Mapping and validation of a major QTL affecting resistance to pancreas disease (salmonid alphavirus) in Atlantic salmon (Salmo salar)

Abstract

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.

Fine mapping QTL for resistance to VNN disease using a high-density linkage map in Asian seabass

“…Similar results were also reported in other aquatic species for disease resistance, such as QTL in Atlantic salmon40, turbot363738, eastern oyster ( Crassostrea virginica )41 for resistance against viruses, bacteria and parasites. However, we also noticed that several studies reported major QTL for resistance to infectious pancreatic necrosis (IPN) virus424344 and salmonid alphavirus45, explaining up to 50% phenotypic variation, in Atlantic salmon. Due to their large effect on the trait, these QTL have already been applied in MAS in Atlantic salmon, greatly reducing the economic losses of the salmon industry46.…”

“…In addition, mapping QTL in multi-family would allow precise mapping as the LD block is smaller and cross-validation of these QTL to reduce the false positives. This was demonstrated in Atlantic salmon, as most of these studies were performed on multi-family43444547. Therefore, future studies should focus on QTL mapping on multi-family using GBS, which could allow detection of common QTL for resistance to VNN in Asian seabass.…”

Viral encephalopathy and retinopathy in aquaculture: a review

“…) and salmonid alphavirus (SAV) resistance (Gonen et al . ). Like for IPNV, the IHNV QTLs explained a high part of the phenotypic variance (up to 32.5% according to Barroso et al .…”

Half a century of genetic interaction between farmed and wild Atlantic salmon: Status of knowledge and unanswered questions

“…Recent developments in genomic tools and their application in animal breeding have opened new opportunities to understand the underlying genetic basis of commercially important traits and how to exploit them in breeding programmes. For example, QTLs (quantitative trait loci) have been identified and validated for a variety of traits including growth (Baranski, Moen, & Vage, ; Tsai, Hamilton, Guy et al., ; Tsai, Hamilton, Tinch et al., ), susceptibility to pancreatic disease (Gonen et al., ), susceptibility to infectious pancreatic necrosis (Houston et al., ; Moen, Baranski, Sonesson, & Kjoglum, ) and survival in the wild (Besnier et al., ). Furthermore, genomewide association studies identified single genes that influence important phenotypes, such as the vgll3 locus acting on age of maturation in adult salmon (Ayllon et al., ; Barson et al., ).…”