Submitted to: Midwestern Section of the American Society of Animal Science
Publication Type: Abstract Only
Publication Acceptance Date: March 20, 2007
Publication Date: March 21, 2007
Repository URL: http://asas.org/abstracts/2007sectional/2007MWAbstracts.pdf
Citation: Kuehn, L.A., Nonneman, D.J., Jiang, Z., Leymaster, K.A., Wise, T.H. 2007. Associations of candidate SNP on age, leptin concentration, backfat, and body weight at puberty in gilts [abstract]. Journal of Animal Science. 85(Suppl. 2):63. Abstract #50. Technical Abstract: Body weight (BW), backfat thickness (BF), and leptin play important roles in livestock reproduction. The objective of this study was to determine whether polymorphisms in the leptin (LEP), leptin receptor (LEPR), PAX5, and POMC genes were associated with age, leptin concentration, body condition as backfat, and body weight at puberty in gilts. Age at puberty was monitored in three lines. The first two lines, born in 2001, were formed by crossing maternal White Cross (Yorkshire x Maternal Landrace) gilts to either Duroc (n = 210) or (lean) Landrace (n = 207) boars. The remaining line (n = 483), born in 2002, was formed by crossing progeny of the Duroc- and Landrace-sired lines. At estrus, BW and BF were recorded and blood collected for leptin assays. Seven SNP were detected in candidate genes/regions: 1 in LEP, 3 in LEPR, 1 in PAX5, and 2 in POMC. Animals were genotyped for each of the SNP; genotypes were validated using GenoProb. The association model included fixed effects of farrowing group, covariates of genotypic probabilities (from GenoProb), and random additive polygenic effects to account for genetic similarities between animals not explained by SNP. Variance components for polygenic effects and error were estimated using MTDFREML. Each SNP was fitted in a separate model. Leptin concentrations were logarithmically transformed for data analysis. Significant additive associations (a) were detected at PAX5 for age at puberty (a = 4.0 d; P < 0.05) with trends (P < 0.10) toward associations in BW and BF (a = 2.2 kg and a = 0.55 mm, respectively). One SNP in LEPR was associated with leptin concentration (a = 0.38 log units; P < 0.05), while another affected age at puberty (a = 3.7 d; P < 0.10). The associations from PAX5 correspond to a QTL peak for age at puberty detected on SSC1. While not necessarily the causative mutation, this result does imply that a QTL that can decrease age at puberty without increasing BF and BW may exist in this region.