Characterising the mechanisms underlying genetic resistance to amoebic gill disease in Atlantic salmon using RNA sequencing

Abstract

Background: 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. Results: 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 allelespecific 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. Conclusions: 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.

Exploring genetic resistance to infectious salmon anaemia virus in Atlantic salmon by genome-wide association and RNA sequencing

“…Furthermore, this information can feed into genome editing efforts to enhance disease resistance, whether it is exploiting existing genetic variation or generating de novo mutations based on the functional basis of disease resistance [ 38 , 39 ]. One route to achieving this is to integrate transcriptomic data with genetic mapping data to identifying putative functional genes and pathways connected to resistance, and this approach has been applied for genetic resistance to viral and parasitic diseases in Atlantic salmon [ 40 , 41 ].…”

Exploring genetic resistance to Infectious Salmon Anaemia Virus in Atlantic salmon by genome-wide association and RNA sequencing

“…Furthermore, this information can feed into genome editing efforts to enhance disease resistance, whether it is exploiting existing genetic variation or generating de novo mutations based on the functional basis of disease resistance [37,38]. One route to achieving this is to integrate transcriptomic data with genetic mapping data to identifying putative functional genes and pathways connected to resistance, and this approach has been applied for genetic resistance to viral and parasitic diseases in Atlantic salmon [39,40].…”

Host-Parasite Interaction of Atlantic salmon (Salmo salar) and the Ectoparasite Neoparamoeba perurans in Amoebic Gill Disease

“…Pathogens released by the parasite may be recognized by the lectin-C pattern recognition receptor, macrophage mannose receptor 1-like which also stimulates interleukin-1b and the Th1/Th17 proinflammatory cytokine response (91). Interestingly, the Th1, Th2 and Th17 cell differentiation pathways reported to be associated with AGD through quantitative trait locus (QTL) and quantitative PCR analyses, were not markedly enriched pathways in our analysis (15,120). Furthermore, the data were contradictory with previous studies, exhibiting upregulation of Th17 genes and downregulation of several other genes in the Th1, Th2 and Th17 cell differentiation pathways leading to their expression.…”