16 research outputs found

    Seasonal Differences in Relative Gene Expression of Putative Central Appetite Regulators in Arctic Charr (Salvelinus alpinus) Do Not Reflect Its Annual Feeding Cycle

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    The highly seasonal anadromous Arctic charr (Salvelinus alpinus) was used to investigate the possible involvement of altered gene expression of brain neuropeptides in seasonal appetite regulation. Pro-opiomelanocortin (POMCA1, POMCA2), Cocaine and amphetamine regulated transcript (CART), Agouti related Peptide (AgRP), Neuropeptide Y (NPY) and Melanocortin Receptor 4 (MC4-R) genes were examined. The function of centrally expressed Leptin (Lep) in fish remains unclear, so Lep (LepA1, LepA2) and Leptin Receptor (LepR) genes were included in the investigation. In a ten months study gene expression was analysed in hypothalamus, mesencephalon and telencephalon of immature charr held under natural photoperiod (69°38’N) and ambient temperature and given excess feed. From April to the beginning of June the charr did not feed and lost weight, during July and August they were feeding and had a marked increase in weight and condition factor, and from November until the end of the study the charr lost appetite and decreased in weight and condition factor. Brain compartments were sampled from non-feeding charr (May), feeding charr (July), and non-feeding charr (January). Reverse transcription real-time quantitative PCR revealed temporal patterns of gene expression that differed across brain compartments. The non-feeding charr (May, January) had a lower expression of the anorexigenic LepA1, MC4-R and LepR in hypothalamus and a higher expression of the orexigenic NPY and AgRP in mesencephalon, than the feeding charr (July). In the telencephalon, LepR was more highly expressed in January and May than in July. These results do not indicate that changes in central gene expression of the neuropeptides investigated here directly induce seasonal changes in feeding in Arctic charr

    Seaward migrating Atlantic salmon smolts with low levels of gill Na+, K+ -ATPase activity : is sea entry delayed?

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    Two groups of migrating wild Atlantic salmon (Salmo salar) smolts caught within a 1 week interval in the River Alta, northern Norway, were tagged with acoustic transmitters and measured for gill Na+, K+ -ATPase activity in order to compare their smolt status with timing of sea entry. The first group of smolts had low levels of gill Na+, K+ -ATPase activity and resided in the lower part of the river twice as long as the second group that had high levels of gill Na+, K+ -ATPase activity. This indicates that early migrating smolts may not be completely physiologically adapted for salt water and delay their sea entry, thereby also synchronizing their seaward migration with the later migrating smolts.Seaward migrating Atlantic salmon smolts with low levels of gill Na+, K+ -ATPase activity; is sea entry delayed? [Published online: 16 november 2010

    Body mass development (A) and Fulton’s Condition Factor <i>K</i> (B) of the fish sampled for mRNA quantification.

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    <p>Black dots: Sampled in May 2012, White dots: Sampled in July 2012, Triangles: Sampled in January 2013. Data are presented as mean (n = 10) ± s.e.m. Dotted line: temperature profile. White area: hours of daylight.</p

    Testing for differences across sampling time points (p-values for ANOVA and Tukey’s Honestly-Significant-Test).

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    <p>Ma—Ju = May tested against July, Ju—Ja = July tested against January, Ma—Ja = May tested against January. n.d.: no data (due to low expression level and/or poor melt curve). n.s.: not significant</p><p>Testing for differences across sampling time points (p-values for ANOVA and Tukey’s Honestly-Significant-Test).</p

    Stomach content in % of body mass (BM), and gonadosomatic index (<i>GSI</i>) in % of BM of anadromous Arctic charr (<i>n</i> = 10) sampled during study.

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    <p>Stomach content in % of body mass (BM), and gonadosomatic index (<i>GSI</i>) in % of BM of anadromous Arctic charr (<i>n</i> = 10) sampled during study.</p

    Relative gene expression in the hypothalamus (A), the mesencephalon (B), and the telencephalon (C) in May 2012 and January 2013.

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    <p>Expression levels in brain compartments sampled in May 2012 and January 2013 are presented relative to those sampled in July 2012 (July data were used as calibrator samples and were set equal to one as indicated by the dashed line). Data are presented as mean (n = 8–10) ± s.e.m.</p

    Forward (F) and reverse (R) primer sequences used for cDNA amplification by qPCR.

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    <p>All primers were produced and verified by PrimerDesign Ltd (Southampton, UK). Bp = product length in base pairs. Efficiencies were tested using serial dilutions.</p><p>Forward (F) and reverse (R) primer sequences used for cDNA amplification by qPCR.</p

    Diversified regulation of circadian clock gene expression following whole genome duplication

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    Across taxa, circadian control of physiology and behavior arises from cell-autonomous oscillations in gene expression, governed by a networks of so-called ‘clock genes’, collectively forming transcription-translation feedback loops. In modern vertebrates, these networks contain multiple copies of clock gene family members, which arose through whole genome duplication (WGD) events during evolutionary history. It remains unclear to what extent multiple copies of clock gene family members are functionally redundant or have allowed for functional diversification. We addressed this problem through an analysis of clock gene expression in the Atlantic salmon, a representative of the salmonids, a group which has undergone at least 4 rounds of WGD since the base of the vertebrate lineage, giving an unusually large complement of clock genes. By comparing expression patterns across multiple tissues, and during development, we present evidence for gene- and tissue-specific divergence in expression patterns, consistent with functional diversification of clock gene duplicates. In contrast to mammals, we found no evidence for coupling between cortisol and circadian gene expression, but cortisol mediated non-circadian regulated expression of a subset of clock genes in the salmon gill was evident. This regulation is linked to changes in gill function necessary for the transition from fresh- to sea-water in anadromous fish. Overall, this analysis emphasises the potential for a richly diversified clock gene network to serve a mixture of circadian and non-circadian functions in vertebrate groups with complex genomes
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