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ABSTRACT: Population genomics of seal lice

PROVIDER: PRJNA1103082 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28763119_1.fastq.gz	Fastqsanger.gz
	SRR28763119_2.fastq.gz	Fastqsanger.gz
	SRR28763120_1.fastq.gz	Fastqsanger.gz
	SRR28763120_2.fastq.gz	Fastqsanger.gz
	SRR28763121_1.fastq.gz	Fastqsanger.gz

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Project description:The salmon louse is an ectoparasitic copepod that causes major economic losses in the aquaculture industry of Atlantic salmon. This host displays a high level of susceptibility to lice which can be accounted for by several factors including stress. In addition, the parasite itself acts as a potent stressor of the host, and outcomes of infection can depend on biotic and abiotic factors that stimulate production of cortisol. Consequently, examination of responses to infection with this parasite, in addition to stress hormone regulation in Atlantic salmon, is vital for better understanding of the host pathogen interaction. Atlantic salmon post smolts were exposed to stress hormone cortisol, lice and their combination. The transcriptomic effects of hormone treatment in salmon skin were significantly greater than lice-infection induced changes. Cortisol stimulated expression of genes involved in metabolism of steroids and amino acids, chaperones, responses to oxidative stress and eicosanoid metabolism and suppressed genes related to antigen presentation, B and T cells, antiviral and inflammatory responses. Cortisol and liceBoth treatments equally down-regulated a large panel of motor proteins that can be important for wound contraction. Cortisol also suppressed multiple genes involved in wound healing, parts of which were activated by the parasite. Down-regulation of collagens and other structural proteins was in parallel with the induction of proteinases that degrade extracellular matrix (MMP9 and MMP13). Cortisol reduced expression of genes encoding proteins involved in formation of various tissue structures, regulators of cell differentiation and growth factors. Atlantic salmon post smolts were organised into four experimental groups: lice + cortisol, lice + placebo, no lice + cortisol, no lice + placebo. Infection levels were equal in both treatments upon termination of the experiment. Gene expression changes in skin were assessed with 21 k oligonucleotide microarray and qPCR at the chalimus stage 18 days post infection at 9oC.

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