A considerable number of single nucleotide polymorphisms (SNPs) are required to elucidate genotype-phenotype associations and determine the molecular basis of important traits. In this work, we carried out de novo SNP discovery accounting for both genome duplication and genetic variation from American and European salmon populations. A total of 9 736 473 nonredundant SNPs were identified across a set of 20 fish by whole-genome sequencing. After applying six bioinformatic filtering steps, 200 K SNPs were selected to develop an Affymetrix Axiom(®) myDesign Custom Array. This array was used to genotype 480 fish representing wild and farmed salmon from Europe, North America and Chile. A total of 159 099 (79.6%) SNPs were validated as high quality based on clustering properties. A total of 151 509 validated SNPs showed a unique position in the genome. When comparing these SNPs against 238 572 markers currently available in two other Atlantic salmon arrays, only 4.6% of the SNP overlapped with the panel developed in this study. This novel high-density SNP panel will be very useful for the dissection of economically and ecologically relevant traits, enhancing breeding programmes through genomic selection as well as supporting genetic studies in both wild and farmed populations of Atlantic salmon using high-resolution genomewide information.
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.
Pancreas disease (PD) of farmed Atlantic salmon Salmo salar L., which is caused by an alphavirus known as salmon pancreas disease virus (SPDV), can have serious economic consequences. An epidemiological survey carried out in Ireland in 2003 indicated that within individual farms there were significant differences in the susceptibility of different strains of farmed Atlantic salmon to infection with SPDV, as measured by levels of clinical disease and mortality. The aim of this preliminary study was to investigate this field observation by comparing lesion development, viraemia and serological responses of 3 commercial strains of Atlantic salmon (A, B and C) experimentally infected with SPDV. Highly significant differences in the severity of lesions in the pancreas at Day 21 post-infection (pi) were detected (p < 0.01), with Group B being more severely affected. There were also significant differences in the prevalence and severity of lesions in heart and skeletal muscle at Day 21 and 35 pi respectively, with Group B results again significantly higher than those from both Groups A and C (p < 0.05). There was no overlap between viraemia and the presence of specific SPDV antibody. Some fish in all groups had no viraemia, lesions or evidence of seroconversion. There were no significant differences seen between the challenged groups in relation to the percentage of viraemic fish at each time point. Viral loads were not determined. Differences between the number of antibody-positive fish in each challenge group were found at Days 28 and 35 pi (p < 0.1). Highly significant differences (p < 0.01) in the geometric mean titres of seropositive fish were detected at Day 28. These results, obtained using a challenge model, confirm that there are strain differences in the susceptibility to experimental SPDV infection in commercial farmed Atlantic salmon. KEY WORDS: Salmon Pancreas Disease Virus · SPDV · Atlantic salmon · Disease susceptibility · Experimental challenge Resale or republication not permitted without written consent of the publisherDis Aquat Org 72: [125][126][127][128][129][130][131][132][133] 2006 (SPDV), the aetiological agent of PD, was isolated in 1993 (Nelson et al. 1995) and was subsequently classified as a salmonid alphavirus (SAV) (Weston et al. 1999(Weston et al. , 2002.National surveys in Ireland from 1989 to 1994 indicated that mortality owing to PD could be up to 48%, with 94% of Irish marine sites affected, and that PD was the major cause of disease losses at that time (Menzies et al. 1996). From 1996 to 2001 there appeared to be a lower incidence and severity of PD in Ireland (McLoughlin et al. 1998). However, in 2002 there was an increase in both the severity and incidence of PD recorded in Ireland ).An epidemiological survey undertaken in 2003 revealed that 13 of 21 sites (61%) had experienced PD, with mortality reaching 40% in some cages . There have also been reports from Scotland and Norway that PD has re-emerged as a significant problem in specific regions of both countries, resu...
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.