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Every breed of cattle—every type of
every human and livestock species—has genetic defects. They
rarely come to the phenotypic surface in offspring, though,
because such a defect in one parent has so few opportunities to
line up with the same deleterious gene in the other parent.
So, it’s news when this type of
genetic defect crops up in cattle. When it’s linked to one of
the most used sires in Angus—far and away the most heavily used
beef cattle breed—the news takes on a life of its own.
That’s sure how it seemed
September 17 when the American Angus Association (AAA) told its
members that Arthrogryposis Multiplex (AM—previously commonly
known as Curly Calf Syndrome) was a genetic defect within the
breed that appeared to be transmitted through a simple mode of
inheritance (more later). Further, AAA told members it likely
stemmed from GAR Precision 1680.
For perspective, Precision 1680’s
AAA performance record includes nearly 10,000 direct sons and
daughters that are part of the breed’s genetic evaluation.
Multiply that by a likely factor of 30 or 40 and you get closer
to the number of his descendents within the breed.
Subsequently, AM has only been linked to Precision 1680 and to
his maternal grandsire 9J9.
Sale barn chatter, phone lines and the Internet ran double-time
with discussion and conjecture when the news first broke. In
fact, Mark Gardiner of Gardiner Angus Ranch (GAR) at Ashland, KS
says, “It created a hysteria I’d never seen before among some
seedstock producers.”
That’s saying plenty. The
Gardiner herd is one of the breed’s stalwarts. Their seedstock
herd descends from the commercial Angus herd begun by Mark’s
grandfather in the 1930’s. Mark’s dad bought his first
registered Angus females in the late 1940’s. The Gardiner’s have
collected individual performance data on all of their seedstock
and commercial calves since 1964. You get the idea.
Emotion Fueled by History
Reaction to AM was understandable at the outset. AM is a
lethal genetic defect. Calves affected with the syndrome are
born dead, with bent and twisted spines. Add to that the history
of past genetic cattle disorders, as well as the unknowns
surrounding AM early on, and you had the makings for emotion
lapping logic.
If you didn’t live through
dwarfism in the 1960’s, Mule Foot in the 1970’s, or other
genetic maladies in other breeds more recently, chances are
you’ve heard the stories about entire lines of cattle, entire
herds, being decimated.
Until just a few years ago,
really, the only way to find carriers of genetic recessive
disorders was by line-breeding suspected carriers. If you made
enough matings that were closely related enough, without
uncovering the problem, you were statistically sure that the
animal wasn’t a carrier. Since such a testing process is so
expensive and time consuming, it was typically more practical to
avoid the affected lines altogether, despite any unique genetic
benefits they also offered.
In the case of Precision 1680
that would have meant discarding one of the first Angus sires to
bend the breed’s genetic curve, providing low birth weight but
superior weaning and yearling growth. Though the bull died a
decade ago (he was born in 1990), seedstock and commercial
producers continue to use his progeny heavily. He’s stacked five
and six deep in some pedigrees.
Arthrogryposis Multiplex Basics
So far, it appears the mode of AM inheritance is transmitted
via a simple mode of inheritance. That means a single gene is
responsible for the abnormality and that affected calves must
inherent the deleterious gene from both parents. Animals
inheriting it from a single parent are AM carriers.
If you understand how coat color
is inherited in Angus cattle, then you already understand the
likely way that AM is inherited.
In Angus the color red is
recessive and the color black is dominant. If a calf receives
the gene for black from one or both parents, its coat color will
be black. In order for the animal to be red, it must inherit the
recessive gene (red), from both parents. So it appears to be
with AM (see How AM is Inherited).
This simple mode of inheritance,
combined with science and DNA technology mean that AM can be
managed easily and accurately. That’s how the Gardiners and AAA
were able to deduce the genetic link so quickly.
By way of brief history, the
Gardiners first encountered AM in 1991, though they didn’t
realize it at the time. The Gardiners brought a stillborn calf
with a bent and twisted spine to renowned Kansas State
University geneticist Horst Leipold. He said AM was a
possibility, but there was no way of being sure. It wasn’t an
ongoing problem. The Gardiners have bred and raised about 27,000
calves since that time. Of those, 11 were stillborn and
anatomically abnormal; six had no Precision in their pedigrees.
The veterinarians and researchers consulted determined the
likely cause was environmental or disease-related.
Fast forward to March of 2007
when AAA received notice of a handful of calves born dead with
bent and twisted spines. Necropsies and some of the calves were
sent, at AAA’s request, to David Steffen, a University of
Nebraska DVM and a longtime consultant to AAA. He was unable to
determine the cause as environmental, genetic or due to viral
infection.
In April 2008, another nine calves with a similar condition were
reported to AAA. Based on Steffen’s recommendation and growing
belief the abnormality was genetic, AAA alerted members on Sept.
5 and requested they report any problems consistent with AM. AAA
received verbal and written reports on another 48 calves.
By this time, Jonathan Beever, a
University of Illinois molecular geneticist, was also working
with AAA and Steffen; he’s shouldered developing a DNA test to
identify AM carriers.
It wasn’t until August 2008 that Beever told the Gardiners he
believed the cause was AM and likely stemmed from Precision. The
Gardiners quickly provided semen and DNA on Precision
descendents. More analysis was done. As soon as researchers
confirmed the genetic defect and the probability of the link to
1680, the Gardiners informed their long list of customers.
Gardiner spent plenty of 16-20-hour days on the phone providing
folks with information. What he told customers and others then
holds up just as well now that more information is known about
AM.
Managing AM
“If I’m a commercial producer and I haven’t line-bred, my
risk is essentially zero,” Gardiner says. In other words, the
odds of mating a carrier bull to cows that are also carriers is
extremely low. For commercial producers mating Angus bulls to
cows of another breed, or vice versa, there is no risk, even if
the Angus being used is a carrier.
For seedstock producers, it’s a
matter of knowing the AM status of their genetics and those they
intend to use. As of the December 1, AAA officials expected a
DNA test for AM to be available by January.
By early November the test was
already well on its way to validation with the help of a
coalition of beef bull studs. All told, 761 Angus sires were
tested; 60 bulls turned up carriers, all directly related to
Precision 1680 and to his grand sire, 9J9. That 8% says nothing
about the actual gene frequency within the breed. It does
suggest, however, that the gene isn’t nearly as pervasive as
some may have feared.
The bull studs made the list of
genotypes available to AAA, which in turn released it to members
November 3.
Such lightening speed in test
development has much to do with the willingness of the Gardiners
and AAA to address the situation earnestly and transparently.
Until now, though breed associations and breeders didn’t exactly
sweep such problems beneath the proverbial rug, they were
reluctant to get too vocal or public.
Bottom line, the DNA test means
individuals within the affected bloodline can be used without
fear of propagating the recessive gene. The test allows users to
keep using a line of genetics for the reasons that made the
genetics so widespread to begin with, while avoiding the
recessive baggage that was recently identified.
For Angus seedstock producers,
managing AM is also a matter of understanding AAA’s preliminary
guidelines regarding registration of AM carriers and
non-carriers (see www.angus.org).
Even without the test, the
Gardiners and buyers at their last sale demonstrated how such
knowledge can be utilized. The sale was September 29 when AM
emotion was surging like wild fire. The Gardiners provided
buyers with the probability of each bull being an AM carrier,
based on pedigree (see How AM is Inherited). All told, 214
18-month-old bulls sold for an average of $4,620, which was $500
more than the previous year.
These auction results speak
volumes about the relationship the Gardiners have with their
customers and their long-standing reputation for standing behind
their cattle. But it also speaks to the notion that genetic
users are willing to embrace science rather than emotion in
dealing with the challenge.
As Dahrr Bullock, extension beef
cattle specialist at the University of Kentucky told producers
soon after the AAA announcement, “For beef producers that use
Angus in their breeding program this is a serious situation that
does require some precautions. However, this is a very
manageable situation that can be resolved over time and should
not be handled in a rash manner.”
How AM is Inherited
Arthrogryposis Multiplex (AM—previously known most commonly
as Curly Calf Syndrome) is a lethal genetic disorder that
results in stillborn calves that have bent and twisted spines.
All evidence so far suggests that AM is transmitted via a simple
recessive gene and mode of inheritance. In other words, the
phenotypic expression of the disorder is only expressed if
calves inherit the recessive gene from both parents—if the calf
is homozygous for the trait. Since AM is a lethal disorder,
there should never be a live animal that is homozygous for the
trait.
If progeny receive the recessive
gene from one parent, they are carriers for the trait—capable of
passing the gene to their offspring—though there will be no
phenotypic expression of it.
You can calculate the probability of an animal receiving the
recessive gene by using what’s termed the Punnett Square. The
examples below illustrate the calculations associated with
mating a carrier animal to a carrier animal (Figure 1), and
mating a carrier animal to a non-carrier animal (Figure 2).
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