Beef Leanness Gene Pinpointed
This Piedmontese-Hereford crossbred calf displays classic double muscling
because it inherited a defective myostatin gene from both of its parents.
Superbly leanbut tenderbeef rump roasts may reach more tables
when new technology helps cattle breeders turn a possibly undesirable gene into
a sure asset.
On a genetic map for cattle, Agricultural
Research Service scientists and their colleagues have pinpointed a gene
that codes for a form of protein called myostatin. In its usual active form,
myostatin puts the brakes on the number of muscle fibers produced in a calf
fetus. Another, less common version of the gene produces inactive myostatin.
Researchers now know that two copies of the gene for inactive myostatin are
responsible for double musclingthat is, extreme muscularity in the hind
quarters of cattle.
Double muscling is considered an undesirable trait from a production
standpoint. Sometimes, birth of double-muscled calves must be assisted by such
extraordinary means as Cesarean section.
Cattle with only one copy of the gene for inactive myostatin look normal,
but their carcasses typically yield about 7 percent more beef that has about 14
percent less overall carcass fat than beef with active myostatin, says Timothy
P. Smith. He is a chemist at ARS' Roman L. Hruska U.S. Meat Animal Research
Center (MARC) in Clay Center, Nebraska.
After several years of mapping research, MARC scientists had nearly
pinpointed the location of the genetic defect causing extremely large
musclesor muscular hypertrophyin double-muscled cattle to a small
segment of bovine chromosome 2. Then, scientists at the Johns Hopkins School of
Medicine in Baltimore, Maryland, discovered a gene they named
myostatin that increased muscularity in mice.
Putting the two findings together, MARC researchers teamed up with
scientists at the Ruakura Agricultural Research Centre in New Zealand and
within months were able to show that changes in the bovine myostatin
gene cause double muscling. Similar results were reported from a team of
European labs. The Johns Hopkins team has also found myostatin genes
in pigs, chickens, and turkeys.
Smith and his colleagues at MARC have since developed DNA tests for
slightly differing versions of the myostatin gene that are often found
in Belgian Blue and Piedmontese cattle breeds. "We hope to see these tests
become available for commercial use in the near future," says Smith.
Cattle breeders could obtain test results from blood, semen, or a small
sample of a cow's ear to plan sure-bet mating strategies for producing cattle
with just one copy of a gene that signals production of inactive or weakly
active myostatin. Such cattle would provide the kind of beef today's consumer
wants without increasing the risks of difficult calvings, Smith says.
The researchers found that cattle with at least one gene for inactive
myostatin produce beef that has less marbling, or intramuscular fat, as well as
less extramuscular fat.
Contrary to popular opinion, Smith says, less marbling doesn't always mean
less tender. The researchers expect to pinpoint a number of genes that,
together, control tenderness.By Ben Hardin, Agricultural Research
Service Information Staff.
This research is part of Animal Germplasm Resources, Conservation, and
Development, an ARS National Program described on the World Wide Web at
Timothy P. Smith is at the
USDA-ARS Roman L. Hruska U.S. Meat Animal
Research Center, P.O. Box 166, State Spur 18D, Clay Center, NE 68933; phone
(402) 762-4366, fax (402) 762-4390.
"Beef Leanness Gene Pinpointed" was published in the
June 1999 issue of Agricultural