Genome wide analysis of infectious salmon anemia resistance in commercial Saint John River Atlantic salmon

Infectious salmon anemia (ISA) is an economically costly viral disease to the global Atlantic salmon aquaculture industry due to the high virulence and high mortality rate. Selective breeding for disease resistance traits using genomic information has been suggested to increase the resistance to various diseases in the breeding population. The aim of this study was to perform a genome wide association (GWA) analysis to identify regions of the genome associated with ISA resistance in the commercial Saint John River population. A total of 2233 parr from 72 families from the 2015 year class were challenged with ISA using a cohabitation trial. The heritability of ISA resistance was 0.16 ± 0.04 on the observed scale for the binary trait of ISA survival at 50% mortality of all cohabitating fish. Binary phenotypes were recorded for all fish with those that survived the challenge being classified as resistant and those that died being classified as susceptible. Selective genotyping using a custom North American 50 K SNP chip was performed by choosing, where possible, four resistant fish and four susceptible fish from each challenged family (n = 572). After quality control a total of 547 fish and 38,954 SNP markers remained for GWA analysis. Two survival traits were analyzed for the genotyped fish: ‘survival to day 37’ when mortality had reached 50% and ‘survival at trial termination’ on day 54. Two SNPs on Ssa03 and on Ssa07 were significant associated with ‘survival to day 37’ but only at the chromosome wide level. More notably nine significant SNPs on nine different chromosomes, were significantly associated with ‘survival at trial termination’ at the genome wide level. The most significant SNP, on Ssa13, explained 8.6% of the phenotypic variation, while SNPs on Ssa12 and Ssa11 explained 7.6% and 6.4% respectively. The remaining six SNPs explained between 4 and 6% of the phenotypic variation, indicating oligogenic architecture of the ‘survival at trial termination’ trait. A total of 33 genes known to be differentially expressed during infection with ISA were located downstream on the same chromosome arm of the nine significant SNPs. Identification of causal mutations is not necessary to implement genomic information into selective breeding programs but improves understanding of the genetic basis of ISA resistance.