Background Infectious Salmonid Anaemia Virus (ISAV) causes a notifiable disease that poses a large threat for Atlantic salmon ( Salmo salar ) aquaculture worldwide. There is no fully effective treatment or vaccine, and therefore selective breeding to increase resistance to ISAV is a promising avenue for disease prevention. Genomic selection and potentially genome editing can be applied to enhance host resistance, and these approaches benefit from improved knowledge of the genetic and functional basis of the target trait. The aim of this study was to characterise the genetic architecture of resistance to ISAV in a commercial Atlantic salmon population and study its underlying functional genomic basis using RNA Sequencing. Results A total of 2833 Atlantic salmon parr belonging to 194 families were exposed to ISAV in a cohabitation challenge in which cumulative mortality reached 63% over 55 days. A total of 1353 animals were genotyped using a 55 K SNP array, and the estimate of heritability for the trait of binary survival was 0.13–0.33 (pedigree-genomic). A genome-wide association analysis confirmed that resistance to ISAV was a polygenic trait, albeit a genomic region in chromosome Ssa13 was significantly associated with resistance and explained 3% of the genetic variance. RNA sequencing of the heart of 16 infected (7 and 14 days post infection) and 8 control fish highlighted 4927 and 2437 differentially expressed genes at 7 and 14 days post infection respectively. The complement and coagulation pathway was down-regulated in infected fish, while several metabolic pathways were up-regulated. The interferon pathway showed little evidence of up-regulation at 7 days post infection but was mildly activated at 14 days, suggesting a potential crosstalk between host and virus. Comparison of the transcriptomic response of fish with high and low breeding values for resistance highlighted TRIM25 as being up-regulated in resistant fish. Conclusions ISAV resistance shows moderate heritability with a polygenic architecture, but a significant QTL was detected on chromosome 13. A mild up-regulation of the interferon pathway characterises the response to the virus in heart samples from this population of Atlantic salmon, and candidate genes showing differential expression between samples with high and low breeding values for resistance were identified.

Sea lice threaten the welfare of farmed Atlantic salmon and the sustainability of fish farming across the world. Chemical treatments are the major method of control but drug resistance means that alternatives are urgently needed. Selective breeding can be a cheap and effective alternative. Here, we combine experimental trials and diagnostics to provide a practical protocol for quantifying resistance to sea lice. We then combined quantitative genetics with epidemiological modelling to make the first prediction of the response to selection, quantified in terms of reduced need for chemical treatments. We infected over 1400 young fish with Lepeophtheirus salmonis, the most important species in the Northern Hemisphere. Mechanisms of resistance were expressed early in infection. Consequently, the number of lice per fish and the ranking of families were very similar at 7 and 17 days post infection, providing a stable window for assessing susceptibility to infection. The heritability of lice numbers within this time window was moderately high at 0.3, confirming that selective breeding is viable. We combined an epidemiological model of sea lice infection and control on a salmon farm with genetic variation in susceptibility among individuals. We simulated 10 generations of selective breeding and examined the frequency of treatments needed to control infection. Our model predicted that substantially fewer chemical treatments are needed to control lice outbreaks in selected populations and chemical treatment could be unnecessary after 10 generations of selection. Selective breeding for sea lice resistance should reduce the impact of sea lice on fish health and thus substantially improve the sustainability of Atlantic salmon production.

This study investigated the effect of a major QTL for resistance to IPN in salmon on performance and production traits. The traits studied were related to growth, fillet and gutted yields, and fat content. Two different analyses were performed: (1) regression of the phenotypic data of the production traits on the predicted number of resistant IPN-QTL alleles in individuals and (2) a variance component analysis using the (co)variance matrix calculated at the putative location of the QTL. No significant effect of the QTL was detected on any of the traits investigated by either method. The result has important practical implications in that it encourages the use of MAS to reduce the risks and impact of IPN mortality.

In a previous study, three significant quantitative trait loci (QTL) associated with resistance to Infectious Pancreatic Necrosis (IPN) disease were identified by analysing challenge data from one sub-population of Landcatch Atlantic salmon (Salmo salar) smolt. While these QTL were shown to affect the resistance in seawater, their effect in freshwater was unknown. This study investigates the effect of these QTL on IPN resistance in salmon fry in freshwater. Twenty families with intermediate levels of IPN mortality were analysed from a freshwater challenge trial undertaken on a different sup-population of LNS salmon to that studied previously. Only the QTL from linkage group 21 (LG21) appeared to have a significant and large effect on resistance in freshwater; the same QTL was found to have the largest effect in seawater in the previous study. Variance component analysis showed a high heritability for the QTL: 0.45±0.07 on the liability scale and 0.25±0.05 on the observed scale. In a family where both parents were segregating for the QTL, there was a 0% vs. 100% mortality in homozygous offspring for resistant and susceptible QTL alleles. The finding that the same QTL has major effect in both freshwater and seawater has important practical implications, as this will allow the improvement of resistance in both phases through marker assisted selection by targeting this QTL. Moreover, the segregation of the LG21 QTL in a different sub-population gives further evidence of its association with IPN-resistance.

Infectious pancreatic necrosis (IPN) is a viral disease with a significant negative impact on the global aquaculture of Atlantic salmon. IPN outbreaks can occur during specific windows of both the freshwater and seawater stages of the salmon life cycle. Previous research has shown that a proportion of the variation seen in resistance to IPN is because of host genetics, and we have shown that major quantitative trait loci (QTL) affect IPN resistance at the seawater stage of production. In the current study, we completed a large freshwater IPN challenge experiment to allow us to undertake a thorough investigation of the genetic basis of resistance to IPN in salmon fry, with a focus on previously identified QTL regions. The heritability of freshwater IPN resistance was estimated to be 0.26 on the observed scale and 0.55 on the underlying scale. Our results suggest that a single QTL on linkage group 21 explains almost all the genetic variation in IPN mortality under our experimental conditions. A striking contrast in mortality is seen between fry classified as homozygous susceptible versus homozygous resistant, with QTL-resistant fish showing virtually complete resistance to IPN mortality. The findings highlight the importance of the major QTL in the genetic regulation of IPN resistance across distinct physiological lifecycle stages, environmental conditions and viral isolates. These results have clear scientific and practical implications for the control of IPN.

Genetic variation in performance and quality traits measured at harvest has previously been demonstrated in Atlantic salmon aquaculture populations. To map major loci underlying this variation, we utilized data from 10 families from a commercial breeding programme. Significant QTL were detected affecting harvest weight and length traits on linkage group 1, and affecting waste weight on linkage group 5. In total, 11 of the 29 linkage groups examined showed at least suggestive evidence for a QTL. These data suggest that major loci affecting economically important harvest characteristics are segregating in commercial salmon populations.

Infectious pancreatic necrosis (IPN) is a viral disease currently presenting a major problem to the aquaculture of Atlantic salmon (Salmon salar), during both the freshwater and seawater stages of production. Genetic variation in resistance to IPN has previously been demonstrated and the purpose of this study was to determine whether this variation includes loci of major effect. The initial QTL detection methodology Utilized the limited recombination seen in male salmon to detect QTL in ten large full-sib families, using a genome-wide scan of two to three markers per linkage group. QTL were then positioned by adding additional markers to the significant linkage groups in a female-based analysis. The most significant QTL was mapped to LG 21, and further confirmation of the LG 21 QTL is provided in an analysis of the QTL flanking markers in an additional nine full-sib families from the same population. The size of QTL effect is such that the QTL flanking markers can be immediately applied in marker-assisted selection programmes to improve the resistance of salmon populations to IPN, thus reducing mortality due to the disease.