A noteworthy result was the down regulation of elovl2 in salmon presenting higher flesh lipid, independent of LC PUFA content. Elovl2 has substrate specificity towards LC PUFA and is highly responsive to dietary n 3 LC PUFA levels in sal mon. However, the expression of this gene is often co ordinately regulated with other genes of LC PUFA either biosynthesis, such as 5fad and 6fad, which was not the case here. Hence, the biological significance of this result is not clear and may indicate other roles of elovl2 in lipid metabolism. For instance, an association between overexpression of elovl2 and enhanced triacyl glycerol synthesis and lipid droplet accumulation, as well as induction of PPAR�� target genes, was shown in mouse preadipocyte cell lines.

In addition, elovl2 was up regulated in the liver transcriptome of rats with nephrotic syndrome, a condition characterized by hyper lipidemia. Elovl2 was only recently characterized in salmon, and this is the first indication of an associ ation between its expression and lipid accumulation in a non mammalian vertebrate, with results suggesting that increased lipid level in salmon flesh repressed elovl2 expression independent of n 3 LC PUFA level although this requires further investigation. Another gene down regulated at higher lipid levels was a mitochondrial acyl carrier protein, involved in acyl transfer steps, including roles in fatty acid synthesis and functioning of the elec tron transport chain, which could conceptually be responding to similar regulatory mechanisms affecting elovl2.

In contrast, stearoyl CoA desaturase, responsible for the synthesis of monounsaturated fatty acids from saturated precursors, was up regulated in salmon with higher flesh lipid levels. This gene was positively corre lated with fat accumulation in bovine skeletal muscle, consistent with up regulation in salmon families with increased fat stores. Possible association between flesh n 3 LC PUFA contents and immune response The predominance of immune response genes responding to total lipid level and, particularly, n 3 LC PUFA con tents in salmon flesh was unexpected. This was a true over representation as GO enrichment analysis enabled identification of several GO terms related to regulation of immune and inflammatory responses in relation to the total lipid factor.

However, as mentioned above, the tran scriptomic comparison, although balanced Batimastat for total lipid, was not balanced for viral disease resistance and, as a consequence, higher contrast between families was imposed on the high lipid group due to the fortuitous selection of family HH presenting a much higher viral resistance EBV. Nonetheless, if family HH biased the results of the two way ANOVA we would expect a preponderance of immune related genes to occur only when comparing these two families, presenting higher and lower flesh n 3 LC PUFA contents at the higher lipid level.