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Porcine NAMPT gene: search for polymorphism, mapping and association studies

Čepica, S., Bartenschlager, H., Óvilo, C., Zrůstová, J., Masopust, M., Fernández, A., López, A., Knoll, A., Rohrer, G. A., Snelling, W. M., Geldermann, H.
Animal genetics 2010 v.41 no.6 pp. 646
Meishan, NAD (coenzyme), backfat, biosynthesis, chromosome mapping, color, cooling, energy metabolism, fatty acid composition, finishing, genes, haplotypes, intramuscular fat, landraces, linkage disequilibrium, lipid metabolism, meat, meat quality, nicotinamide phosphoribosyltransferase, single nucleotide polymorphism, stress tolerance, swine, synthetic populations, wild boars
NAMPT encodes an enzyme catalysing the rate-limiting step in NAD biosynthesis. The extracellular form of the enzyme is known as adipokine visfatin. We detected SNP AM999341:g.669T>C (referred to as 669T>C) in intron 9 and SNP FN392209:g.358A>G (referred to as 358A>G) in the promoter of the gene. RH mapping linked the gene to microsatellite SW944. Linkage analysis placed the gene on the current USDA – USMARC linkage map at position 92 cM on SSC9. Association analyses were performed in a wild boar x Meishan F2 family (W x M), with 45 traits recorded (growth and fattening, fat deposition, muscling, meat quality, stress resistance and other traits), and in a commercial Landrace x Chinese-European (LCE) synthetic population with records for 15 traits (growth, fat deposition, muscling, intramuscular fat, meat colour and backfat fatty acid content). In the W x M, SNP 669T>C was associated with muscling, fat deposition, growth and fattening, meat quality and other traits and in the LCE with muscling, meat quality and backfat fatty acid composition. In the W x M, SNP 358A>G was associated with muscling, fat deposition, growth and other traits. After correction for multiple testing, the NAMPT haplotypes were associated in the W x M with, in descending order, muscling (q = 0.0056), growth (q = 0.0056), fat deposition (q = 0.0109), fat-to-meat ratio (q = 0.0135), cooling losses (q = 0.0568) and longissimus pHU (q = 0.0695). The SNPs are hypothesized to be in linkage disequilibrium with a causative mutation affecting energy metabolism as a whole rather than fat metabolism alone.