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ABSTRACT: AGD resistant and susceptible Atlantic salmon RNA-seq

PROVIDER: PRJNA552604 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9642620_1.fastq.gz	Fastqsanger.gz
	SRR9642620_2.fastq.gz	Fastqsanger.gz
	SRR9642630_1.fastq.gz	Fastqsanger.gz
	SRR9642630_2.fastq.gz	Fastqsanger.gz
	SRR9642640_1.fastq.gz	Fastqsanger.gz

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Project description:Infectious Pancreatic Necrosis (IPN) is a highly contagious birnavirus disease of farmed salmonid fish, which often causes high levels of morbidity and mortality. A large genetic component underlying resistance to this disease has been previously described for Atlantic salmon (Salmo salar L.), which mediates high mortality rates in some families and zero mortality in others. A global comparison of the gene expression profiles of resistant and susceptible Atlantic salmon fry following challenge with the IPN virus was undertaken. Full sibling salmon fry from two IPNV-resistant and two IPNV-susceptible families were challenged with the virus and sampled at 1 day, 7 days and 20 days post-challenge. Significant viral titre was observed in both resistant and susceptible fish at all timepoints, although generally at higher levels in susceptible fish. Microarray interrogations were performed using a custom-designed, oligonucleotide microarray platform (Agilent) with 44 K probes per slide (Salar_2; Agilent Design ID:025520). The design is lodged with ArrayExpress ( under accession number A-MEXP-2065. Dual-label hybridisations were undertaken, with each experimental sample (Cy3 labelled) being competitively hybridised against a pooled reference control (Cy5 labelled) comprising equimolar amounts from each experimental RNA sample. The interrogations comprised 144 separate hybridisations; 2 genotypes (susceptible, resistant) Ã 2 families for each genotype Ã 2 challenge states (control, challenged) Ã 3 timepoints (1, 7, 20 dpi) Ã 4 biological replicates for resistant (2 from each of two tanks) and 8 biological replicates for susceptible (4 from each of two tanks). A preliminary analysis suggested evidence for a segregating QTL in both the susceptible families and therefore twice as many offspring were screened. It was later established that the evidence for QTL segregation in one of the families was inconclusive and therefore comparisons were made at the family level only. The analyses took the unbalanced design into account.

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