4.3 Article

Interactions between genes involved in growth and muscularity in pigs: IGF-2, myostatin, ryanodine receptor 1, and melanocortin-4 receptor

Journal

DOMESTIC ANIMAL ENDOCRINOLOGY
Volume 37, Issue 4, Pages 227-235

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.domaniend.2009.06.002

Keywords

Interactions; IGF-2; Myostatin; Melanocortin-4 receptor; Ryanodine receptor 1

Funding

  1. Institute for the Promotion of Innovation through Science and Technology (IWT), Brussels, Belgium

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In the swine breeding industry, two economical traits are of particular importance in sires, namely, muscle growth and average daily gain (ADG). These traits are quantitative, which implies that they are under the control of multiple genes. Mutations in these genes, associated with either muscularity or growth, are useful quantitative trait nucleotides (QTN) for unraveling genetic variation of these traits and can be used in marker-assisted selection. Until now, QTN involved in muscle growth and/or ADG in pigs were identified in porcine ryanodine receptor 1 (RYR1), insulin-like growth factor-2 (IGF-2), and melanocortin-4 receptor (MC4R). Recently, a fourth possible QTN was found in porcine myostatin (MSTN). All four QTN have an influence on muscle growth and/or somatic growth, so an influence of one mutation on one or more of the other mutations should not be excluded. However, although the polymorphisms in the RYR1 and the MC4R gene affect the function of the respective protein, the polymorphisms of the IGF-2 and MSTN gene influence the mRNA expression of the respective gene. Therefore, this study investigated possible interactions between the genotypes of MSTN, IGF-2, and MC4R (population 1) or the RYR1, IGF-2, and MSTN QTN (population 2) on IGF-2 and MSTN expression in different muscle types in pigs. In both skeletal muscle and heart muscle growth, the IGF-2:MSTN ratio seems to play an important role. Also, the RYR1 genotype had a significant effect on IGF-2 expression in m. longissimus dorsi. No effect of the MC4R QTN could be seen. (C) 2009 Elsevier Inc. All rights reserved.

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