ARS | Publication request: MYOSTATIN MUTATIONS CAUSE DOUBLE MUSCLING IN CATTLE

Submitted to: Plant and Animal Genome VX Conference Abstracts
Publication Type: Proceedings
Publication Acceptance Date: January 1, 1998
Publication Date: N/A

Technical Abstract: A visibly distinct muscular hypertrophy (mh) occurs with high frequency in a number of cattle breeds that have been selected for this trait. The increase in muscle mass caused by the mh locus is a major component of the double muscled syndrome that includes a reduction in internal organ size, general shortening of limb bones, and reduction in fat deposition. There has been considerable interest in double muscled breeds due to their increased proficiency of converting feed to lean beef. However, problems associated with the trait, such as reduction in stress tolerance, fertility, and calf viability in some double muscled breeds have hindered exploitation of the desirable carcass composition. Mapping studies in populations segregating for the mh locus show that it lies near the centromere of BTA2, between the genes PROC and COL3A1 genes. This is the same location as myostatin (MSTN), a TGF-beta gene family member that has dramatic effects on muscle development in mice. Sequencing of MSTN in double muscled breeds has revealed mutations that are predicted to interfere with or abolish the function of the protein, indicating that loss of MSTN function in cattle is the basis of the double muscled condition. Indeed, knockout mice homozygous for targeted disruption of MSTN display an extreme increase in muscle mass with significant similarities to that observed in double muscled cattle, confirming this hypothesis. The fact that muscular hypertrophy is the result of a loss of function suggests the exciting possibility that interference with MSTN in other breeds and livestock species may lead to increased efficiency of meat production.