Modern technology and good old-fashioned management minimize the challenge of genetic abnormalities caused by recessive genes.
The science and application of genetics has allowed animal breeders to make tremendous strides in production efficiency. Coupled with modern nutrition and management, U.S. beef producers today produce a beef tonnage equivalent to that of 30 years ago — but with 25 million fewer head of cattle.
There's no doubt that the industry's ability to identify outlier animals that defy genetic antagonisms and excel for a variety of traits has been a boon to the industry.
One downside, though, since true genetic curve benders are so few and far between, is that their magnified use can become a problem if it turns out they also drag some unwanted genetic baggage with them.
That's what rocked the beef industry a year ago when Arthrogryposis Multiplex (AM), a lethal genetic defect, was discovered in one of the Angus breed's most used and coveted bloodlines — GAR Precision 1680.
According to Precision 1680's performance record from the American Angus Association (AAA), nearly 10,000 direct sons and daughters are part of the breed's genetic evaluation. He was one of the first Angus sires to bend the curve and provide low birth weight but superior weaning and yearling growth.
Every breed, species and individual contains recessive genes that are seldom expressed and thus rarely known about. In the case of Precision 1680, inadvertent propagation was the catalyst. His genes were being multiplied and magnified because of his genetic merit, but no one knew he also carried the recessive gene for AM.
Also known as Curly Calf Syndrome, AM results in stillborn calves with bent and twisted spines.
Science offers options
In the old days of genetic defects like Snorter Dwarfsm, such a discovery would have been the death knell for an entire line of cattle and a major blow to the breed itself. In those days, the only way to manage such defects was to avoid them, period.
Many are familiar with coat color in Angus as an example of how the simple mode of genetic inheritance works; red is recessive and 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.
Though genetic defects inherited in this manner create challenges, especially for seedstock producers, new technology means these simple recessive genetic defects — which AM appears to be — can be managed without throwing away the bloodline.
In the case of AM, a genomic test that screens for the presence of the defective gene also means seedstock producers can still utilize the bloodline while avoiding the problem.
For commercial producers, the odds of mating a carrier bull to cows that are also carriers are extremely low.
Managing genetic defects
AAA breed officials took a proactive approach to AM. Rather than insist on testing and printing results for full disclosure, then letting breeders and the marketplace assign values, AAA moved to eliminate the problem more quickly by banning the registration of carrier animals in the future. For more on this issue, see “Dealing With Curly Calf” at http://beefmagazine.com/genetics/1201-curly-calf-issue/.
This model offers direction to other breeds that possess other genetic defects.
There are 21 genetic abnormalities under management by beef breed associations — conditions ranging from fawn calf syndrome to hypotrichosis to dwarfism in its various forms (see Table 1).
“For commercial producers, the trick to avoiding calves with lethal or performance-threatening abnormalities is never to mate a carrier bull to a carrier female,” Kent Andersen, then the executive vice president of the North American Limousin Foundation, said last spring. “The first and easiest line of defense is to use only bulls free of the relevant defect in a given population.
“Mutations that cause abnormalities always will be a reality of the livestock business,” he says. “Fortunately, with advances in genomics technology and thoughtful management by associations and breeders, we can mitigate the adverse effects substantially.”
During the 2009 Beef Improvement Federation meeting in Sacramento, CA last spring, Jonathon Beever, University of Illinois in Urbana-Champaign geneticist and one of the nation's top authorities on genetic defects in cattle, told producers of four options in dealing with a potential genetic defect carrier in a cowherd population. He said producers could:
Ignore the issue and risk future problems.
Completely eliminate the genetic source, which would be contrary to overall breed improvement
Find outcross genetics to breed away from the gene pool with the defect. While this isn't a practical option for seedstock breeders, it would be for commercial operations, particularly if they produce a terminal cross.
Accurately identify the carriers through genetic testing, and then manage the problem.
Beever called the latter point the most responsible choice, given the high accuracy and growing cost-effectiveness of genetic testing. Beever adds that how producers develop their response within the beef industry will also be influenced by their place in the production system, with seedstock breeders being particularly proactive. (See “The Lowdown On Genetic Defects” on page 24.)
About this table
This listing of genetic defects is exclusive and limited to diseases that are still of concern, reflecting genes that are still present in beef cattle populations, or were in the last 5-10 years. Specific breed listings may seem over-represented because of recent genetic discoveries and proactive steps in management.
It is imperative to understand the inheritance pattern regarding genetic defects. In a simple recessive mode of inheritance, it takes a Carrier x Carrier mating to have a calf with a genetic defect. Even in that mating, the resulting offspring will have a genetic defect 25% of the time.
— Alaina Mousel
|Genetic abnormality||Primary breed(s) of incidence||Lethal or nonlethal||Mode of inheritance||DNA test available?||Management stage|
|Arthrogryposis Multiplex (AM, or “Curly Calf Syndrome”)||Angus & derivatives||Lethal||Simple recessive||Yes||DNA testing underway|
|Beta (β)-Mannosidosis||Salers||Lethal||Simple recessive||Yes||Effectively eradicated|
|Fawn Calf Syndrome (FCS)||Angus & derivatives||Nonlethal||Simple recessive||No||Under investigation|
|Neuropathic hydrocephalus (NH)||Angus & derivatives||Lethal||Simple recessive||Yes||DNA testing underway|
|Hypotrichosis (hairless calf)||Hereford||Nonlethal||Simple recessive||Yes||DNA testing underway|
|Idiopathic epilepsy (IE)||Hereford||Nonlethal1||Simple recessive||Yes||DNA testing underway|
|Osteopetrosis (marble-bone disease)||Angus & Red Angus derivatives||Lethal||Simple recessive||Yes||DNA testing underway2|
|Protoporphyria||Limousin||Nonlethal||Simple recessive||Yes||Effectively eradicated|
|Pulmonary hypoplasia & anasarca (PHA)||Maine-Anjou, Shorthorn & Dexter||Lethal||Simple recessive||Yes||DNA testing underway|
|Tibial hemimelia (TH)||Shorthorn & derivatives||Lethal||Simple recessive||Yes||DNA testing underway|
|Double Muscling||Multiple breeds||Nonlethal||Simple recessive||Yes||DNA testing underway|
|Syndactyly (Mule Foot)||Angus, Simmental, Holstein||Nonlethal||Simple recessive||No||Under investigation|
|Dwarfism (snorter)||Angus||Nonlethal||Simple recessive||Yes|
|Dwarfism (bulldog)||Multiple breeds (non Dexter)||Lethal||Simple recessive||No||Under investigation|
|Dwarfism (bulldog)||Dexter||Lethal||Simple recessive||Yes||DNA testing underway|
|Dwarfism (long headed)||Angus||Nonlethal||Simple recessive||Yes||DNA testing underway|
|Heterochromia Irides (white eye)||Angus||Nonlethal||Simple recessive||No||Carriers identified by affected offspring|
|Red color gene||Multiple breeds||C||Simple recessive||Yes||Routine testing|
|Wild-type color gene||Multiple breeds||Nonlethal||Variable||Yes||Routine testing|
|Dilution of coat color||Hereford, Simmental, Gelbvieh||Nonlethal||Dominant||Yes||DNA testing underway|
|Alpha (α)-Mannosidosis||Angus, Red Angus, Murray Grey, Gallaway||Lethal||Simple recessive||Yes||Test available|
| 1The American Hereford Association lists Idiopathic epilepsy (IE) as a lethal genetic defect; |
2A DNA test for Osteopetrosis is not available for Angus cattle, but the test available for Red Angus may work for Black Angus
|Source: North American Limousin Foundation, Dr. David Steffan, Dr. Jon Beever|
Steve Foglesong heads up the Black Gold Ranch and Feedlot (www.blackgoldranchandfeedlot.com) in Astoria, IL. The family operation consists of 5,000 acres of cropland and pasture under intensive rotational grazing by 1,200 cows. A few years ago, they added a slatted-floor confinement feeding facility of 5,000-head capacity.
“On our place, we've never had a problem with genetic defects and haven't worried about it much due to our reliance on crossbreeding; that will cut any potential problems in half right there,” Foglesong says. “Plus, I assume our seedstock provider and our herdsman are taking care of any potential for genetics problems and not sending carrier animals down the line.”
Bryan Gill, marketing manager with Gill Red Angus (http://www.bigredgenetics.com/), says the production goal of this Timber Lake, SD, operation is “to produce the best-footed, easy-keeping maternal cows and performance bulls with muscle, length and calving ease so our commercial customers are profitable.”
Gill says the family operation, which markets about 200 bulls annually, most of them via their production sale the first Tuesday in February, has few problem pedigrees, thanks to careful development.
“We follow the rules of the Red Angus Association of America (RAAA) and test the sons and daughters of any known carrier in the pedigree. We haven't necessarily culled anything due to that testing, but we have located the carriers in our herd. We then breed away from it, just like the RAAA recommends. Now that we have a test available, we won't bring a sire or cow into our program that has been tested as being a carrier. From here on out, all our herd sires and donor cows will be tested before being used in our herd,” Gill says.
He reports that many of their commercial customers work with Gill Red Angus exclusively: “We recommend to all of our customers that they not worry about this issue and let us take care of the problem, as their seedstock supplier.”
Dave Nichols knows the heartbreak of this issue. As a 13-year-old, some 50 odd years ago, he absorbed the shock of his first grand champion heifer producing a dwarf calf.
“My veterinarian attributed it to lepto; my feed salesman said it was a vitamin E issue. Folks either didn't know or wouldn't tell me, but my county Extension director took me to see Jay Lush at Iowa State University, who was to cattle genetics what Einstein was to physics. Dr. Lush explained recessives to me.
“If not for Jay Lush, I'd probably be pumping gas at a Philips 66 station,” Nichols says with his trademark humor.
Today, Nichols heads up Nichols Farms, Bridgewater, IA, a family-owned seedstock operation that annually markets more than 1,000 Angus, Simmental, Salers and composite bulls, as well as semen and embryos throughout the world. The operation is a leader in performance testing (1956), Certified Meat Sires (1961), EPDs (1977), real-time ultrasound (1989), and genomic profiles (2005).
“All breeds, all mammals have congenital defect lethal and sub-lethal recessives. What we have to do is eliminate them, and we do that with science and objectivity, and it's a lot easier to eliminate them today thanks to DNA testing,” Nichols says.