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Domestication of Atlantic salmon started approximately forty years ago, using both artificial and natural selection strategies. Such selection methods are likely to have imposed distinctive selection signatures on the salmon genome. Therefore, identifying differences in selection signatures may give insights into the mechanism of selection and candidate genes of biological and productive interest. Here, we used two complementary haplotype-based statistics, the within-population integrated Haplotype Score test (|iHS|) and the cross-population Extended Haplotype Homozygosity test (XP-EHH) to compare selection signatures in four populations of Atlantic salmon with a common genetic origin. Using |iHS| we found 24, 14, 16 and 26 genomic regions under selection in Pop-A, Pop-B, Pop-C, and Pop-D, respectively. While using the XP-EHH test we identified 27, 25 and 15 potential selection regions in Pop-A/Pop-B, Pop-A/Pop-C and Pop-A/Pop-D, respectively. These genomic regions harbor important genes such igf1r and sh3rf1 which have been associated with growth related traits in other species. Our results contribute to the detection of candidate genes of interest and help to understand the evolutionary and biological mechanisms for controlling complex traits under selection in Atlantic salmon.

Pancreas disease (PD), caused by a salmonid alphavirus (SAV), has a large negative economic and animal welfare impact on Atlantic salmon aquaculture. Evidence for genetic variation in host resistance to this disease has been reported, suggesting that selective breeding may potentially form an important component of disease control. The aim of this study was to explore the genetic architecture of resistance to PD, using survival data collected from two unrelated populations of Atlantic salmon; one challenged with SAV as fry in freshwater (POP 1) and one challenged with SAV as post-smolts in sea water (POP 2). Analyses of the binary survival data revealed a moderate-to-high heritability for host resistance to PD in both populations (fry POP 1 h2~0.5; post-smolt POP 2 h2~0.4). Subsets of both populations were genotyped for single nucleotide polymorphism markers, and six putative resistance quantitative trait loci (QTL) were identified. One of these QTL was mapped to the same location on chromosome 3 in both populations, reaching chromosome-wide significance in both the sire- and dam-based analyses in POP 1, and genome-wide significance in a combined analysis in POP 2. This independently verified QTL explains a significant proportion of host genetic variation in resistance to PD in both populations, suggesting a common underlying mechanism for genetic resistance across lifecycle stages. Markers associated with this QTL are being incorporated into selective breeding programs to improve PD resistance.