DECR1 and ME1 genotypes are associated with lipid composition traits in Duroc pigs. (10th April 2013)

• Record Type: Journal Article
• Authors: Ramírez, O.; Quintanilla, R.; Varona, L.; Gallardo, D.; Díaz, I.; Pena, R.N.; Amills, M.
• Is Part Of: Journal of animal breeding and genetics. Volume 131:Number 1(2014:Feb.)
• Page Start: 46
• Page End: 52
• Publication Date: 2013-04-10
• Subjects: Livestock -- Breeding -- Periodicals; Livestock -- Genetics -- Periodicals; 636.0820
• DOI: 10.1111/jbg.12035
• Languages: English
• ISSNs: 0931-2668

Abstract

<abstract abstract-type="main" id="jbg12035-abs-0001"> <title>Summary</title> <p>Variation at the porcine <italic>DECR1</italic> and <italic>ME1</italic> genes has been associated with meat quality traits and backfat thickness in Landrace pigs, respectively. However, it has not been investigated yet whether <italic>DECR1</italic> and <italic>ME1</italic> genotypes influence lipid composition. With this aim, we have genotyped two missense <italic>DECR1</italic> substitutions (c.160G>C and c.437G>C) and one silent <italic>ME1</italic> (c.576C>T) polymorphism in 361 Duroc barrows distributed in five half‐sib families and phenotyped for serum lipid concentrations and intramuscular fat content and composition traits. At the whole‐population level, relevant associations, that is, with a posterior probability of the allele substitution effect to be over or below zero (PPN0) > 0.90, were observed between <italic>DECR1</italic> genotype and serum cholesterol (CHOL) (PPN0 = 0.932) and LDL concentrations (PPN0 = 0.945) at 190 days, as well as between <italic>ME1</italic> genotype and <italic>longissimus dorsi</italic> saturated fatty acid content (PPN0 = 0.924). At the within‐family level, we found relevant associations between <italic>DECR1</italic> and <italic>ME1</italic> genotypes and diverse lipid composition traits, but most of them were family‐specific. Discrepancies in allele substitution effects estimated in half‐sib families might be produced by many factors such as number of individuals, marker allele frequencies and informativeness in each family, unaccounted random genetic and environmental effects, epistasis and family‐specific differences in the linkage phase or amount of linkage disequilibrium between causal and marker mutations. This lack of consistency across families, combined with the fact that the <italic>ME1</italic> mutation is synonymous and that the two <italic>DECR1</italic> polymorphisms are conservative, suggests that the associations found are not causative.</p> </abstract>