|Appears in Collections:||Aquaculture Journal Articles|
|Peer Review Status:||Refereed|
|Title:||Transcriptional control mechanisms of genes of lipid and fatty acid metabolism in the Atlantic salmon (Salmo salar L.) established cell line, SHK-1|
Tocher, Douglas R
SHK-1 cell line
|Citation:||Minghetti M, Leaver M & Tocher DR (2011) Transcriptional control mechanisms of genes of lipid and fatty acid metabolism in the Atlantic salmon (Salmo salar L.) established cell line, SHK-1, 1811 (3), pp. 194-202.|
|Abstract:||The regulatory control mechanisms of lipid and fatty acid metabolism were investigated in Atlantic salmon. We identified sterol regulatory element binding protein (SREBP) genes in salmon and characterised their response, and the response of potential target and other regulatory genes including liver X receptor (LXR), to cholesterol and long-chain polyunsaturated fatty acids (LC- PUFA) in the salmon established cell line, SHK-1. Two cDNAs for SREBPs homologous to mammalian SREBP-1 and SREBP-2 were characterised. We identified three groups of genes whose expression responded differently to the treatments. One group of genes, including cholesterol biosynthetic genes, showed increased expression in response to lipid depletion but supplementary cholesterol or LC- PUFA had no further effect. The expression of a second group of genes belonging to fatty acid biosynthetic pathways, included fatty acid synthase, Δ6 and Δ5 fatty acyl desaturases, also increased after lipid depletion but this was negated by cholesterol or by LC-PUFA supplementation. The expression of a third group of genes including acyl-CoA oxidase, HMG-CoA reductase and Elovl5 elongase was increased by cholesterol treatment but was not affected by lipid depletion or by LC-PUFA. This same pattern of expression was also shown by liver X receptor (LXR), indicating that acyl-CoA oxidase, HMG-CoA reductase and Elovl5 are possible direct targets of LXR. This suggests that salmon Elovl5 may be regulated differently from mammalian Elovl5, which is an indirect target of LXR, responding to LXR-dependent increases in SREBP-|
|Rights:||Published in Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids by Elsevier. Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids, Volume 1811, Issue 3, March 2011, pp. 194 - 202.; This is the peer reviewed version of this article.; NOTICE: this is the author’s version of a work that was accepted for publication in Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids, VOL 1811, ISSUE 3, (March 2011). DOI: 10.1016/j.bbalip.2010.12.008|
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