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Transcriptomics of selenium toxicity and deficiency in C. elegans (374.1)
Author(s) -
Boehler Christopher,
Raines Anna,
Sunde Roger
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.374.1
Subject(s) - transcriptome , caenorhabditis elegans , toxicity , selenium , biology , gene , selenoprotein , phenotype , axenic , gene expression profiling , microarray analysis techniques , gene expression , microbiology and biotechnology , biochemistry , genetics , chemistry , oxidative stress , catalase , glutathione peroxidase , organic chemistry , bacteria
Selenium (Se) is a trace element that is both essential and toxic. C. elegans expresses only 1 selenoprotein, and we have shown recently that Se is not essential but is toxic to C. elegans (PLOS ONE 8:e71525). To characterize Se regulation of the transcriptome, we conducted a microarray study in C. elegans cultured in axenic media with 0, 0.05, 0.1, 0.2 and 0.4 mM Se as selenite. Because worms cultured in 0.2 and 0.4 mM Se display delayed growth, all cultures were staged for harvest at the L4‐larval stage. Relative to 0.1 mM Se, this resulted in 2, 10, 6 and 2%, respectively, of the transcriptome being altered 蠅 2‐fold. C. elegans cultured in low Se (0 mM Se) exhibited no signs of deficiency, but a set of 222 genes changed 蠅 2‐fold; functional analysis revealed up‐regulation of genes related to lipid modification. Se toxicity (0.2 and 0.4 mM Se) altered the expression of 183 Se toxicity‐specific genes, after filtering against gene sets for sulfur and cadmium toxicity, that were significantly enriched in oxidoreductase genes, and significantly depleted in genes related to structural components of collagen and the cuticle. This study shows that while there is no phenotype associated with Se deficiency in C. elegans, low Se elicits a transcriptomic phenotype. In contrast, Se is toxic and elicits transcript changes supporting a hypothesis that derangement of cuticle thiols underlies altered development. Grant Funding Source : Supported by WIS 01435 and by UW Selenium Nutrition Research fund