Mapping and validation of a major QTL affecting resistance to pancreas disease (salmonid alphavirus) in Atlantic salmon (Salmo salar).
Mapping and validation of a major QTL affecting resistance to pancreas disease (salmonid alphavirus) in Atlantic salmon (Salmo salar).
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DOI：
10.1038/hdy.2015.37
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发表时间：
2015-11
期刊：
影响因子：
3.8
通讯作者：
Houston RD
中科院分区：
文献类型：
--
作者：
Gonen S;Baranski M;Thorland I;Norris A;Grove H;Arnesen P;Bakke H;Lien S;Bishop SC;Houston RD
胰腺疾病（PD），由鲑鱼甲病毒（SAV）引起，对大西洋鲑鱼养殖业的经济和动物福利有很大的负面影响。据报道，宿主对这种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一个重要组成部分。本研究的目的是探索耐PD的遗传结构，使用从两个不相关的大西洋鲑鱼种群收集的生存数据;一个挑战与SAV作为鱼苗在淡水中（POP 1），一个挑战与SAV作为后小鲑鱼在海水中（POP 2）。二进制生存数据的分析表明，在两个群体中，寄主对PD的抗性的遗传力为中等至高（鱼苗POP 1 h2~0.5;二龄鲑后POP 2 h2~0.4）。这两个群体的亚组进行基因型的单核苷酸多态性标记，并确定了6个假定的抗性数量性状位点（QTL）。其中一个QTL被定位在两个群体的3号染色体上的同一位置，在POP 1中基于父系和母系的分析中都达到了全染色体显著性，在POP 2中的组合分析中达到了全基因组显著性。这一独立验证的QTL解释了两个种群中PD抗性的宿主遗传变异的显著比例，表明了整个生命周期阶段遗传抗性的共同潜在机制。与该QTL相关的标记正被纳入选择性育种计划以提高PD抗性。
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 h2~0.5; post-smolt POP 2 h2~0.4). 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.