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C. Elegans expression: toxic vs. adequate vs. low selenium

ABSTRACT: Genome-wide expression analysis in C. Elegans grown in axenic media with low to toxic selenium concentrations We performed Affymetrix micorarray-based transcriptional profiling on wild-type C. Elegans Bristol N2 grown in low Se axenic media supplemented with five concentrations of selenium, from low to toxic, and harvested at the L4-larva stage.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE54011 | GEO | 2014/07/03

SECONDARY ACCESSION(S): PRJNA234349

REPOSITORIES: GEO

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C. Elegans expression: toxic vs. adequate vs. low selenium

Project description:Genome-wide expression analysis in C. Elegans grown in axenic media with low to toxic selenium concentrations We performed Affymetrix micorarray-based transcriptional profiling on wild-type C. Elegans Bristol N2 grown in low Se axenic media supplemented with five concentrations of selenium, from low to toxic, and harvested at the L4-larva stage. RNA was prepared for hybridization to Affy microarrays from synchronized cultures of wild-type C. elegans seeded in low Se axenic media, supplemented with graded 0, 0.05, 0.1, 0.2, and 0.4 mM Se added as sodium selenite, and harvested at the L4-larva stage (1 culture/sample per Se concentgration).

2014-07-03 | E-GEOD-54011 | biostudies-arrayexpress

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Project description:C. Elegans expression: toxic vs. adequate vs. low selenium

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Deep sequencing of endogenous mRNA from Caenorhabditis elegans in the presence and absence of arsenite

Project description:Background: Arsenite is one of the most toxic chemical substances known and is assumed to exert detrimental effects on viability even at lowest concentrations. By contrast and unlike higher concentrations, we here find that exposure to low-dose arsenite promotes growth of cultured mammalian cells. In the nematode C. elegans, low-dose arsenite promotes resistance against thermal and chemical stressors, and extends lifespan of this metazoan, whereas higher concentrations reduce longevity. While arsenite causes a transient increase in reactive oxygen species (ROS) levels in C. elegans, co-exposure to ROS scavengers prevents the lifespan-extending capabilities of arsenite, indicating that transiently increased ROS levels act as transducers of arsenite effects on lifespan, a process known as mitohormesis. The RNA-seq data comprises 2 biological replicates for worms exposed to 100nM Arsenite 48h after L4 and 2 biological replicates of the same age as controls 4 samples: 2 mRNA profiles of C.elegans 48h after L4 exposed to Arsenite; 2 mRNA profiles of C.elegans 48h after L4 as controls (H20). The N2 wild type (var. Bristol) strain was used.

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Expression analysis of Caenorhabditis elegans Bristol N2 prg-1 and Bristol N2 prg-1; daf-2 double mutant

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Sequencing of endogenous mRNA from Caenorhabditis elegans at two time points in the presence and absence of arsenite

Project description:Background: Arsenite is one of the most toxic chemical substances known and is assumed to exert detrimental effects on viability even at lowest concentrations. By contrast and unlike higher concentrations, we here find that exposure to low-dose arsenite promotes growth of cultured mammalian cells. In the nematode C. elegans, low-dose arsenite promotes resistance against thermal and chemical stressors, and extends lifespan of this metazoan, whereas higher concentrations reduce longevity. While arsenite causes a transient increase in reactive oxygen species (ROS) levels in C. elegans, co-exposure to ROS scavengers prevents the lifespan-extending capabilities of arsenite, indicating that transiently increased ROS levels act as transducers of arsenite effects on lifespan, a process known as mitohormesis. Worms were exposed to 100nM Arsenite 48h after L4. Jena Centre for Systems Biology of Ageing - JenAge (www.jenage.de)

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Copper impairs hepatic selenoprotein P release

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.

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Deep sequencing of endogenous mRNA from Caenorhabditis elegans in the presence and absence of arsenite

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Expression analysis of Caenorhabditis elegans Bristol N2 prg-1 and Bristol N2 prg-1; daf-2 double mutant

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2013-06-01 | E-GEOD-40569 | biostudies-arrayexpress

Expression analysis of Caenorhabditis elegans Bristol N2 rsd-2 and rsd-6 single mutants at 25Â°C and 20Â°C

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