Abstract
Increasing muscle mass is one of the primary breeding objectives in domestic animals as it translates in enhanced carcass yield in livestock or improved athletic performances in companion animals. Naturally occurring loss-offunction mutations in the MSTN gene have been shown to underlie the “double-muscling” phenotype in cattle, the “increased muscle mass” phenotype in sheep and the “bully” phenotype in sprinter dogs. Hypomorphic MSTN alleles associated with weaker but sometimes more advantageous effects on muscle mass have been identified in cattle and sheep. MSTN is a prime target for transgenic approaches aimed at enhancing meat production in livestock. Strategies that are being explored include the generation of MSTN “knock-out” animals and the expression in skeletal muscle of MSTN transinhibitors. More elaborate transgenic approaches targeting post-natal or sex-specific inhibition of MSTN are also being pursued. Finally, MSTN is an obvious target for pharmacological inhibition as well as immunomodulation with the aim to increase muscle mass in animals.
Keywords: Myostatin, GDF8, double-muscling, marker assisted selection, transgenics, genetic engineering, phenotype, Hypomorphic, immunomodulation, QTL, hypertrophy, muscle fibers, glycolytic, TGF, BBCB, mutation, heterogeneity, inheritance, homozygosity, balanced polymorphism, alleles, genotype, increased muscle mass, Dog, Horse, FLRG, Follistatin, MLC, Oncorhynchus mykiss, Cre recombinase, Y chromosome, RMCE, trans-inhibitors, fibroblasts, antibodies, Carassius auratus, Clarias gariepinus, Oreochromis aureus
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