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Mechanisms of nickel toxicity in bacteria

ABSTRACT: We report the effects of a nickel stress on the transcriptome of Escherichia coli coli cells, evaluated by RNA-Seq experiments

ORGANISM(S): Escherichia coli

PROVIDER: GSE76167 | GEO | 2016/07/01

SECONDARY ACCESSION(S): PRJNA306510

REPOSITORIES: GEO

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Mechanisms of nickel toxicity in bacteria

Project description:We report the effects of a nickel stress on the transcriptome of Escherichia coli coli cells, evaluated by RNA-Seq experiments Comparison between wild type E. coli grown in miminal media in the presence or not of 50 ÂµM NiCl2 during 10 min - 2 conditions compared with 3 replicates each

2016-07-01 | E-GEOD-76167 | biostudies-arrayexpress

Transcriptomics data on E. coli lacking queuosine tRNA modification (tgt deficient strain) exposed or not to nickel stress.

Project description:Purpose: to observe differences in E. coli transcripts levels due to the absence of the tRNA modification queuosine and due to exposure to excess nickel. Methods: RNAseq was performed using the total RNA isolated from E. coli MG1655 WT and Δtgt strains grown in LB medium only or in LB added by 2 mM NiCl2. Results: in nickel-treated WT compared to untreated WT (WT_Ni/WT_LB) 734 genes were found up-regulated and 1,642 genes down-regulated in the treated cells; in the tgt mutant compared to the WT strain (tgt_LB/WT_LB), 417 genes were found up regulated and 1,053 genes down regulated in the tgt mutant. Conclusions: the gene expression pattern of the tgt deficient cell in LB medium resembles the one of the WT strain exposed to nickel, showing repression of iron-import genes and genes associated to anaerobic metabolism; increased resistance to nickel stress observed in the tgt mutant is explained by the repression of the nickel import system nikABCCDE.

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Project description: Not available

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Nickel Chloride (NiCl2) effect on human T cells from whole blood

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Project description:Our findings demonstrate that nickel-challenged skin in subjects with allergy to nickel is characterized by a specific miRNA signature compared to vehicle-challenged skin. In addition, we found that miRNA expression changes are different in allergic contact dermatitis (ACD to nickel) compared to irritant contact dermatitis (ICD).

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Project description:Nickel-resistant Saccharomyces cerevisiae mutant was obtained by evolutionary engineering. The reference strain which was used to select this nickel-resistant mutant could not grow even at 0.5 mM NiCl2 whereas this mutant was shown to be resistant upto 5.3 mM NiCl2 concentration. Whole-genome microarray analysis might be promising to identify the nickel resistance mechanisms in the yeast cells.

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Nickel-induced transcriptional memory in lung epithelial cells promotes interferon signaling upon nicotine exposure

Project description:Nickel is an environmental toxicant prevalent in the atmosphere. Nickel exposure is associated with a multitude of human health hazards including chronic respiratory ailments and lung and nasal cancers. Our earlier studies on nickel exposure in lung cells showed that a majority of the gene expression changes caused by nickel exposure persisted even after termination of exposure (nickel-washed-out cells (NiW)). In this study, we wanted to examine the impact of a secondary toxicant exposure on the nickel-washed-out (NiW) cells as compared to the cells that were never exposed to nickel. To accomplish this, we exposed the untreated control cells (UT) and the nickel-washed-out cells (NiW) to multiple doses of nicotine (NTE). RNA-Seq analysis showed that the exposure of NiW cells to nicotine (NiW-NTE) caused unique gene expression changes that were markedly different from the gene expression changes caused by nicotine exposure of UT cells, which were never exposed to nickel. Analysis of the differentially expressed genes using Reactome Pathway analysis predicted interferon signaling only in the NiW-NTE cells. Upstream Regulator Analysis (URA) predicted STAT-1, a transcription factor that mediates cellular response to interferons, as the top potential upstream regulator in the NiW-NTE cells. Furthermore, chromatin immunoprecipitation (ChIP) analysis revealed increased STAT-1 binding at the promoters of genes associated with interferon signaling in NiW-NTE cells. Aberrant STAT-1 activation has been shown to promote carcinogenesis and interferon signaling promotes pathogenesis of autoimmune disease. Therefore, our results suggest that the epigenetic and transcriptional memory of the cells from the previous nickel exposure could negatively influence the outcome of secondary exposure to nicotine.

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Allergic contact dermatitis to nickel is characterized by a specific microRNA signature [PBMCs]

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