Abstract

Mitigation of stress is of great importance in poultry production, as chronic stress can affect the efficiency of production traits. Selective breeding with a focus on stress responses can be used to combat the effects of stress. To better understand the genetic mechanisms driving differences in stress responses of a selectively bred population of Japanese quail, we performed genomic resequencing on 24 birds from High Stress (HS) and Low Stress (LS) lines of Japanese quail using Illumina HiSeq 2 × 150 bp paired end read technology in order to analyze Single Nucleotide Polymorphisms (SNPs) within the genome of each line. SNPs are common mutations that can lead to genotypic and phenotypic variations in animals. Following alignment of the sequencing data to the quail genome, 6,364,907 SNPs were found across both lines of quail. 10,364 of these SNPs occurred in coding regions, from which 2886 unique, non-synonymous SNPs with a SNP% ≥ 0.90 and a read depth ≥ 10 were identified. Using Ingenuity Pathway Analysis, we identified genes affected by SNPs in pathways tied to immune responses, DNA repair, and neurological signaling. Our findings support the idea that the SNPs found within HS and LS lines of quail could direct the observed changes in phenotype.

Highlights

  • IntroductionPhenotypic diversities occur due to genetic variations within and between populations

  • Phenotypic diversities occur due to genetic variations within and between populations.Many genotypic variations arise as the result of genetic mutations

  • 10,364 Single Nucleotide Polymorphisms (SNPs) were uniquely found across the High Stress (HS) and Low Stress (LS) line of Japanese quail with SNP% ≥ 0.90 and present within the CDS region

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Summary

Introduction

Phenotypic diversities occur due to genetic variations within and between populations. Many genotypic variations arise as the result of genetic mutations. One of these mutations is known as a Single Nucleotide Polymorphism (SNP). Non-synonymous SNPs occur within coding regions of chromosomes and may be either missense or nonsense mutations. Both alter the amino acid at the point of mutation, though in differing ways. Each type of mutation alters the protein produced [2] These protein alterations may lead to alterations in phenotype. Due to this simple mechanism, SNPs are employed as biomarkers in studies surrounding population genetics [3]

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