of 20 to 30 mane or tail hairs, pulled out rather than cut; the hair root is needed for the DNA test. This sample can be sent to a laboratory to be analyzed.
The test kit can be ordered through your own veterinarian or from a genetics lab that does this type of test, such as VetGen or the UC-Davis Veterinary Genetics Laboratory. A carrier horse can still be used for breeding if the potential mate is free of SCID because they will never produce a SCID foal. Half of all offspring from such a mating would be carriers, but the other half would not have the recessive gene; therefore, you would not have to sacrifice the bloodline from an outstanding individual who happens to be a carrier. If you test all offspring, you would know which ones could be safely bred. The others could be used in performance careers.
GBED is a mutation that causes inability of tissues to store sugar properly, and foals with this defect are usually aborted, stillborn, or weak, dying within the first days or weeks of life. The glycogen in their skeletal muscles, heart, and liver can’t be mobilized very well, so they have no energy reserves. This inherited defect was first recognized in 1997 and is now present in about 10 percent of all Quarter Horses and related bloodlines (Paints, Appaloosas, and so on, that have incorporated Quarter Horse breeding). This mutation traces back to King, a popular foundation Quarter Horse born in 1932.
Some of the affected foals may be alive at birth but need help to stand and nurse. They may seem healthy for the first hours or days and then die suddenly, develop seizures, or become weak and unable to get up. With intensive care, some have lived to be two or three months old, but all have eventually died or been euthanized.
Researchers discovered that GBED appears only in offspring who inherit the recessive, mutated gene from both parents. If a carrier is mated to a normal horse, the offspring have a 50 percent chance of being a carrier, but none would be affected themselves. But when a carrier is mated with another carrier, resultant foals have a 50 percent chance of being carriers, 25 percent chance of being affected by GBED (and dying), and 25 percent chance of not receiving the defective gene at all. There is a genetic test for GBED, and if any descendent of King produces a foal lost to abortion, stillbirth, or early death for any unknown reason, that animal should be tested. If breeders test their horses and choose not to mate carriers with carriers, no more GBED foals will be produced. Testing can be done at VetGen laboratory or at University of California, Davis.
WFFS is a connective tissue disorder. Affected foals have extremely fragile skin that is easily torn or ulcerated by minimal contact, and their limb joints are extremely lax; these foals cannot stand normally, and must be euthanized soon after birth. Some are aborted, and in some cases the pregnancy may be lost fairly early.
The original mutation traces back through an extremely old bloodline, which afforded more opportunities for this recessive trait to spread. One researcher traced it back to a French Thoroughbred stallion in the 1800s who was used widely in France and Germany to upgrade warhorses. Some descendants of that stallion, 150 years later, became popular and were bred to each other, and this defect is now surfacing more frequently as more of these horses are bred. Researchers identified the mutant gene in 2011; they estimate that more than 10 percent of warmblood horses carry it.
This is a recessive trait, so unless each parent is a carrier and they produce a defective foal, you don’t realize it’s there. A genetic test is now available, and conscientious breeders will test to ensure that no more WFFS foals are born.
LFS, also called coat color dilution lethal (CCDL), is a recessive genetic disease that affects newborn foals of certain Arabian horse bloodlines. Egyptian bloodlines have the most documented cases with 10.3 percent of Egyptian Arabians being carriers, in contrast to only 1.8 percent of non-Egyptian Arabians.
Affected foals have severe neurological abnormalities, and cannot stand. They must be euthanized shortly after birth. The name originates from the diluted color of the hair coat, which in some cases appears to have a purple or lavender hue. The coat color may range from silver to light chestnut to pale pink.
In 2009, Cornell University researchers developed a DNA test to detect carriers of LFS, and now Arabian breeders can test their horses for this defect.
There are other defects that are not as lethal, but some of them can eventually lead to death of the horse. These include abnormalities in muscle metabolism that may result in collapse of the horse, muscles chronically cramping, defects in the skin, and defects in the ligaments that support the fetlock joints.
HYPP is a muscle disorder that occurs in certain family lines of Quarter Horses, Appaloosas, and Paints. Affected horses usually have heavy muscling, as is popular in halter classes. The problem is characterized by sporadic attacks of muscle tremors (shaking), weakness, and/or collapse and inability to get up. Attacks may be accompanied by noisy breathing from paralysis of muscles in the upper air passages. Sometimes, sudden death follows an attack, with the horse dying from heart failure or paralysis of the respiratory muscles. The problem is sometimes mistaken for colic, choking, tying up, or a respiratory ailment.
HYPP is inherited as a dominant trait. Homozygous individuals who inherit the defective gene from each parent (H/H) are severely affected (many do not survive to adulthood); heterozygous individuals with one normal gene and one defective gene (N/H) are more moderately affected and may survive if they have proper temperament and metabolism. With careful management (feeding a low-potassium diet and maintaining a steady, careful exercise program), many of them survive and function, but this can be a headache for the horse owner.
Breeding a heterozygous animal (N/H) to a normal animal (N/N) will result in offspring with a 50 percent chance of being normal, and a 50 percent chance of having the defective gene (N/H). Breeding a homozygous (H/H) animal, sometimes called a double positive, will result in all offspring inheriting the HYPP gene, regardless of the status of the other parent. Breeding an H/H horse to an N/H horse will produce offspring with a 50 percent chance of being H/H and a 50 percent chance of being N/H. Breeding N/H to N/H gives a 50 percent chance of being N/H, a 25 percent chance of being completely normal (N/N), and a 25 percent chance of being H/H.
The HYPP-affected horse must be kept on a low-potassium diet (little if any alfalfa hay). Some owners give the horse frequent doses of a diuretic (acetazolamide), which helps the body eliminate potassium. Treatment of an attack will vary with its severity. Giving the horse glucose (such as Karo syrup) may resolve a mild attack, but immediate veterinary treatment and IV fluids will be needed for a more severe attack in which the horse collapses.
The primary symptoms of PSSM are muscle cramping, trembling, unwillingness to move forward, and tense and swollen muscles of the hindquarters (see here). In some affected animals, however, the owners merely notice poor performance, lack of energy, difficulty in backing up, stiff gait or gait abnormalities, unwillingness to lift the feet for hoof care, or sensitivity to pressure over certain muscles of the back and hindquarters. PSSM occurs in many breeds — mostly heavily muscled horses — and is a dominant trait; therefore, it only takes one copy of the mutant gene to express it. This is different from GBED (see here) or HERDA (see below), which are recessive (the horse must inherit two copies, one from each parent). The risk of having affected offspring from a horse with PSSM is much higher because there is always at least a 50 percent chance of the foal inheriting the dominant gene. And if a foal gets two copies of the PSSM gene, that foal will often be more severely affected.
Over many decades, horse breeders have inadvertently selected for PSSM, especially in draft horses and Quarter Horses, in an effort to get more muscling — often doubling up these defective genes. There is now a DNA test that can detect one type of PSSM (which involves about 80 percent of affected animals), and researchers are working on a test that will detect another type that has recently been recognized.
This genetic defect has been recognized in certain family lines of Quarter Horses. It is similar to MH in humans, in that it generally isn’t noticed until the individual is exposed to gas anesthesia (as for surgery). An affected horse may have a severe reaction and die. Some horses have MH along with PSSM, which makes their muscle typing-up episodes even more severe. The horses who die during a muscle cramping problem are likely to also be affected with MH. The genetics of this problem are still being studied, but there is now a DNA test for this defect.
Also called hyperelastosis cutis, this skin defect was first documented in the 1960s and traced back to the famous Quarter Horse sire Poco Bueno. HERDA is an inherited connective-tissue disorder characterized by abnormal skin that tears easily and separates readily from the underlying tissue. Any pressure or trauma can pull the skin apart. The problem is often not discovered until the young horse goes into training and the simple act of wearing a saddle creates massive injury to the skin.
All affected horses are related, but the defective gene did not cause problems in the earliest offspring of Poco Bueno because they only carried half the equation; the defect did not show up until some of his descendants were bred to each other. During early research, skin biopsies were used to diagnose this problem, but now there is a DNA test and breeders can readily determine whether a horse is a carrier.
DSLD is an untreatable genetic defect that causes abnormalities in certain body tissue, particularly the supportive structures of the legs. The most noticeable problem is weakness of the suspensory ligaments and dropping of the fetlock joints, especially in the hind legs. Originally identified in Peruvian Paso horses, it was first thought to be a problem only in that breed, but this condition has since been seen in several other breeds, including Quarter Horses, Thoroughbreds, warmbloods, and draft horses. Research on this defect is still ongoing; the genetic basis for this problem is not yet known.
To be a successful breeder, you must not only be a good judge of horses when assessing conformation and ability but also know their genetics. You will be mating not only two individuals but also two separate ancestries, combining their genes. You must be able to predict with reasonable accuracy what the product of each mating will be, complementing the sire’s and dam’s characteristics as well as creating foals who inherit the best of both ancestries. There are no perfect horses; therefore, you must try to mate sound individuals who will produce even better offspring.
If a horse has faults, mate it with one who has strengths in that area. If you mate two horses with the same faults, you will most likely produce a foal who is worse than his parents. Never double up bad points of conformation or any known defects. Genetic tests for certain defects are now available and can help horse breeders make informed decisions.
Breeding good horses is a time-consuming job that involves much work and expense. It costs no more to keep and feed a good broodmare than a poor one, so make every effort to have the best you can afford. If you have a stallion, a good one will help sell your foals. If you consistently have good foals, people will come back for more; but if you sell a few poor ones, or some who carry a serious defect, the word will get around. If you are conscientious about breeding good horses, you won’t let fads popular in the show ring overrule your best judgment regarding what is best for the breed. If you strive to attain consistently high goals, there will always be a market for your horses even if you aren’t chasing the latest fad.