Dissection of additive genetic variability for quantitative traits in chickens using SNP markers

• Published in: Journal of animal breeding and genetics (1986) Vol. 131; no. 3; pp. 183 - 193
• Main Authors: Abdollahi‐Arpanahi, R, Pakdel, A, Nejati‐Javaremi, A, Moradi Shahrbabak, M, Morota, G, Valente, B.D, Kranis, A, Rosa, G.J.M, Gianola, D
• Format: Journal Article
• Language: English
• Published: Germany Blackwell Wissenschafts-Verlag 01-06-2014; Blackwell Publishing Ltd
• Subjects: Animals; body weight; breast muscle; Chickens - genetics; chromosomes; Chromosomes - genetics; egg production; Gene Frequency; Genetic diversity; Genetic markers; Genetic Markers - genetics; genetic variance; genetic variation; Genomic relationships; genomic variance; Genomics; genotype; genotyping; hens; marker density; minor allele frequency; Polymorphism, Single Nucleotide; Poultry; quantitative traits; single nucleotide polymorphism; ultrasonics; variance; marker density; Genomic relationships; minor allele frequency; genomic variance
• ISSN: 0931-2668; 1439-0388
• DOI: 10.1111/jbg.12079

The aim of this study was to separate marked additive genetic variability for three quantitative traits in chickens into components associated with classes of minor allele frequency (MAF), individual chromosomes and marker density using the genomewide complex trait analysis (GCTA) approach. Data were from 1351 chickens measured for body weight (BW), ultrasound of breast muscle (BM) and hen house egg production (HHP), each bird with 354 364 SNP genotypes. Estimates of variance components show that SNPs on commercially available genotyping chips marked a large amount of genetic variability for all three traits. The estimated proportion of total variation tagged by all autosomal SNPs was 0.30 (SE 0.04) for BW, 0.33 (SE 0.04) for BM, and 0.19 (SE 0.05) for HHP. We found that a substantial proportion of this variation was explained by low frequency variants (MAF <0.20) for BW and BM, and variants with MAF 0.10–0.30 for HHP. The marked genetic variance explained by each chromosome was linearly related to its length (R² = 0.60) for BW and BM. However, for HHP, there was no linear relationship between estimates of variance and length of the chromosome (R² = 0.01). Our results suggest that the contribution of SNPs to marked additive genetic variability is dependent on the allele frequency spectrum. For the sample of birds analysed, it was found that increasing marker density beyond 100K SNPs did not capture additional additive genetic variance.