Evidence map›Paper›PMID 25990876›Full record

ArticleHeredity2015

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

S Gonen, M Baranski, I Thorland, A Norris, H Grove, P Arnesen, H Bakke, S Lien, S C Bishop, R D Houston

Open access · hybridAbstract read
In one paragraph

Article in Heredity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
7.9field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

40 citing papers in PubMed, 95 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Genome-wide association study forFrontiers in genetics · 2023
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 2 countries.

S GonenThe Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Midlothian, UK.
M BaranskiNofima, Ås, Norway.
I ThorlandAkvaforsk Genetics Center AS, Sunndalsøra, Norway.
A NorrisMarine Harvest, Bergen, Norway.
H GroveDepartment of Animal and Aquacultural Sciences and Centre for Integrative Genetics, Norwegian University of Life Sciences, Ås, Norway.
P ArnesenMarine Harvest, Bergen, Norway.
H BakkeSalmoBreed AS, Bergen, Norway.
S LienDepartment of Animal and Aquacultural Sciences and Centre for Integrative Genetics, Norwegian University of Life Sciences, Ås, Norway.
S C BishopThe Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Midlothian, UK.
R D HoustonThe Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Midlothian, UK.
Roslin Institute · GBAkvaforsk Genetics Center (Norway) · NOFafo Foundation · NOUniversity of Edinburgh · GB

Funding

Biotechnology and Biological Sciences Research Council BB/H022007/1
6 · The paper itself

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 h(2)~0.5; post-smolt POP 2 h(2)~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.

Indexed as

Quantitative Trait LociAlphavirusAnimalsChromosome MappingDisease ResistanceFemaleFish DiseasesGenetics, PopulationGenotypeInheritance PatternsMaleModels, GeneticPancreatic DiseasesPolymorphism, Single NucleotideSalmo salar

Identifiers

PMID25990876
PMCPMC4611234
OpenAlexW1482490553

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.