Investigation of the transcriptomic response in Atlantic salmon (Salmo salar) gill exposed to Paramoeba perurans during early onset of disease

• Published in: Scientific Reports
• Main Authors: Talbot, Anita, Gargan, Laura, Moran, Grainne, Prudent, Louis, O’Connor, Ian, Mirimin, Luca, Carlsson, Jens, MacCarthy, Eugene
• Other Authors: Department of Agriculture, Food and the Marine, Ireland
• Format: Article in Journal/Newspaper
• Language: English
• Published: Springer Science and Business Media LLC 2021
• Subjects: Multidisciplinary; Atlantic salmon; Salmo salar
• Online Access: http://dx.doi.org/10.1038/s41598-021-99996-1; https://www.nature.com/articles/s41598-021-99996-1.pdf; https://www.nature.com/articles/s41598-021-99996-1

Abstract Amoebic Gill Disease (AGD), caused by the protozoan extracellular parasite Paramoeba perurans ( P. perurans ) is a disease affecting Atlantic salmon ( Salmo salar ). This study investigated the gill transcriptomic profile of pre-clinical AGD using RNA-sequencing (RNA-seq) technology. RNA-seq libraries generated at 0, 4, 7, 14 and 16 days post infection (dpi) identified 19,251 differentially expressed genes (DEGs) of which 56.2% were up-regulated. DEGs mapped to 224 Gene Ontology (GO) terms including 140 biological processes (BP), 45 cellular components (CC), and 39 molecular functions (MF). A total of 27 reference pathways in the Kyoto Encyclopedia of Genes and Genomes (KEGG) and 15 Reactome gene sets were identified. The RNA-seq data was validated using real-time, quantitative PCR (qPCR). A host immune response though the activation of complement and the acute phase genes was evident at 7 dpi, with a concurrent immune suppression involving cytokine signalling, notably in interleukins, interferon regulatory factors and tumour necrosis factor-alpha ( tnf- α) genes. Down-regulated gene expression with involvement in receptor signalling pathways (NOD-like, Toll-like and RIG-1) were also identified. The results of this study support the theory that P. perurans can evade immune surveillance during the initial stages of gill colonisation through interference of signal transduction pathways.