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Farmed salmon strains have been selected to improve growth rates as well as other traits of commercial interest but the 2 million farmed salmon escaping annually may enhance the risk of extinction of wild populations through genetic and ecological interactions. Here, we compare the transcription profiles of 3557 genes in the progeny of farmed and wild Atlantic salmon from Norway and Canada grown in controlled conditions, and demonstrate that five to seven generations of artificial selection led to heritable changes in gene transcription profiles, the average magnitude of the differences being 25% and 18% for at least 1.4% and 1.7% of the expressed genes in juvenile salmon from Norway and Canada, respectively. Moreover, genes showing significant transcription profile differences in both farmed strains (16%) all exhibited parallel changes. These findings, along with the identification of several genes whose expression profiles were modified through artificial selection, provide new insights into the molecular basis of parallel evolution, and suggest how gene flow from farmed escapees may affect the genetic integrity of wild populations. [ABSTRACT FROM AUTHOR]

A sequence critical for phenobarbital (PB) induction, the PB response unit (PBRU), situated upstream of the rat CYP2B1 and CYP2B2 genes, includes two nuclear receptor binding sites, NR1 and NR2. When NR1 and NR2 are mutated PB responsiveness is abolished. While no nuclear receptor for which PB is an agonist ligand has yet been identified, PB is a ligand of GABAA receptors and it can displace [3H] 1-(2-chlorophenyl)-N-methyl-N-(1-methylpropyl)-3-isoquinolinecarboxamide (PK 11195) from its binding site on the peripheral benzodiazepine receptor (PBR). We assessed CYP2B levels in primary rat hepatocytes following treatment with 10 ligands of either or both of these receptors. All compounds tested were found to be CYP2B1/CYP2B2 inducers and most were CYP3A inducers. Five had not previously been described as CYP2B1/CYP2B2 inducers: bicuculline, flunitrazepam, 4′-chlorodiazepam (Ro5-4864), N,N-dihexyl-2-(4-fluorophenyl)indole-3-acetamide (FGIN 1–27) and 7-(dimethylcarbamoyloxy)-6-phenylpyrrolo-[2,1-d][1,5]benzothiazepine (DCPPBT). Reporter gene analysis demonstrated that CYP2B induction by these agents and other PBR or GABAA receptor ligands is mediated through the PBRU and the NR1/NR2 sites, suggesting a molecular mechanism similar to that for PB induction. The potencies for PBRU-dependent induction by 11 ligands of PBR or the GABAA receptor was evaluated. FGIN-127, DCPPBT and PK 11195 exhibited EC50 values for PBRU-dependent transcription activation about three orders of magnitude higher than the reported affinities of the PBR for these agents, arguing against the involvement of the PBR in PB induction. However the EC50 values found for the agents tested encourage further investigation on the possible involvement of the GABAA receptor in PB induction. [Copyright &y& Elsevier]