4.7 Article

Genome wide association analysis for bacterial kidney disease resistance in a commercial North American Atlantic salmon (Salmo salar) population using a 50 K SNP panel

Journal

AQUACULTURE
Volume 495, Issue -, Pages 465-471

Publisher

ELSEVIER
DOI: 10.1016/j.aquaculture.2018.06.014

Keywords

Genome wide association; Atlantic salmon, pathogen resistance; Bacterial kidney disease; SNP

Funding

  1. Genome Canada (Genome Atlantic and Ontario Genomics) through the Genomic Applications Partnership Program Salmon and Chips award
  2. NSERC Industrial Postgraduate Scholarship
  3. University of Guelph teaching assistantships

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Renibacterium salmoninarum is the causative agent of bacterial kidney disease (BKD), an important disease of commercial Atlantic salmon causing substantial economic loss. Genetic improvement programs have been developed for many aquaculture species for a variety of economically important traits, and selective breeding has been proposed for low to moderate heritability disease traits to increase disease resistance. The aim of this study was to perform a genome wide association (GWA) analysis to identify the genomic architecture of BKD resistance and detect SNP markers associated with BKD resistance in a commercial population of Atlantic salmon held in seawater. We experimentally challenged 652 post smolts from 63 families with R. salmoninarum through intraperitoneal injection. A binary trait, overall challenge survival, and a quantitative trait, day of death, were recorded for each challenged individual. DNA extraction and 50 K SNP genotyping was performed for 576 individuals. Fish and loci that did not pass quality control and fish with > 10% European ancestry were removed leaving 507 post smolts genotyped for 44,527 SNPs. GWA for survival and time to death was conducted using a mixed model approach using the relationship matrix to account for population and family structure and a Cox proportional hazards model, respectively. A single marker on Ss alpha 08 was significantly associated with survival at the chromosome wide level. One marker located on Ss alpha 04 was significantly associated with time to death at the chromosome wide level. The two significant SNPs explained a small percentage of the phenotypic variance and were located on different chromosomes, 4.0% (Ss alpha 08) and 5.3% (Ss alpha 04), indicating a polygenic trait.

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