The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Midlothian, EH25 9RG, UK.
Landcatch Natural Selection Ltd., Roslin Innovation Centre, University of Edinburgh, Midlothian, EH25 9RG, UK.
BMC Genomics. 2020 Mar 30;21(1):271. doi: 10.1186/s12864-020-6694-x.
Gill health is one of the main concerns for Atlantic salmon aquaculture, and Amoebic Gill Disease (AGD), attributable to infection by the amoeba Neoparamoeba perurans, is a frequent cause of morbidity. In the absence of preventive measures, increasing genetic resistance of salmon to AGD via selective breeding can reduce the incidence of the disease and mitigate gill damage. Understanding the mechanisms leading to AGD resistance and the underlying causative genomic features can aid in this effort, while also providing critical information for the development of other control strategies. AGD resistance is considered to be moderately heritable, and several putative QTL have been identified. The aim of the current study was to improve understanding of the mechanisms underlying AGD resistance, and to identify putative causative genomic factors underlying the QTL. To achieve this, RNA was extracted from the gill and head kidney of AGD resistant and susceptible animals following a challenge with N. perurans, and sequenced.
Comparison between resistant and susceptible animals primarily highlighted differences mainly in the local immune response in the gill, involving red blood cell genes and genes related to immune function and cell adhesion. Differentially expressed immune genes pointed to a contrast in Th2 and Th17 responses, which is consistent with the increased heritability observed after successive challenges with the amoeba. Five QTL-region candidate genes showed differential expression, including a gene connected to interferon responses (GVINP1), a gene involved in systemic inflammation (MAP4K4), and a positive regulator of apoptosis (TRIM39). Analyses of allele-specific expression highlighted a gene in the QTL region on chromosome 17, cellular repressor of E1A-stimulated genes 1 (CREG1), showing allelic differential expression suggestive of a cis-acting regulatory variant.
In summary, this study provides new insights into the mechanisms of resistance to AGD in Atlantic salmon, and highlights candidate genes for further functional studies that can further elucidate the genomic mechanisms leading to resistance and contribute to enhancing salmon health via improved genomic selection.
吉尔健康是大西洋鲑鱼养殖的主要关注点之一,由变形虫 Neoparamoeba perurans 感染引起的阿米巴性吉尔病(AGD)是发病率高的常见原因。在没有预防措施的情况下,通过选择性繁殖增加鲑鱼对 AGD 的遗传抗性可以降低疾病的发生率并减轻鳃损伤。了解导致 AGD 抗性的机制和潜在的致病基因组特征可以为此提供帮助,同时也为其他控制策略的发展提供关键信息。AGD 抗性被认为具有中度遗传性,已经确定了几个假定的 QTL。本研究的目的是提高对 AGD 抗性的潜在机制的理解,并确定潜在的导致 QTL 的致病基因组因素。为了实现这一目标,从经 N. perurans 挑战后具有 AGD 抗性和易感的动物的鳃和头肾中提取 RNA,并进行测序。
抗性和易感动物之间的比较主要突出了在鳃中的局部免疫反应中的差异,涉及红细胞基因和与免疫功能和细胞黏附相关的基因。差异表达的免疫基因表明 Th2 和 Th17 反应的差异,这与在连续受到变形虫的挑战后观察到的遗传力增加一致。五个 QTL 区域候选基因表现出差异表达,包括与干扰素反应相关的基因(GVINP1)、参与全身炎症的基因(MAP4K4)和凋亡的正调节剂(TRIM39)。等位基因特异性表达分析突出了染色体 17 上 QTL 区域中的一个基因,细胞 E1A 刺激基因 1 的抑制剂(CREG1),表现出等位基因差异表达,暗示存在顺式作用调节变异。
总之,本研究为大西洋鲑鱼对 AGD 抗性的机制提供了新的见解,并强调了候选基因进行进一步的功能研究,这可以进一步阐明导致抗性的基因组机制,并通过改进基因组选择来提高鲑鱼的健康。