Resistance to amoebic gill disease (AGD) is characterised by the transcriptional dysregulation of immune and cell cycle pathways.
Amoebic gill disease (AGD) is a parasite-mediated proliferative gill disease capable of affecting a range of teleost hosts. While a moderate heritability for AGD resistance in Atlantic salmon has been reported previously, the mechanisms by which individuals resist the proliferative effects remain poorly understood. To gain more knowledge of this commercially important trait, we compared gill transcriptomes of two groups of Atlantic salmon, one designated putatively resistant, and one designated putatively susceptible to AGD. Utilising a 17k Atlantic salmon cDNA microarray we identified 196 transcripts that were differentially expressed between the two groups. Expression of 11 transcripts were further examined with real-time quantitative RT-PCR (qPCR) in the AGD-resistant and AGD-susceptible animals, as well as non-infected naïve fish. Gene expression determined by qPCR was in strong agreement with the microarray analysis. A large number of differentially expressed genes were involved in immune and cell cycle responses. Resistant individuals displayed significantly higher expression of genes involved in adaptive immunity and negative regulation of the cell cycle. In contrast, AGD-susceptible individuals showed higher expression of acute phase proteins and positive regulators of the cell cycle. Combined with the gill histopathology, our results suggest AGD resistance is acquired rather than innately present, and that this resistance is for the most part associated with the dysregulation of immune and cell cycle pathways.
Wynne
James W
JW
CSIRO National Food Futures Flagship, CSIRO Marine and Atmospheric Research Hobart, GPO Box 1538, Hobart, Tasmania 7001, Australia. james.wynne@sciro.au
O'Sullivan
Maree G
MG
Stone
Glenn
G
Cook
Mathew T
MT
Nowak
Barbara F
BF
Lovell
David R
DR
Taylor
Richard S
RS
Elliott
Nicholas G
NG
D000562:Amebiasis / Q000276:immunology* / Q000473:pathology; D000818:Animals; D002453:Cell Cycle / Q000276:immunology*; D004198:Disease Susceptibility / Q000276:immunology; D005260:Female; D005393:Fish Diseases / Q000276:immunology* / Q000469:parasitology / Q000473:pathology; D020869:Gene Expression Profiling; D005880:Gills / Q000276:immunology* / Q000469:parasitology / Q000473:pathology; D006790:Host-Parasite Interactions / Q000276:immunology; D007113:Immunity, Innate / Q000276:immunology; D016840:Lobosea / Q000276:immunology* / Q000472:pathogenicity; D008297:Male; D020317:Salmo salar / Q000276:immunology / Q000469:parasitology; D015398:Signal Transduction / Q000276:immunology*; D014158:Transcription, Genetic / Q000276:immunology*