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Progress in
the field of genetics has been moving by leaps and bounds during the past
few years. It wasn't long ago that researchers discovered ways to
unravel and study DNA, that elusive strand of genes that inhabits each and
every cell. Once that breakthrough was made, discoveries cane at an
almost dizzying pace. Specific genes were identified and located.
Another startling and, to many disturbing, step forward came recently.
Scientist cloned sheep.
What does all this mean to horsemen? It can
and should mean a great deal. By taking advantage of past and present
knowledge, we can take steps to produce stronger, healthier horses and steer
away from some crippling diseases.
Genetics progress in the horse world has been slower than in other phases
of agriculture. There likely are a couple of reasons for that.
Many of the horses in existence are bred strictly for the pleasure of the
owners. Beef cattle, hogs, chickens, dairy cows and sheep, however all
are creatures that are bred and raised for food and profit.
With profit as an incentive, there has been great genetic progress with
animals produced for meat. For example, one can buy just-hatched baby
chicks, put them on the put them on the proper feed program, and eight weeks
later pack them into the freezer as four- to five-pound broilers. With
hogs, there has been a complete change in the type of animal produced only a
few decades ago. When the consumer complained of too much fat,
the geneticists developed a longer, leaner hog that packed only a small
amount of fat on its frame. It has been the same with beef and sheep. Of Course, it is easier to facilitate relatively rapid changes in the
chicken and population because of the numbers involved. The number of
fertilized chicken eggs with which researchers could work, for example, was
basically limitless. And with hogs, one sow can deliver a dozen
offspring at a time.
It isn't the same with horses. If the breeders is lucky, his or her
broodmare will produce a single foal each year of her productive life.
The late Daniel Gainey, founder of Jostens Company in Owatonna,
Minnesota, and a prominent Arabian breeder for many years, used to put it
something like this: "In business, I count on progress by the decade. With horses, it takes longer."
So how does this business of genetics work? How can we determine
which mare to put to which stallion? The answer is both simple and
complicated. It is simple because the offspring will receive a set of
genes from each parent and they will determine the newcomer's physical and
mental makeup. It is complicated because the deeper we get into the
process, the more variable come into play.
It is also complex because it sometime is difficult to differentiate
between genetic and environmental factors. Does the colt start chewing
on fences because it was genetically predisposed to do so, or did the colt
learn to chew from watching its mother. Or is it a combination of
both.
It's the same with temperament. Is a particular foal mean-spirited
because he inherited those genes, or because its mother has a bad temper and
it learned the same through observation? In this scenario, the problem
becomes more complicated if the sire of the foal is a mild-mannered horse.
And how about the differences between full brothers or sister. One
might be large and robust and the other small and lacking in strength. Genetics? Or,
was it a difference in feeding programs when the two were young?
How about breeding decisions? If we have a 17-hand mare and want a
smaller offspring, what will happen when we breed her to a 13-hand stallion?
Will the foal be 15 hands, splitting the difference for each parent, so to
speak.
If we breed a fast stallion to a slow mare, will we get an offspring that
will have moderate speed?
Because this article is designed to be a primer on genetics, we must
start at the beginning of this relatively new science if we are to find some
answers to these questions.
Back to Basics
The first realization we must have is that because of the complex nature
of our genetics makeup, there is great variation. We need only look
around us in a crowded room or in a stadium filled with thousands of people. There might be similarities, but very few will look alike.
Yet, there also are traits that are passed down in families from
generation to generation. If one studies photos of the European
royalty family Hapsburg, it quickly will become evident that a protruding
lower lip shows up in generation after generation, the result of a
particular gene being expressed.
When we refer to the field of genetics as a relatively new science, we
are being accurate. The father of the study of genetics was an
Austrian monk named Gregor Mendel. He was born in 1822 and died in
1884. We he was conducting his experiments, science did not know of
the existence of chromosomes. For Mendel to accomplish what he did
without knowledge of chromosomes is truly one of the greatest intellectual
accomplishments in the field of science.
Mendel was the son of peasant parents. He was educated in the
monastery in Czechoslovakia and from there went to the University of Vienna,
where he studied science and mathematics. Then misfortune, or more
likely fortune, struck. (It was unfortunate for Mendel at the time,
but fortunate of the science of genetics.) Mendel failed to pass his
examination for a teaching certificate. He returned to the monastery
and remained there for the rest of his life.
At the monastery Mendel initiated a series of studies aimed at unraveling
some of the mysteries of genetics. For his experiments, Mendel
selected the common garden pea.
It was a good choice, because garden peas are small plants that are easy
to grow, with a short germination time that meant several generations could
be produced and studied in a single year.
Studying Mendel's progress with the pea plants can serve to open the door
of knowledge on genetics at the basic level because the concepts are
the same, be the subject pea plants or horses.
First, Mendel simply studied the plants that grew in the monastery garden
for several generations. He found, for example, that plants with white
flowers when fertilized by like plants always produced plants with white
flowers, regardless of the number of generations involved. When
fertilized with the plants that produced purple flowers. When fertilized by
like plants, the new plants always bore purple flowers.
Now for the experiment. The monk decided to produce hybrid plants by
crossing purple flowered plants with white flowered plants. Mendel
removed the male part from a plant that produced white flower and fertilized
that plant with pollen from a plant that always produced purple flowers. He did the reverse--fertilizing a plant that produced purple plants with
pollen from a white-flower plant
At that time, one of the prevailing theories was that if plants with
opposing colors were crossed, the result would be a plant that was
intermediate in color. In the case of white-flowered plants being
crossed with the purple-flowered, the result was expected to be light
lavender.
Mendel proved that theory to be groundless. He did not get any
plants with intermediate coloration with his crossbreeding program. Remember the question about crossing tall mare with short stallion? The
likely result would be that the offspring would basically be either tall or
short. This does not mean that the offspring would basically be either short
or tall. This does not mean that the offspring would be the exact size
of one of the parents. Since one or the other of the genes--tall or
short--would be expressed, it is unlikely that the resultant foal would wind
up midway between the parents in size.
However, we are getting ahead of ourselves. Back to Mendel and his
pea plants.
Mendel found that in each case where he crossed a white flowered plant
with a a purple flowered plant, the resultant offspring were all purple. This first generation of plants would be referred to as the first filial or
the F1 generation.
Mendel referred to the trait expressed as the color purple as being
"dominant." The trait not expressed he referred to as "recessive."
Thus, the purple flowered plant was dominant over the white flowered plant.
The terms dominant and recessive have become the most common terms used when
discussing genetics.
After the F1 plants with their purple flowers had matured, Mendel allowed
them to self pollinate in an effort to see what would happen in the second
filial or F2 generation. Then the results were different. Not
all of the plants in the second or F2 generation had purple flowers. Some of the flowers were white, meaning that the recessive trait had been
latent in the first generation, but now was active.
Mendel discovered something else. The white flower F2 plants always
produced white flowers when allowed to self-fertilize. By contrast,
only one-third of the purple flowered plants produced offspring with purple
flowers, despite the fact that they were dormant. That led to the
conclusion that one-fourth of the plants were not pure-breeding dominant
individuals; one-fourth were pure breeding recessive individuals.
The 3:1 ratio of dominant over recessive is referred to as the Mendelian
ratio.
Armed with the knowledge that these are dominant traits and recessive
traits, let's switch our attention to genetics in horse breeding.
Each horse's body contains multitudinous cells. Within each cell is
the genetic blueprint for that animal. The blueprint or genetic
material is carried on chromosome, which are slender, threadlike structures
that are paired. A horse has 64 chromosomes or 32 pairs. At
various locations--referred to as loci or locus--on these chromosomes are
genes. A gene is comprised of a DNA nucleotide sequence. Just
as is the case with chromosomes, genes exist in pairs. The two genes
that are paired are referred to as alleles. However, just because in
pairs, doesn't mean the pairs are identical. Often they are not.
If paired genes are identical, the individual is referred to as being
homozygous. If the paired genes are not identical, the term used
heterozygous. Homozygous individuals have only one allele to pass on
to their offspring. Heterozygous individuals can pass on either of the
two different alleles possessed in their genetic makeup.
This passing of traits all occurs at the moment of conception. When the
sperm fertilizes the egg, the paired chromosomes from parent split with a
single set of 32 chromosomes from each joining pair for a total of 64
individual chromosomes. This means, of course, that there is a new
pairing of genes or alleles.
So, now the potential offspring of these two individuals is endowed with
a complete set of genes from each parent. The way in which the genes
pair up will determine which genes are expressed.
The genetic rule of thumb is that the dominant gene always will have its
way when paired with a recessive gene. Sometimes, however, both
parents pass on a recessive gene for a particular trait, and it is then that
the recessive gene will be expressed.
A case in point. For some years, a particular breed of beef cattle
suffered from dwarfism as a result of a recessive gene. Any time
a bull and cow were mated with each carrying the recessive gene ant those
genes paired up at the time of fertilization, the recessive gene would be
expressed and the offspring would be a dwarf. Selective breeding
that made certain that at least one parent carried a dominant gene for
growth has pretty much wiped out the problem.
There are a couple of genetic health problems in particular breeds of
horses today that are the result of recessive genes. More about that
later.
First there are two other terms with which we should become acquainted:
genotype and phenotype. The phenotype is the outward manifestation of
the genes being carried. In other words, the genotype is the blueprint and
the phenotype is the realized outcome.
"There are two basic types of genetic action--qualitative and
quantitative," writes E.I. Johnson, PhD, of the University of Florida, in a
paper on equine genetics. "In qualitative gene action, a particular
trait is influenced by a single pair of genes, or maybe two or three pairs
of genes. In quantitative gene action, a trait such as speed is
influenced by a number of genes that all have some influence on the trait."
"In traits affected by qualitative gene action, there are three primary
types of gene action that affect the trait. The types of gene action are
dominance, codominance, and partial dominance. Dominance is defined as
the ability to mask or cover up its recessive allele. Codominance in gene
action results in an intermediate state between the two parents. An
example of codominance is blood type. Each blood type is different and
known and thus indicates the genotype. Partial dominance also results
in an intermediate state, but not necessarily an exact intermediate state. An example of a partial dominant state is the dilution gene affecting color. The base color, such as bay or sorrel, have no dilution genes. When
one dilution gene is present, the base color is altered (diluted) to
buckskin or palomino. If two dilution genes are present, the base
color will be diluted to cremello or perlino."
Most traits in horses are influenced by quantitative gene action. A
good example would be speed in a Thoroughbred, Quarter Horse, or Standardbred. there is no single gene that determines speed at which
one animal can run. Instead, multiple genes are involved, with factors
like size, sturdiness of leg, heart and lung capacity, coordination, muscle
efficiency, strong tendons, ligaments, and joints and mental traits that
govern the horse's will to win.
Then, of course, environmental factors become involved. Training
and nutrition, for example, can strongly influence how well a horse
performs.
Johnson contends that all genetic traits have a heritable estimate:
"The heritability estimate is essentially the percentage of a horse's
expressed trait that is due to genetics. The percentage that is due to
genetics indicates the probability of the being passed on from one
generation to the next. Specifically, the heritability estimate of a
trait refers to the ability to select horses to mate based on superior
performance for the trait and to predict the improvement in the offspring.
Some traits are highly heritable and other are low. In any selection
process, greater progress can be made when keeping the number of traits
selected to a minimum."
"If a horse is selected for only one trait, then greater selection
pressure (horses more outstanding in that trait) can be applied on that
trait. Selecting for traits that are highly heritable also greatly
increase the chance for improvement. For the traits that have a low
heritability estimate, much greater success can be achieved by controlling
the environment and management regimes."
Johnson provides these heritability estimates for certain traits in
horses.
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Height at withers--45 to 50
-
Body weight--25 to 30
-
Body length--35 to 40
-
Heart girth circumference--20 to 25
-
Cannon bone circumference--20 to 25
-
Pulling power--20 to 30
-
Running speed--35 to 40
-
Walking speed--40 to 45
-
Trotting speed--35 to 45
-
Movement--40 to 50
-
Temperament--25 to 30
-
Cow sense--Moderate to high
-
Type and conformation--Moderate
-
Reproductive traits--Low
-
Intelligence--Moderate to high
So, one can conclude there are no magic genetic formulas in breeding. The old adage of "breed the best to the best'" has some validity, but it
does not guarantee a highly improved offspring.
The great Secretariat is an example. He was one of the mightiest
runners ever to set foot on a track, yet few of his offspring even came
close to duplicating his performances. Somehow, some to those key
quantitative genes involved in racing success were not expressed in his get.
While the goal always should be to improve the offspring, there are
far too many breeding programs that breed for only a single trait and forget
all the others. Racing is a case in point. Far too many runners
which cannot compete because of weaknesses in leg bones, joints, ligaments
and tendons are put into the breeding shed and mated with others who cannot
compete for the same reason. It doesn't take a Gregor Mendel to
determine the probable outcome for such a cross. The colt or filly might
inherit blazing speed, but the opportunity to display it likely will be
short-lived before the same weakness that ended the careers of the parents
will do the same for the offspring.
Unfortunately, genes do not always remain in unaltered form. Sometimes
defects occur and when that is the case, certain weakness or diseases are
easily passed from one generation to another.
Remember that the entire blueprint for a horse resides in the minuscule
amount of DNA found in the nucleus of a single microscopic cell.
Jill J. McClure, D.V.M., MS, of Louisiana State University, used this
colorful description to describe DNA: "The DNA consists of a series of genes
aligned like the Christmas tree lights on a string."
Defects in the DNA blueprint, she writes, can result in the failure to
form essential proteins or the formation of abnormal proteins that can
result in death and disease.
Diseases involving DNA, she explained, can be divided into two
categories--those that result from mutant genes and those that occur from
chromosome aberrations, which are the result of accidental damage to
chromosomes during reproduction.
The diseases that result from mutations can be passed from one generation
to another. A case in point is combined immunodeficiency (CID), an
inherited disease of Arabian and part-0Arabian horses. Foals with the
malady are born bereft of a normal immune system and usually die shortly
after birth as the result of infections against which their bodies have no
defense.
"The defect" reports McClure, " is believed to have
arisen originally from a mutation in a single gene in a single individual
(point mutation), which was then perpetuated by the intense breeding of the
affected line. Some estimates suggest that as many as 25% of Arabians in the
United States carry the gene for CID and that two to three percent of
all Arabian foals are born affected."
Two recessive genes are required for CID to be exhibited.
If an Arabian has one dominant gene and one recessive--heterozygous--the
dominant gene will prevail, but the will still be a carrier. If a
heterozygous horse is mated to one that is homozygous normal, all the foals
will be normal, but half of them would be carriers. In the
heterozygous horses, all would be normal, but all also would be carriers.
If two heterozygous horses were mated, the expected outcome would be that
25% would inherit two copies of the normal dominant gene; 50% would be phenotypically normal with one dominant and one recessive gene, but would be
carriers, and 25% would inherit two copies of the recessive gene and have
CID.
Hyperkalemic period paralysis (HYPP) is another example
of a gene mutation that started with one Quarter Horse stallion, Impressive. The affliction is characterized by intermittent attacks of muscle
tremors, weakness, disorientation, or convulsions. The HYPP gene
differs from the CID gene in that the HYPP gene is dominant. McClure
gives this explanation:
"The disease (HYPP) is transmitted by an autosomal
dominant mode of inheritance. At least one of the parents of an
affected animal must also carry the gene and be affected, but not
necessarily both, because this is a dominant condition and only one abnormal
gene need be present. The defect is believed to have originated as a
point mutation in the gene that controls the protein that regulates the
movement of sodium into and out of muscle. Both the normal and
abnormal alleles for this gene have been identified. Only one
amino acid is different between the normal and abnormal proteins,
emphasizing how even small changes can make significant clinical
differences."
Because of the popularity of Impressive and his
offspring, it is estimated that approximately 100,000 Quarter Horses carry
the gene for HYPP.
HYPP and CID are only two of a number of genetic
diseases. When genetics problem stems from chromosome damage or
abnormalities, the result is frequently early embryonic death. When
there is survival, reports McClure, the horses tend to exhibit growth
defects and infertility. Here is her explanation of chromosome damage:
"During reproduction, the chromosomes of each parent are
copied and then packaged individually into germ cells (either sperm or
eggs). During the process of copying and packaging, things can go
wrong, resulting in chromosomal breakage, deletion, duplication, or
misalignment. Chromosomal defects are associated with alterations of either
whole or relative large sections of the chromosomes containing many genes."
"They have no consistent mode of inheritance because they
are largely the result of sporadic accidents of nature. Chromosomal
abnormalities involving large segments of chromosomes and significant
numbers of genes are incompatible with life and result in early embryonic
death. this probably explains why manifestation of chromosomal defects
in horses that are actually born relatively uncommon."
There is much that is known in the field of equine
genetics and much to be learned. Horse owners who stay abreast of the
exciting research will discover many benefits that will help them produce a
better horse.
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Les Sellnow is a free-lance
writer specializing in articles on equine research. Based in Riverton,
Wyoming, Sellnow also is author of fiction and non-fiction books.
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