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Shorthorn mutation was beginning of current genetic research
"Breeders really need to use the test in order to eradicate this problem. Knowing an animal's status will help producers make informed breeding decisions," said Indiana Shorthorn breeder Nick Steinke.
By Jennifer Bremer  Shorthorn breeders were hit with a genetic defect after the turn of the millennium that has helped other breeds eradicate similar problems and has led to extensive research for identification of other genetic mutations. In 2000, Tibial Hemimelia, a lethal genetic defect began showing up predominantly in Shorthorn cattle. The defect, carried as a recessive gene, causes multiple congenital defects according to Dr. Jon Beever at the University of Illinois. "TH really came to the forefront in 2003, but was first described in Galloway cattle in the 1960s," said Dr. Beever. Translated, TH refers to the absence of all or part of the tibia--the bone between the stifle and hock--and the absence of all or part of a limb. These calves also have large abnormal hernias, twisted legs, and can have a skull deformity. Genetic information from affected calves and their sires and dams led Dr. Beever to determine the genetic defect was a deletion of part of the gene. Producer action Nick Steinke, a Shorthorn breeder from Indiana, had heard rumors of the problem in 2002, but it wasn't until 2003 when he really became interested. Steinke along with his local veterinarian, Dr. Chuck Hannon, encountered some of the deformed calves and after investigation realized it was a genetic problem. "I heard from some of my customers and some other breeders that they were having some deformed calves," said Steinke. "In the spring of 2003, my neighbor had one and then I had one. We figured it was more than just a freak of nature." After doing extensive pedigree searches on the affected calves, a common ancestor was identified. Hannon then searched for more affected calves in order to have enough samples to submit to determine the problem. Dr. Beever then came into the picture, as Hannon had contacted him about the unknown defect since he had been involved in work with a genetic defect in sheep. "He was the first one to call us back," said Hannon. "And then everything else developed quite quickly." Genotypes Dr. Beever studied the pedigrees of affected and unaffected cattle, which led to his conclusion that TH is a recessive disorder. In order for a calf to be affected, it must inherit the defective gene from both sire and dam. "Since the carrier animals look normal in a recessive disorder, we then realized how important it would be to develop a test," said Hannon. Although affected calves are rarely tested, they would be homozygous for the mutation and a TH carrier (THC) would be heterozygous for the mutation. Using the known genetic information from two animals, a breeder can determine the chances of having an affected calf, according to Dr. Beever. He explained: If the normal gene is "T" and the defective gene is "t," mating a carrier bull with the genotype Tt for the TH gene to a carrier cow also with the genotype Tt for the TH gene will result in three calves that look normal at birth, but two of the three will be TH carriers (Tt). The fourth calf will be born with TH (tt). Thus, mating two carriers gives a breeder a 25 percent chance of having a TH calf every time this mating is repeated. Mating a carrier bull or cow to a non-carrier cow or bull will result in 50 percent of the calves being TH carriers (Tt). A non-carrier or TH-free (THF) animal would have the genotype TT. Managing the problem Hannon said he's seen very few TH calves in the past few years and, when he hears of one, he blames it on an accidental breeding in most cases. "Since we now have a test for TH and people know which pedigrees it is normally seen in, a full-fledged TH calf is very uncommon," he said. Steinke said he has had some TH carrier females in his herd and has continued to breed to THF bulls to phase out those genetics. "The American Shorthorn Association is trying to manage the problem of TH carriers, but they need to completely eradicate it from the breed," said Steinke. In November 2003, the initial ASA Genetic Defect Protocol was approved, and then revised in April 2004. The ASA Genetic Defect Protocol outlines the steps Shorthorn breeders should take to report and submit samples on defective calves and their parents for parental verification. The protocol also solicits documentation from attending veterinarians. The protocol made possible the listing of carrier animals. In August 2005, the ASA Genetic Defect Policy was approved, outlining policy requirements on AI sires, donor dams, and cloned animals, as well as ASA rights and conditions. "Breeders really need to use the test in order to eradicate this problem," Steinke added. "Knowing an animal's status will help producers make informed breeding decisions." The ASA bylaws state that it is every member's duty to promptly report any abnormal condition or genetic defect found in Shorthorn cattle to the association. With the aid of qualified geneticists, every effort will be made to determine the cause and document parentage for every reported defect. Any effort to conceal such information is considered an unethical practice by the ASA and may result in suspension or expulsion from the membership. While TH is mostly seen in Shorthorn influenced cattle, it is also seen in some other breeds due to crossbreeding. Hannon said any animal that traces back to the original Shorthorn bull imported to the U.S. in the 1970s has the potential to be a carrier of the defective gene. "Most of the TH calves we are seeing now is because of a mistake in breeding," said Hannon. "It looks like we have this problem pretty well under control." Jennifer Bremer can be reached by phone at 515-833-2120 or by e-mail at jbremermaj@hotmail.com. 12/8/08 Date: 12/4/08
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