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 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 hog 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 breeder 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, Minn., and a
prominent Arabian breeder for many years, used to put it something
like this: "In business, I count progress by the decade. With
horses, it takes a little 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 variables come into play.
It is also
complex because it sometimes is difficult to differentiate between
genetic and environmental factors. Does a young 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 it
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 sisters. One might be
large and robust and the other small and lacking in strength.
Genetics? Or a difference in feeding programs when the two were
very 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 from
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 genetic 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 royal 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. When 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 a 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 for 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
unravelling 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.
It was the same with 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 parts from a plant that produced white flowers and
fertilized that plant with pollen from a plant that always
produced purple flowers. He also 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 the white-flowered plant
being crossed with the purple-flowered, the result was expected to
be a 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 the tall mare with a 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
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
purple flowered plant, the resultant offspring were all purple.
This first generation of plants would be referred to as 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 flowered F2 plants always
produced white flowers when they were 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
dominant. That led to the conclusion that one-fourth of the plants
were pure-breeding dominant individuals; one-half of the plants
were not pure-breeding dominant individuals; and 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 there 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 chromosomes, which are slender, thread-like 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 they exist in pairs, doesn't mean the pairs
are identical. Often they are not.
If the paired
genes are identical, the individual is referred to as being
homozygous. If the paired genes are not identical, the term used
is 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 of each parent split
with a single set of 32 chromosomes from each joining to form a
new 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 the result of a recessive gene. Any time a bull
and cow were mated with each carrying the recessive gene and 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 a
little 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, co-dominance, and partial dominance. Dominance is
defined as the ability to mask or cover up its recessive allele.
Co-dominance in gene action results in an intermediate state
between the two parents. An example of co-dominance 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
partial dominance is the dilution gene affecting color. The base
color, such as bay or sorrel, has 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 the speed at which the
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 heritability 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 that being passed
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
others 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
increases 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:
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 of 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 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 weaknesses 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, DVM, MS, of Louisiana State University, used this
colorful description to describe DNA: "The DNA consists of a
series of genes aligned like 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 or 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-Arabian 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 defence.
"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 gene--heterozygous--the dominant
gene will prevail, but the horse will still be a carrier. If a
heterozygous horse is mated to one that is homozygous normal, all
of the foals would 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 would have CID.
Hyperkalemic
periodic 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 the genetic
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 the 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 manifestations of chromosomal
defects in horses that are actually born are 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.
