Evidence map›Paper›PMID 31287894›Full record

ArticleThe Journal of heredity2019

QTLs Associated with Resistance to Cardiomyopathy Syndrome in Atlantic Salmon.

Solomon Boison, Jingwen Ding, Erica Leder, Bjarne Gjerde, Per Helge Bergtun, Ashie Norris, Matthew Baranski, Nicholas Robinson

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of heredity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

20 citing papers in PubMed, 36 citations in OpenAlex.

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  7. Genome-wide association study forFrontiers in genetics · 2023
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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

8 authors at 5 institutions in 2 countries.

Solomon BoisonDepartment of Breeding and Genetics, Nofima AS, Osloveien, Ås, Norway.
Jingwen DingDepartment of Aquaculture, Norwegian University of Life Sciences, Ås, Norway.
Erica LederDepartment of Breeding and Genetics, Nofima AS, Osloveien, Ås, Norway.
Bjarne GjerdeDepartment of Breeding and Genetics, Nofima AS, Osloveien, Ås, Norway.
Per Helge BergtunDepartment of Breeding and Genetics, Nofima AS, Osloveien, Ås, Norway.
Ashie NorrisDepartment of Breeding and Genetics, Nofima AS, Osloveien, Ås, Norway.
Matthew BaranskiDepartment of Breeding and Genetics, Nofima AS, Osloveien, Ås, Norway.
Nicholas RobinsonSustainable Aquaculture Laboratory - Temperate and Tropical (SALTT), School of BioSciences, The University of Melbourne, Parkville, Victoria, Australia.
Fafo Foundation · NOMowi (Norway) · NONofima · NONorwegian University of Life Sciences · NOUniversity of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiomyopathy syndrome (CMS) caused by piscine myocarditis virus is a major disease affecting the Norwegian Atlantic salmon industry. Three different populations of Atlantic salmon from the Mowi breeding program were used in this study. The first 2 populations (population 1 and 2) were naturally infected in a field outbreak, while the third population (population 3) went through a controlled challenged test. The aim of the study was to estimate the heritability, the genetic correlation between populations and perform genome-wide association analysis for resistance to this disease. Survival data from population 1 and 2 and heart atrium histology score data from population 3 was analyzed. A total of 571, 4312, and 901 fish from population 1, 2, and 3, respectively were genotyped with a noncommercial 55,735 Affymetrix marker panel. Genomic heritability ranged from 0.12 to 0.46 and the highest estimate was obtained from the challenge test dataset. The genetic correlation between populations was moderate (0.51-0.61). Two chromosomal regions (SSA27 and SSA12) contained single nucleotide polymorphisms associated with resistance to CMS. The highest association signal (P = 6.9751 × 10-27) was found on chromosome 27. Four genes with functional roles affecting viral resistance (magi1, pi4kb, bnip2, and ha1f) were found to map closely to the identified quantitative trait loci (QTLs). In conclusion, genetic variation for resistance to CMS was observed in all 3 populations. Two important quantitative trait loci were detected which together explain half of the total genetic variance, suggesting strong potential application for marker-assisted selection and genomic predictions to improve CMS resistance.

Indexed as

Quantitative Trait LociAlgorithmsAnimalsCardiomyopathiesDisease ResistanceFish DiseasesGenetic Association StudiesGenome-Wide Association StudyGenotypeModels, GeneticPhenotypeQuantitative Trait, HeritableSalmo salarAtlantic salmoncardiomyopathy syndromefield outbreakgenetic correlationsheritabilityQTL analysis

Identifiers

PMID31287894
PMCPMC6785937
OpenAlexW2956395522

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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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.