SRP328014 PRJNA745995 GSE179972 Investigation of the transcriptomic response of Atlantic salmon (Salmo salar) exposed to Neoparamoeba perurans. Purpose: The aim of this study was to RNA-sequencing (RNA-seq) to investigate further the gill transcriptome during the early stage of infection, prior to the appearance of mucoid lesions on the gills of amoebic gill disease (ADG)-affected fish. Methods: 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 inoculation (dpi) RNA-seq data was validated using real-time, quantitative PCR (qPCR) analysis. Results: This study identified 29,357 Differentially Expressed Genes (DEGs) over the course of 16 days follwing exposure to N.perurans , the caustative agent of Amoebic gill disease. With many genes differentially regualted at more tehn one time point, the number of individual gene identified as down-regulated was 8,524 and up-regulated was 10,826. DEGs mapped to 224 Gene Ontology (GO) terms, 27 reference pathways in the Kyoto Encyclopedia of Genes and Genomes (KEGG) and 15 Reactome Gene Sets. Conclusions:Molecular diagnostics and histopathology, but not gill scores, provided an accurate record of disease progression during early stage onset of AGD, prior to evidence of clinical signs on the gill. At 7 days post infection (dpi), there was evidence of innate immune response activation and a concomitant immune suppression involving signalling pathways for cytokines, specifically interleukins. Overall design: Atlantic salmon were exposed to N.perurans, the causative agent of AGD with samples collected over time five timepoints: 0, 4, 7, 14 and 16 dpi. There were 6 fish control and AGD-affected fish sampled at each of teh four time points. Total RNA was extracted from gill tissue. 30 RNA-seq libraries were generated. The RNA-seq data was validated using qPCR. Differential gene expression was identified by comparing the individaul libraries at each point with the T0 control (T0_GCRL1 to T0_GCRL6). GSE179972 pubmed 34667245