Identification of genetic loci associated with higher resistance to pancreas disease (PD) in Atlantic salmon (Salmo salar L.)

Summary

Background: Pancreas disease (PD) is a contagious disease caused by salmonid alphavirus (SAV) with significant
economic and welfare impacts on salmon farming. Previous work has shown that higher resistance against PD has
underlying additive genetic components and can potentially be improved through selective breeding. To better
understand the genetic basis of PD resistance in Atlantic salmon, we challenged 4506 smolts from 296 families of
the SalmoBreed strain. Fish were challenged through intraperitoneal injection with the most virulent form of the
virus found in Norway (i.e., SAV3). Mortalities were recorded, and more than 900 fish were further genotyped on a
55 K SNP array.
Results: The estimated heritability for PD resistance was 0.41 ± 0.017. The genetic markers on two chromosomes,
ssa03 and ssa07, showed significant associations with higher disease resistance. Collectively, markers on these two
QTL regions explained about 60% of the additive genetic variance. We also sequenced and compared the cardiac
transcriptomics of moribund fish and animals that survived the challenge with a focus on candidate genes within
the chromosomal segments harbouring QTL. Approximately 200 genes, within the QTL regions, were found to be
differentially expressed. Of particular interest, we identified various components of immunoglobulin-heavy-chain
locus B (IGH-B) on ssa03 and immunoglobulin-light-chain on ssa07 with markedly higher levels of transcription in
the resistant animals. These genes are closely linked to the most strongly QTL associated SNPs, making them likely
candidates for further investigation.
Conclusions: The findings presented here provide supporting evidence that breeding is an efficient tool for
increasing PD resistance in Atlantic salmon populations. The estimated heritability is one of the largest reported for
any disease resistance in this species, where the majority of the genetic variation is explained by two major QTL.
The transcriptomic analysis has revealed the activation of essential components of the innate and the adaptive
immune responses following infection with SAV3. Furthermore, the complementation of the genomic with the
transcriptomic data has highlighted the possible critical role of the immunoglobulin loci in combating PD virus.

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DOI : doi.org/10.1186/s12864-020-067...
NVA : hdl.handle.net/11250/2681776