Release 56
(Apr 24, 2025)

Reference # 20952696 Details:

Authors:Hu G, Wang SZ, Wang ZP, Li YM, Li H (Contact: lihui@neau.edu.cn)
Affiliation:College of Animal Science and Technology, Northeast Agricultural University, Harbin, 150030, P. R. China
Title:Genetic epistasis analysis of 10 peroxisome proliferator-activated receptor {gamma}-correlated genes in broiler lines divergently selected for abdominal fat content
Journal:Poultry Sci, 2010, 89(11): 2341-50 DOI: 10.3382/ps.2010-00857
Abstract:

Chicken peroxisome proliferator-activated receptor γ (PPARγ), which is highly expressed in adipose tissues, is a key factor in fat accumulation in the abdominal fat pad. In this study, association and pairwise epistasis analyses were performed for all the polymorphisms detected in PPARγ and for 9 genes from PPARγ-correlated lipid metabolic pathways for abdominal fat weight (AFW) in 10th-generation populations of Northeast Agricultural University broiler lines divergently selected for abdominal fat content. Epistatic networks were then reconstructed with the identified epistatic effects. Single-marker association analyses showed that 5 of the 20 screened polymorphisms were significantly associated with AFW (P < 0.05), and CCAAT/enhancer-binding protein α (C/EBPα) c.552G>A was 1 of the 5 significant loci. Pairwise interaction analyses showed that 15 pairs of polymorphisms reached a significance level of P < 2.64 × 10(-4) (adjusted by Bonferroni correction) in the lean line, 41 pairs reached significance in the fat line, and 7 pairs reached significance in both lines. Interestingly, many other loci interacted with C/EBPα c.552G>A in both lines. In epistatic network analyses, C/EBPα c.552G>A seemed to behave as a hub for the epistatic network in both lines. All these results revealed that the genetic architecture of C/EBPα c.552G>A for AFW seemed to be an apparent individual main-effect QTL but that it could be dissected into a genetic epistatic network. Our results suggest that C/EBPα c.552G>A might be the most important locus contributing to phenotypic variation in AFW among all the polymorphisms detected in this study.

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