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.

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Body weight, occurrence of spinal deformity, and sexual maturity were recorded in 51 full-sib families of the strains coastal and Arctic cod at two years of age. The family groups were located at three sites along the Norwegian coast including Hordaland, Møre and Romsdal (M&R), and Nordland County to detect genetic variation in important production traits and to investigate interactions between genetic composition and production environment. Body weight varied among locations partly owing to different production conditions. There were also large differences among the locations with respect to spinal deformity. M&R had the highest occurrence of spinal deformity (p < 0.001). Comparison of sexual maturity among the locations was made difficult owing to the different ways the trait was recorded. Only small differences were found between coastal and Arctic cod in spinal deformity (p < 0.05 in Hordaland) and sexual maturity (p = 0.06 in M&R), while no differences were found for body weight. Heritability estimates for body weight (0.51), spinal deformity (0.27), and sexual maturity (0.21) indicate the potential for improvement of all three traits by selective breeding using a family-based selection programme. Final recordings at the end of the growing period will provide further information. Genetic correlations estimated between weight and occurrence of spinal deformity (rg = 0.50) suggest that caution be used when selecting for growth, and that a need exists for including spinal deformity in the selection index. No significant correlations were found between these two traits and the incidence of sexual maturity.