The callipyge mutation and other genes that affect muscle hypertrophy in sheep

Abstract

-Genetic strategies to improve the profitability of sheep operations have generally focused on traits for reproduction. However, natural mutations exist in sheep that affect muscle growth and development, and the exploitation of these mutations in breeding strategies has the potential to significantly improve lamb-meat quality. The best-documented mutation for muscle development in sheep is callipyge (CLPG), which causes a postnatal muscle hypertrophy that is localized to the pelvic limbs and loin. Enhanced skeletal muscle growth is also observed in animals with the Carwell (or rib-eye muscling) mutation, and a double-muscling phenotype has been documented for animals of the Texel sheep breed. However, the actual mutations responsible for these muscular hypertrophy phenotypes in sheep have yet to be identified, and further characterization of the genetic basis for these phenotypes will provide insight into the biological control of muscle growth and body composition.sheep / muscle / hypertrophy / callipyge / mutation

Impacts of the Callipyge Mutation on Ovine Plasma Metabolites and Muscle Fibre Type

“…There was also a slight increase in the level of circulating lipoproteins at this age which may also reflect an enhanced mobilization of fatty acids in Callipyge lambs. These results are also consistent with the overall lean Callipyge phenotype [8]–[10].…”

“…The changes in plasma metabolites associated with the Callipyge mutation may be derived from metabolic changes in affected muscles or were also due to direct and/or indirect effects of the mutation in other large metabolically active tissues. The N mat C pat genotype is linked with a postnatal rostro-claudal gradient of muscle hypertrophy as well as whole body leanness [4], [10]–[14]. The latter trait may arise as an indirect response of adipose tissue depots to the affected hypertrophied muscles or directly as a result of gene expression changes surrounding the site of the mutation in adipose tissue which drive changes in adipose tissue metabolism, deposition and released metabolites.…”

“…The phenotype is first expressed 1–3 months post-birth and occurs along a rostro-claudal gradient in the affected N mat C pat animal with greatest impact on skeletal muscles innervated through lumbar and sacral roots e.g. longissimus dorsi and semimembranosus muscles [4], [10]–[14]. There are also decreases in the proportional sizes of several non-muscle organs, as well as increased animal leanness and improved feed conversion efficiency but live-weight is unaffected [1]–[3], [6], [8], [9], [12].…”

“…In particular, skeletal muscles affected by the mutation are likely to be more dependent on glycolytic metabolism for energy generation as a result of a shift toward fast twitch glycolytic fibres, although the details of specific fibre type changes are not yet clear [8]–[10]. The mutation may therefore cause indirect effects in other tissues through changes in blood metabolites or endocrine factors derived from the affected muscles.…”

Mapping Quantitative Trait Loci (QTL) in sheep. III. QTL for carcass composition traits derived from CT scans and aligned with a meta-assembly for sheep and cattle carcass QTL

“…Two full and 12 partial genome scans have reported QTL for carcass composition including bone density on chromosomes 1-6, 8, 18, 20, 21, and 24 in populations of Coopworth, Scottish Blackface, British Texel, Charollais, Suffolk, Texel and different cross-breed sheep populations [8,11-18]. At present two DNA tests (LoinMax and MyoMax; http://www.pfizeranimalgenetics.com.au/sites/PAG/aus/Pages/sheep.aspx[19]) are commercially available, which test for genetic variants in the Carwell and Myostatin genes [8,10,16,17,20-25]. …”