The susceptibility of Atlantic salmon fry to freshwater infectious pancreatic necrosis is largely explained by a major QTL

Abstract

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.

Quantitative genetics of disease resistance in vaccinated and unvaccinated Atlantic salmon (Salmo salar L.)

“…A quantitative trait loci explaining a very large proportion of the genetic variation in IPN resistance has been detected in Atlantic salmon (Houston et al, 2009;Moen et al, 2009). In our study, evidence was found of significantly favourable genetic correlations of resistance to furunculosis in unvaccinated fish with resistance to both IPN and ISA (unvaccinated fish).…”

Future directions in breeding for disease resistance in aquaculture species

“…Aquaculture species are typically close to their wild ancestors and the relatively new selection and disease pressures in the farm environment raise the possibility that major-effect loci segregate within the populations. A successful example of QTL analyses applied to selective breeding is the case of infectious pancreatic necrosis resistance in Atlantic salmon, in which a major QTL explains the majority of the genetic variance for resistance (Houston et al, 2008;Houston et al, 2010;Moen et al, 2009) and has been demonstrated as a successful means of controlling the disease . Selected other examples of QTL-affecting resistance to disease include the cases of salmonid alphavirus (Gonen et al, 2015), ISAV (Moen et al, 2007), and Gyrodactylus salaris (Gilbey et al, 2006) in salmon, lymphocystis disease in Japanese flounder (Fuji et al, 2006), Bonamiosis in the European Flat Oyster (Lallias et al, 2009), and Flavobacterium psychrophilum in rainbow trout (Vallejo et al, 2014).…”

Genetic and genomic analyses for economically important traits and their applications in molecular breeding of cultured fish

“…This QTL was confirmed in three other families. Several authors have reported QTLs for IPNV, and most show that the anti-IPNV loci are located on LG21 [37][38][39][40], indicating that rainbow trout and Atlantic salmon anti-IPNV QTLs may be evolutionarily conserved. The genetic effects of Atlantic salmon anti-IHN QTLs have been validated in other studies [41].…”