d to avoid confounding effects associated with the

d to avoid confounding effects associated with the selleck chemical lipid level factor. Using these results, four families were identified, two with high levels of lipid, and two with low levels of lipid and, within each level of total lipid, the two fam ilies had significantly contrasting relative n 3 LC PUFA contents. Therefore, the four families constituted a 2 x 2 factorial design, labelling each family by the total lipid n 3 LC PUFA contrasts as LL, LH, HL and HH, respectively, which allowed comparisons of n 3 LC PUFA contents at a con stant lipid level and, similarly, comparisons of total lipid at constant n 3 LC PUFA levels. Microarray analysis A two way ANOVA analysis employing the Benjamini Hochberg multiple testing correction was per formed to assess significant effects of the factors n 3 LC PUFA and total lipid, which returned lists with 43, 109 and 66 entities for each factor and their interaction, respectively.

These significant lists were then analyzed in detail and genes were categorized according to their biological function, in some cases inferred from mam malian homolog genes. Because the focus of this work was to identify genes that are specific ally affected by the trait n 3 LC PUFA content with out the interference of total lipid level, the interaction between the two factors is not presented. Distribution of genes by categories of biological function revealed that there was a preponderance of immune response genes significantly affected by both factors, 38% by n 3 LC PUFA and 29% by total lipid.

Gene Ontology hich enables the identification of GO terms significantly enriched in the input entity list when compared to the whole array dataset, revealed that this is a true over representation in the list of genes sig nificantly affected by the total lipid factor. In contrast, genes involved in the broad category of metabolism only corresponded to 21% of genes sig nificantly affected by n 3 LC PUFA content and 30% by the total lipid factor. Surprisingly, no lipid metabolism genes were significantly altered in liver when comparing families with higher and lower contents of n 3 LC PUFA in their flesh, while about 8% were significantly affected by flesh lipid level. Within these, noteworthy was the down regulation of fatty acyl elongase and of acyl carrier protein transcripts in salmon having a higher lipid level in their flesh, independent of LC PUFA con tent.

On the other hand, stearoyl CoA desaturase was significantly up regulated in Cilengitide fish with higher lipid levels in their flesh. The interaction between both factors is not presented but it did not substantially affect lipid me tabolism genes. Finally, and in general, genes involved in regulation of transcription sellectchem and signalling were also prevalent, 17% in response to n 3 LC PUFA and 12 13% to total lipid. Therefore, the results did not identify lipid metabolism pathways that might underlie differences in flesh n 3 LC PUFA composition between families. However, previous studies demonstrated that hep

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