The effects of dietary selenium on selenocysteine incorporation and selenoprotein expression
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE46038 | GEO | 2013/09/17
SECONDARY ACCESSION(S): PRJNA197001
REPOSITORIES: GEO
Similar Datasets
Project description:The goal of this study was to determine the effects of dietary selenium levels on translational control of selenoprotein synthesis in mouse liver. Wild type mice and mice expressing a mutant Sec-tRNA gene (TrspA37G) were fed diets supplemented with 0, 0.1, or 2 ppm selenium for 6 weeks. Livers were harvested and ribosome and mRNA profiles were generated by deep-sequencing using the Illumina HiSeq 2000.
2013-09-17 | E-GEOD-46038 | biostudies-arrayexpress
Project description:In this study, juvenile rainbow trout were exposed four dietary doses of organic selenium (7.1, 10.7 19.5 and 31.8 mg/kg Selenium) over 60 days. The RNA was exctracted from liver tissue and used for further gene expression analysis.
2015-06-30 | GSE67599 | GEO
Project description:In this study, juvenile rainbow trout were exposed four dietary doses of organic selenium (7.1, 10.7 19.5 and 31.8 mg/kg Selenium) over 60 days. The RNA was exctracted from liver tissue and used for further gene expression analysis. There were 39 samples analyzed (8) control liver tissues (8) 7.1 mg/kg Se dosed fish liver tissues (7) 10.7 mg/kg Se dosed fish liver tissues (8) 19.5 mg/kg Se dosed fish liver tissues (9) 31.8 mg/kg Se dosed fish liver tissues. There was a total of 39 microarrays processed.
2015-06-30 | E-GEOD-67599 | biostudies-arrayexpress
Project description:We tested the hypothesis that the behavioral response to selenium (Se) follows a hormetic dose response pattern, manifested through the functions of selenoproteins within the brain. We measured anxiety-related behaviors in zebrafish (Danio rerio) at deficient, control and supplemented levels of dietary Se, and measured the transcriptional response of selenoprotein genes important for neuroprotection. We also used a microarray approach to assess the transcriptomic response of the midbrain to Se. The behavioral response to Se was characterized by hormesis, and the direction, magnitude, and shape of the hormetic responses were dependent on both sex and zebrafish population. Transcription of selenoproteins within the midbrain also responded to Se in a similar hormetic dose-dependent manner, with sex and population influencing the trajectory of the responses. The hormetic behavioral response to Se may therefore be manifested through selenoproteins in the brain, but the influence is not direct.
2014-05-01 | GSE52484 | GEO
Project description:Expression of selenoproteins requires the co-translational incorporation of selenocysteine (Sec) in response to an in-frame UGA codon. The machinery of UGA/Sec re-coding is complex and many factors affect the hierarchy of expression among selenoproteins, including modification of tRNA[Ser]Sec. Its hyper-modification in the anticodon stem loop is influenced by selenium bioavailability, and a mutation in adenosine 37 (A37) that abrogates isopentenylation, has a profound effect on selenoprotein expression in mice. Patients with mutations in tRNA-isopentenyl-transferase (TRIT1) show a severe neurological disorder and hence we wondered whether mutations in TRIT1 negatively affected the expression of selenoproteins. Fibroblasts from a patient carrying a pathogenic R323Q mutation in TRIT1 in homozygosity did not show decreased selenoprotein expression, although recombinant TRIT1R323Q had significantly reduced activity in vitro towards anticodon stem-loop substrates. We thus engineered mice conditionally deficient in Trit1 in hepatocytes and neurons. Selenoprotein expression as assessed by western blotting, 75Se metabolic labeling, and ribosomal profiling was not decreased despite the general reduction of N6-isopentenyl-adenosine in tRNAs. We show that 5-methylcarboxymethylation and 2’O-methylation of U34 occur independently of isopentenylation of A37 in tRNA[Ser]Sec. Reanalyzing previously published ribosomal profiling datasets, we demonstrate that (i) failure of 5-carboxymethylation at U34 is associated with reduced expression of GPX1, but not GPX4, and that (ii) FTSJ1 is not the elusive U34-2’O-methyltransferase involved in the methylation of tRNA[Ser]Sec.
2021-11-17 | GSE183923 | GEO
Project description:We tested the hypothesis that the behavioral response to selenium (Se) follows a hormetic dose response pattern, manifested through the functions of selenoproteins within the brain. We measured anxiety-related behaviors in zebrafish (Danio rerio) at deficient, control and supplemented levels of dietary Se, and measured the transcriptional response of selenoprotein genes important for neuroprotection. We also used a microarray approach to assess the transcriptomic response of the midbrain to Se. The behavioral response to Se was characterized by hormesis, and the direction, magnitude, and shape of the hormetic responses were dependent on both sex and zebrafish population. Transcription of selenoproteins within the midbrain also responded to Se in a similar hormetic dose-dependent manner, with sex and population influencing the trajectory of the responses. The hormetic behavioral response to Se may therefore be manifested through selenoproteins in the brain, but the influence is not direct. We performed a microarray analysis comparing the midbrain-specific transcriptome between male zebrafish from two populations (Pargana: P and Transgenic Mosaic 1: T) fed either a control, Se deficient, or Se supplemented diet (17 total samples: 9 fish per population, 3 fish per diet: missing 1 P control sample).
2014-05-01 | E-GEOD-52484 | biostudies-arrayexpress
Project description:Protein and mRNA levels for several selenoproteins, such as glutathione peroxidase-1 (Gpx1), are down-regulated dramatically by selenium (Se) deficiency. Selenoprotein levels in rats increase sigmoidally with increasing dietary Se and reach defined plateaus at the Se requirement, making them sensitive biomarkers for Se deficiency, but not high for Se status. Biomarkers for high Se status are needed as super-nutritional Se intakes are associated with beneficial and adverse health outcomes, but conventional biomarkers are not especially useful above the Se requirement. To characterize Se regulation of the transcriptome, we conducted 3 microarray experiments in weanling mice and rats fed Se-deficient diets supplemented with levels of Se up to 5 µg Se/g diet.
2011-01-19 | GSE23895 | GEO
Project description:Selenium is an essential micronutrient. Its recommended daily allowance is not attained by a significant proportion of the population in many countries and its intake has been suggested to affect colorectal carcinogenesis. Therefore, microarrays were used to determine how both selenoprotein and global gene expression patterns in the mouse colon were affected by marginal selenium deficiency comparable to variations in human dietary intakes. Two groups of 12 mice each were fed a selenium-deficient (0.086mg Se/kg) or a selenium-adequate (0.15mg Se/kg) diet. After 6wk, plasma selenium level, liver, and colon glutathione peroxidase (GPx) activity in the deficient group was 12, 34, and 50%, respectively, of that of the adequate group. Differential gene expression was analysed with mouse 44K whole genome microarrays. Pathway analysis by GenMAPP identified the protein biosynthesis pathway as most significantly affected, followed by inflammation, Delta-Notch and Wnt pathways. Selected gene expression changes were confirmed by quantitative real-time PCR. GPx1 and the selenoproteins W, H, and M, responded significantly to selenium intake making them candidates as biomarkers for selenium status. Thus, feeding a marginal selenium-deficient diet resulted in distinct changes in global gene expression in the mouse colon. Modulation of cancer-related pathways may contribute to the higher susceptibility to colon carcinogenesis in low selenium status.
2018-07-13 | GSE117025 | GEO
Project description:Selenoprotein P is a hepatokine which is essential for maintaining systemic selenium homeostasis and is used as serum biomarker for the selenium status in humans. In addition to selenium, also copper homeostasis is mainly regulated by the liver coordinating systemic distribution of copper bound to ceruloplasmin or excreting surplus copper into the bile. Circulating selenium and copper concentrations are most often negatively correlating, e.g. during aging copper levels are increasing while selenium levels are decreasing. Based on these results, we addressed the question of how both trace elements interfere with each other using the liver-derived cell line HepG2. We observed that copper treatment resulted in a substantial increase of intracellular selenium concentrations. In parallel, extracellular SELENOP concentrations were drastically reduced while SELENOP accumulated within the cells. The same observation was made when using primary murine hepatocytes. Indeed, SELENOP was one of the proteins most strongly downregulated by copper in an untargeted secretome approach. Accumulation of hepatic copper is a characteristic of Wilson’s disease. Accordingly, SELENOP levels were decreasing in the serum of LPP rats, a model of Wilson’s disease starting at disease onset. Also, Wilson’s disease patients showed reduced serum SELENOP concentrations when circulating copper concentrations were low. This positive correlation between copper and ceruloplasmin and SELENOP was also observed in a GWAS analysis of EPIC-Potsdam samples identifying SNP rs11708215 as a modulating factor. Our data indicate that under conditions of a suboptimal selenium supply combined with a high copper intake a functional selenium deficit can become even worse because peripheral tissues such as the brain depend on SELENOP for their selenium supply.
2023-07-20 | PXD036300 | Pride
Project description:Protein and mRNA levels for several selenoproteins, such as glutathione peroxidase-1 (Gpx1), are down-regulated dramatically by selenium (Se) deficiency. Selenoprotein levels in rats increase sigmoidally with increasing dietary Se and reach defined plateaus at the Se requirement, making them sensitive biomarkers for Se deficiency, but not high for Se status. Biomarkers for high Se status are needed as super-nutritional Se intakes are associated with beneficial and adverse health outcomes, but conventional biomarkers are not especially useful above the Se requirement. To characterize Se regulation of the transcriptome, we conducted 3 microarray experiments in weanling mice and rats fed Se-deficient diets supplemented with levels of Se up to 5 µg Se/g diet. Rats or mice were fed Se-deficient diets supplemented with sodium selenite up to 5 ug Se/g diet for 28 or 35 days. Affymetrix Rat 230 2.0 and Mouse 430 2.0 Genome Arrays were used to analyze gene expression in liver in all studies plus kidney in the mouse study.
2011-01-19 | E-GEOD-23895 | biostudies-arrayexpress