Identification of genetic loci associated with higher resistance to pancreas disease (PD) in Atlantic salmon (Salmo salar L.)
Abstract 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...
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crspringernat:10.1186/s12864-020-06788-4 2023-05-15T15:31:30+02:00 Identification of genetic loci associated with higher resistance to pancreas disease (PD) in Atlantic salmon (Salmo salar L.) Hillestad, Borghild Makvandi-Nejad, Shokouh Krasnov, Aleksei Moghadam, Hooman K. Research Council of Norway 2020 http://dx.doi.org/10.1186/s12864-020-06788-4 https://link.springer.com/content/pdf/10.1186/s12864-020-06788-4.pdf https://link.springer.com/article/10.1186/s12864-020-06788-4/fulltext.html en eng Springer Science and Business Media LLC https://creativecommons.org/licenses/by/4.0 https://creativecommons.org/licenses/by/4.0 CC-BY BMC Genomics volume 21, issue 1 ISSN 1471-2164 Genetics Biotechnology journal-article 2020 crspringernat https://doi.org/10.1186/s12864-020-06788-4 2022-01-04T10:16:18Z Abstract 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. Article in Journal/Newspaper Atlantic salmon Salmo salar Springer Nature (via Crossref) Norway Sav’ ENVELOPE(156.400,156.400,68.817,68.817) BMC Genomics 21 1 |
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Open Polar |
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Springer Nature (via Crossref) |
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crspringernat |
language |
English |
topic |
Genetics Biotechnology |
spellingShingle |
Genetics Biotechnology Hillestad, Borghild Makvandi-Nejad, Shokouh Krasnov, Aleksei Moghadam, Hooman K. Identification of genetic loci associated with higher resistance to pancreas disease (PD) in Atlantic salmon (Salmo salar L.) |
topic_facet |
Genetics Biotechnology |
description |
Abstract 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. |
author2 |
Research Council of Norway |
format |
Article in Journal/Newspaper |
author |
Hillestad, Borghild Makvandi-Nejad, Shokouh Krasnov, Aleksei Moghadam, Hooman K. |
author_facet |
Hillestad, Borghild Makvandi-Nejad, Shokouh Krasnov, Aleksei Moghadam, Hooman K. |
author_sort |
Hillestad, Borghild |
title |
Identification of genetic loci associated with higher resistance to pancreas disease (PD) in Atlantic salmon (Salmo salar L.) |
title_short |
Identification of genetic loci associated with higher resistance to pancreas disease (PD) in Atlantic salmon (Salmo salar L.) |
title_full |
Identification of genetic loci associated with higher resistance to pancreas disease (PD) in Atlantic salmon (Salmo salar L.) |
title_fullStr |
Identification of genetic loci associated with higher resistance to pancreas disease (PD) in Atlantic salmon (Salmo salar L.) |
title_full_unstemmed |
Identification of genetic loci associated with higher resistance to pancreas disease (PD) in Atlantic salmon (Salmo salar L.) |
title_sort |
identification of genetic loci associated with higher resistance to pancreas disease (pd) in atlantic salmon (salmo salar l.) |
publisher |
Springer Science and Business Media LLC |
publishDate |
2020 |
url |
http://dx.doi.org/10.1186/s12864-020-06788-4 https://link.springer.com/content/pdf/10.1186/s12864-020-06788-4.pdf https://link.springer.com/article/10.1186/s12864-020-06788-4/fulltext.html |
long_lat |
ENVELOPE(156.400,156.400,68.817,68.817) |
geographic |
Norway Sav’ |
geographic_facet |
Norway Sav’ |
genre |
Atlantic salmon Salmo salar |
genre_facet |
Atlantic salmon Salmo salar |
op_source |
BMC Genomics volume 21, issue 1 ISSN 1471-2164 |
op_rights |
https://creativecommons.org/licenses/by/4.0 https://creativecommons.org/licenses/by/4.0 |
op_rightsnorm |
CC-BY |
op_doi |
https://doi.org/10.1186/s12864-020-06788-4 |
container_title |
BMC Genomics |
container_volume |
21 |
container_issue |
1 |
_version_ |
1766362013789847552 |