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Carol Davidson, 2008
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The Dexter Arrives
From 1820 on, small cattle in Ireland with heavy bodies and short legs
were selected out of the general population and grouped together to form
a new ‘breed’ called Dexter. It wasn’t long before these animals were
being exported to England, and cattle in England that had the same
traits were added to the gene pool. It was expected that over time, the
breed would stabilize and all those animals that did not match the
trademark look and size would be bred out, and owners would be left with
the best of the lovely little cattle they preferred.
1: Dexter bull
2: Dexter cow
As time passed, owners found
that while they were getting the preferred ‘shortleg’ type, they
continued also to get larger, more normal-looking cattle (known as
‘longleg’ type), as well as deformed fetuses (later called ‘bulldog’
calves), and they didn’t seem to be able to eliminate these two
undesired types. The statistical proportion of births was ¼ longleg, ½
shortleg, and ¼ bulldog.
With the advent of the science
of genetics, it was discovered that the very trait that made a Dexter a
Dexter (short legs), was unfortunately due to a form of dominant lethal
genetic mutation. As long as the mutation was the primary selection
criterion, all three types would continue, and Dexters would never breed
true. Rather than give up the appearance they preferred, owners chose to
live with the problem.
mutation was better understood, many started to breed their shortleg
Dexters with the normal as they found they still got the same proportion
of shortlegs but avoided the bulldog calves. For those matings, the
statistical proportions were ½ shortleg, ½ normal. Until very recently,
owners continued to breed both ways, with only the shortleg considered
the real Dexter, and many (most) of the longlegs discarded. Since 1980
in North America, some owners have chosen to breed small longlegs,
working to produce a size and look similar to the original selection
criteria, but without using the lethal mutation.
Dexter cattle have a unique genetic mutation that
causes defective bone growth. This mutation is referred to as
chondrodysplasia, and it results in the animals appearing heavy bodied
on short legs. There is a large variation in effect of this single-gene
mutation, with some animals being proportionate and very attractive,
while others are strongly disproportionate with a dwarf-like appearance.
The degree of dwarfism expressed is not consistent. At this time, the
cause for the variation is not known. Carriers of this gene appear to be
much more heavily muscled, but this is because muscle that is designed
to attach to a normal bone is actually compressed onto a shortened one,
causing the muscle to bulge. Carriers often show a greater spring of rib
or can be potbellied because the organs retain their normal size yet
must fit within the reduced skeletal framework, or drop below it.
6, 7, and 8:
examples of the degree of dwarfism expressed in carriers
The mutation affects the
chondrocytes, which are minute particles of specialized cartilage that
ossify to form bones. Chondrocytes are shaped rather like playing
cards. They are released at one side of a ‘growth plate’, and are
attracted to the other side where they go through a process that unites
them into solid bone. There are growth plates on all bones except
the cranium. The normal gene results in the organization of chondrocytes
hundreds of chains or columns, edge to edge (called palisading).
As they pass through the far side of the plate, true ossified bone
conversion takes place. It is this ‘nose to tail’ effect that
creates the length in the bone. The mutated gene disrupts the
normal organization of the chondrocytes, and palisading does
not occur. The chondrocytes simply drift
helter-skelter toward the opposite side and get converted as is.
9: homozygous normal (non-carrier)
10: homozygous for
The effect on the length of
the bone can be compared to the difference in vertical height between a
house of playing cards, and a deck used for 52-pick-up. The result is
most visible in long bone growth because there are growth plates at both
ends of those bones, which doubles the effect. Dr. Julie Cavanagh,
University of Sydney (AU), discovered the genetic location of the
mutated gene and presented her findings at the 2002 International Dexter
Congress, and a test followed soon after. Dr. Cavanagh found that when
she averaged the heights of the cows and bulls with and without
chondrodysplasia that formed her database, there was an overall average
difference between carriers and non-carriers of five and one-half inches in
cows and eight inches in bulls. Individual animals and distinct herds
can be expected to show a variation on the average.
The mutation is a
4-character mistake in a longitudinal growth gene. The mistake causes a
premature ‘stop’ early in the instruction which nullifies the normal
action of the gene. Because genes work in pairs, three different results
are possible depending on the gene combination.
In the case where both genes of the pair are unaffected, the genes work
properly, and long bone growth is normal. This is the Dexter
In the case where one
gene is normal and one gene is mutated, the normal gene works properly
but the other gene’s effect is virtually nil. The normal gene works
alone, and only partial palisading takes place.
While there is long bone growth, it is less than usual, and the result
is shortened bones, especially legs. This is the Dexter
‘carrier’, or the
classic original selection.
In the case where both genes are
affected, all chondrocytes are disorganized. No palisading takes place,
and there is virtually no bone growth. The fetus is aborted most
frequently either between 30 and 60 days (information provided by
experienced English breeders with large herds; less experienced owners
think the cow simply didn’t settle and rebreed her) or between 6 and 8
months (in which case the fetus has vestigial legs, an abdominal hernia
and a ‘bulldoglike’ head). This is the Dexter
always born dead, hence the genetic designation ‘lethal.’
The combinations below are statistical
probabilities. Every calf is a new throw of the dice. There is no
specific bias toward any one direction; no inclination to one result
over another. It is all pure chance. The possible statistical genetic
Non-carrier bull x non-carrier cow:
100% chance of having a non-carrier calf.
Non-carrier bull x carrier cow:
50% chance of having a non-carrier calf;
50% chance of having a carrier calf.
Carrier bull x non-carrier cow:
50% chance of having a non-carrier calf;
50% chance of having a carrier calf.
Carrier bull x carrier cow:
25% chance of having a non-carrier calf;
50% chance of having a carrier calf;
25% chance of having a dead bulldog calf.
A quick examination of the above breeding statistics makes it clear that
only the non-carriers breed true. For those who wish to breed the
carrier, both types will be produced, creating a herd that shows a wide
range of heights because of the effect of the mutation.
Because we are dealing with a form of dominant gene,
many carriers can be identified visually. However this does not
hold true 100% of the time. Only genetic testing can identify the
presence of the mutation. With that knowledge, owners can make informed
The ADCA recommends that owners who wish to breed the
carrier type mate carriers with non-carriers to avoid their cows having
For the instructions and application for
Those who test will receive test result certificates from Texas A&M, the
official ADCA DNA lab.
Here is the test result interpretation table that appears on the