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影响大西洋鲑(Salmo salar)对胰腺疾病(鲑鱼α病毒)抗性的一个主要数量性状位点的定位与验证。

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

作者信息

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

机构信息

The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Midlothian, UK.

Nofima, Ås, Norway.

出版信息

Heredity (Edinb). 2015 Nov;115(5):405-14. doi: 10.1038/hdy.2015.37. Epub 2015 May 20.

DOI:10.1038/hdy.2015.37
PMID:25990876
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4611234/
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.

摘要

胰腺疾病(PD)由鲑鱼α病毒(SAV)引起,对大西洋鲑鱼养殖造成了巨大的负面经济影响和动物福利问题。已有报道表明宿主对该疾病的抗性存在遗传变异,这表明选择性育种可能成为疾病控制的重要组成部分。本研究的目的是利用从两个不相关的大西洋鲑鱼种群收集的存活数据,探索对PD抗性的遗传结构;一个种群在淡水中作为鱼苗时受到SAV攻击(种群1),另一个种群在海水中作为后幼鲑时受到SAV攻击(种群2)。对二元存活数据的分析显示,两个种群中宿主对PD的抗性都具有中等到高度的遗传力(鱼苗种群1 h²0.5;后幼鲑种群2 h²0.4)。对两个种群的子集进行了单核苷酸多态性标记的基因分型,并鉴定出六个假定的抗性数量性状位点(QTL)。其中一个QTL在两个种群中都定位到了3号染色体上的相同位置,在种群1基于父本和母本的分析中均达到全染色体显著水平,在种群2的综合分析中达到全基因组显著水平。这个经过独立验证的QTL在两个种群中都解释了宿主对PD抗性的很大一部分遗传变异,表明在整个生命周期阶段遗传抗性存在共同的潜在机制。与该QTL相关的标记正被纳入选择性育种计划,以提高对PD的抗性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c36d/4611234/49d558c1703a/hdy201537f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c36d/4611234/d071575b00ea/hdy201537f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c36d/4611234/bceb858df5a4/hdy201537f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c36d/4611234/49d558c1703a/hdy201537f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c36d/4611234/d071575b00ea/hdy201537f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c36d/4611234/bceb858df5a4/hdy201537f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c36d/4611234/49d558c1703a/hdy201537f3.jpg

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