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Removing the guesswork

From the edition of Agriculture Today.

A homozygous 'double muscled' heifer, too extreme to meet market specifications for fat, or to be a dependable breeder.

A homozygous 'double muscled' heifer, too extreme to meet market specifications for fat, or to be a dependable breeder.

Gene discovery research conducted by NSW Department of Primary Industries has isolated the genetic basis for the double muscling effect within a number of Australian cattle breeds.

A single gene known as myostatin has a major effect on muscling. The protein encoded by this gene is responsible for the regulation of skeletal muscle development.

The function of Myostatin is to repress or inhibit skeletal muscle growth, playing a small role early in an animal’s life but becoming most active as the animal grows. A mutation in this gene results in a non-functional protein that is unable to regulate skeletal muscle growth with the net result being increased muscularity, correctly termed muscular hypertrophy.

Muscular hypertrophy is characterized by both an increase in the number of muscle fibres and an enlargement of individual fibres. The effect is most prominent in the hindquarters or the extremity muscles.

All cattle have two copies of the myostatin gene and animals without a mutation exhibit normal muscling depending on other genetic influences.

Those with a mutation in each copy of the gene (two copies) exhibit extreme muscular hypertrophy or the ‘double’ muscled phenotype. They have extreme muscle mass and can experience production problems.

Animals with one copy of the mutation offer superior muscling advantages over cattle without a mutation, including increased muscle mass, increased rib eye area and a small reduction in fat. Preliminary data indicates a single copy of this mutation in females is not detrimental; they produce, calve and milk normally.

Experiments at NSW DPI’s Glen Innes Research Station indicate the beef yield (meat out of the boning room) advantage of animals with one copy of the mutation can be in the order of five per cent over ‘normal’ animals, with no copies of the gene.

Previously, muscular hypertrophy has been difficult to manage without breeding the extreme form. Animals with one copy (heterozygotes) are not always visually obvious and it was possible to inadvertently join them together risking some double muscled (two copies) progeny.

The identification of myostatin mutation(s) removes the guesswork from breeding programs avoiding the double muscled condition and its associated problems.

A DNA test that accurately determines the number of copies (0, 1 or 2) of any of the six known myostatin mutations causing muscular hypertrophy is now being offered by the Genetics laboratory at NSW DPI’s Elizabeth Macarthur Agricultural Institute.

Contact: Brendon O’Rourke, Camden on 02 4640 6343.

- BRENDON O'ROURKE

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This story appears in Agriculture Today.

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