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Genome-Wide Association and Genomic Selection for Resistance to Amoebic Gill Disease in Atlantic Salmon.

ABSTRACT: Amoebic gill disease (AGD) is one of the largest threats to salmon aquaculture, causing serious economic and animal welfare burden. Treatments can be expensive and environmentally damaging, hence the need for alternative strategies. Breeding for disease resistance can contribute to prevention and control of AGD, providing long-term cumulative benefits in selected stocks. The use of genomic selection can expedite selection for disease resistance due to improved accuracy compared to pedigree-based approaches. The aim of this work was to quantify and characterize genetic variation in AGD resistance in salmon, the genetic architecture of the trait, and the potential of genomic selection to contribute to disease control. An AGD challenge was performed in ∼1,500 Atlantic salmon, using gill damage and amoebic load as indicator traits for host resistance. Both traits are heritable (h² ∼0.25-0.30) and show high positive correlation, indicating they may be good measurements of host resistance to AGD. While the genetic architecture of resistance appeared to be largely polygenic in nature, two regions on chromosome 18 showed suggestive association with both AGD resistance traits. Using a cross-validation approach, genomic prediction accuracy was up to 18% higher than that obtained using pedigree, and a reduction in marker density to ∼2,000 SNPs was sufficient to obtain accuracies similar to those obtained using the whole dataset. This study indicates that resistance to AGD is a suitable trait for genomic selection, and the addition of this trait to Atlantic salmon breeding programs can lead to more resistant stocks.

SUBMITTER: Robledo D

PROVIDER: S-EPMC5873910 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Amoebic gill disease (AGD) is one of the most important parasitic diseases of farmed Atlantic salmon. It is a source of major economic loss to the industry and poses significant threats to animal welfare. Previous studies have shown that resistance against this disease has a moderate, heritable genetic component, although the genes and the genetic pathways that contribute to this process have yet to be elucidated. In this study, to identify the genetic mechanisms of AGD resistance, we first investigated the molecular signatures of AGD infection in Atlantic salmon through a challenge model, where we compared the transcriptome profiles of the naïve and infected animals. We then conducted a genome-wide association analysis with 1,333 challenged tested fish to map the AGD resistance genomic regions, supported by the results from the transcriptomic data. Further, we investigated the potential of incorporating gene expression analysis results in genomic prediction to improve prediction accuracy. Our data suggest thousands of genes have modified their expression following infection, with a significant increase in the transcription of genes with functional properties in cell adhesion and a sharp decline in the abundance of various components of the immune system genes. From the genome-wide association analysis, QTL regions on chromosomes ssa04, ssa09, and ssa13 were detected to be linked with AGD resistance. In particular, we found that QTL region on ssa04 harbors members of the cadherin gene family. These genes play a critical role in target recognition and cell adhesion. The QTL region on ssa09 also is associated with another member of the cadherin gene family, protocadherin Fat 4. The associated genetic markers on ssa13 span a large genomic region that includes interleukin-18-binding protein, a gene with function essential in inhibiting the proinflammatory effect of cytokine IL18. Incorporating gene expression information through a weighted genomic relationship matrix approach decreased genomic prediction accuracy and increased bias of prediction. Together, these findings help to improve our breeding programs and animal welfare against AGD and advance our knowledge of the genetic basis of host-pathogen interactions.

Project description:BackgroundGill health is one of the main concerns for Atlantic salmon aquaculture, and Amoebic Gill Disease (AGD), attributable to infection by the amoeba Neoparamoeba perurans, is a frequent cause of morbidity. In the absence of preventive measures, increasing genetic resistance of salmon to AGD via selective breeding can reduce the incidence of the disease and mitigate gill damage. Understanding the mechanisms leading to AGD resistance and the underlying causative genomic features can aid in this effort, while also providing critical information for the development of other control strategies. AGD resistance is considered to be moderately heritable, and several putative QTL have been identified. The aim of the current study was to improve understanding of the mechanisms underlying AGD resistance, and to identify putative causative genomic factors underlying the QTL. To achieve this, RNA was extracted from the gill and head kidney of AGD resistant and susceptible animals following a challenge with N. perurans, and sequenced.ResultsComparison between resistant and susceptible animals primarily highlighted differences mainly in the local immune response in the gill, involving red blood cell genes and genes related to immune function and cell adhesion. Differentially expressed immune genes pointed to a contrast in Th2 and Th17 responses, which is consistent with the increased heritability observed after successive challenges with the amoeba. Five QTL-region candidate genes showed differential expression, including a gene connected to interferon responses (GVINP1), a gene involved in systemic inflammation (MAP4K4), and a positive regulator of apoptosis (TRIM39). Analyses of allele-specific expression highlighted a gene in the QTL region on chromosome 17, cellular repressor of E1A-stimulated genes 1 (CREG1), showing allelic differential expression suggestive of a cis-acting regulatory variant.ConclusionsIn summary, this study provides new insights into the mechanisms of resistance to AGD in Atlantic salmon, and highlights candidate genes for further functional studies that can further elucidate the genomic mechanisms leading to resistance and contribute to enhancing salmon health via improved genomic selection.

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Genome-Wide Association and Genomic Selection for Resistance to Amoebic Gill Disease in Atlantic Salmon.

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