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Atlantic salmon migrates from rivers to sea to feed, grow and develop gonads before returning to spawn in freshwater. The transition to marine habitats is associated with dramatic changes in the environment, including water salinity, exposure to pathogens and shift in dietary lipid availability. Many changes in physiology and metabolism occur across this life-stage transition, but little is known about the molecular nature of these changes. Here, we use a long-term feeding experiment to study transcriptional regulation of lipid metabolism in Atlantic salmon gut and liver in both fresh- and saltwater. We find that lipid metabolism becomes significantly less plastic to differences in dietary lipid composition when salmon transitions to saltwater and experiences increased dietary lipid availability. Expression of genes in liver relating to lipogenesis and lipid transport decreases overall and becomes less responsive to diet, while genes for lipid uptake in gut become more highly expressed. Finally, analyses of evolutionary consequences of the salmonid-specific whole-genome duplication on lipid metabolism reveal several pathways with significantly different (p < .05) duplicate retention or duplicate regulatory conservation. We also find a limited number of cases where the whole-genome duplication has resulted in an increased gene dosage. In conclusion, we find variable and pathway-specific effects of the salmonid genome duplication on lipid metabolism genes. A clear life-stage-associated shift in lipid metabolism regulation is evident, and we hypothesize this to be, at least partly, driven by nondietary factors such as the preparatory remodelling of gene regulation and physiology prior to sea migration.

Contamination of drinking water source zones by vinyl chloride (VC), a known human carcinogen and common groundwater contaminant, poses a public health risk. Bioremediation applications involving aerobic, VC-assimilating bacteria could be useful in alleviating environmental VC cancer risk, but their evolution and activity in the environment are poorly understood. In this study, adaptation of ethene-assimilating Mycobacterium strains JS622, JS623, JS624, and JS625 to VC as a growth substrate was investigated to test the hypothesis that VC-assimilating bacteria arise from naturally occurring ethene-assimilating bacteria. VC consumption in the absence of microbial growth was initially observed in cultures grown in both ethene and 1/10-strength trypticase soy agar + 1% (w/v) glucose. After extended incubations (55-476 days), all strains commenced growth-coupled VC consumption patterns. VC-adapted cultures grown on 20 mM acetate subsequently retained their ability to assimilate VC. Three independent purity check methods (streak plates, 16S rRNA gene sequencing, and repetitive extragenic palindromic polymerase chain reaction) verified culture purity prior to and following VC adaptation. Overall, our results suggest that ethene-assimilating mycobacteria have a widespread ability to adapt to VC as a growth substrate.

Atlantic salmon can synthesize polyunsaturated fatty acids (PUFAs), such as eicosapentaenoic acid (20:5n-3), arachidonic acid (20:4n-6) and docosahexaenoic acid (22:6n-3) via activities of very long chain fatty acyl elongases (Elovls) and fatty acyl desaturases (Fads), albeit to a limited degree. Understanding molecular mechanisms of PUFA biosynthesis and regulation is a pre-requisite for sustainable use of vegetable oils in aquafeeds as current sources of fish oils are unable to meet increasing demands for omega-3 PUFAs. By generating CRISPR-mediated elovl2 partial knockout (KO), we have shown that elovl2 is crucial for multi-tissue synthesis of 22:6n-3 in vivo and that endogenously synthesized PUFAs are important for transcriptional regulation of lipogenic genes in Atlantic salmon. The elovl2 -KOs showed reduced levels of 22:6n-3 and accumulation of 20:5n-3 and docosapentaenoic acid (22:5n-3) in the liver, brain and white muscle, suggesting inhibition of elongation. Additionally, elovl2 -KO salmon showed accumulation of 20:4n-6 in brain and white muscle. The impaired synthesis of 22:6n-3 induced hepatic expression of sterol regulatory element binding protein-1 ( srebp-1 ), fatty acid synthase-b, Δ6fad-a , Δ5fad and elovl5 . Our study demonstrates key roles of elovl2 at two penultimate steps of PUFA synthesis in vivo and suggests Srebp-1 as a main regulator of endogenous PUFA synthesis in Atlantic salmon.

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