Ontology highlight
ABSTRACT:
PROVIDER: PRJNA597382 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10762453_1.fastq.gz | Fastqsanger.gz | |||
| SRR10762453_2.fastq.gz | Fastqsanger.gz | |||
| SRR10762454_1.fastq.gz | Fastqsanger.gz | |||
| SRR10762454_2.fastq.gz | Fastqsanger.gz | |||
| SRR10762455_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Living organisms are exposed on a daily basis to widespread mixtures of toxic compounds. Mixtures pose a major problem in the assessment of health effects because they often generate substance-specific effects that cannot be attributed to a single mechanism. Two compounds often found together in the environment are the heavy metal chromium and the polycyclic aromatic hydrocarbon benzo[a]pyrene (B[a]P). We have examined how long-term exposure to a low concentration of Cr(VI) affects the transcriptional response to B[a]P, a second toxicant with an unrelated mechanism of action. Growth of mouse hepatoma cells for 20 passages in medium with 0.1 or 0.5 uM Cr(VI) increases DNA damage and apoptosis and decreases clonogenic ability. These cells also show transcriptome changes indicative of increased expression of DNA damage response and repair genes. In them, B[a]P activates cancer progression pathways, unlike cells never exposed to Cr(VI), where B[a]P activates mostly xenobiotic metabolism pathways. Cells grown in Cr(VI) for 20 passages and then cultured for an additional 5 passages in the absence of Cr(VI) recover from some but not all the chromium effects. They show B[a]P-dependent transcriptome changes strongly weighted towards xenobiotic metabolism, similar to those in B[a]P-treated cells that had no previous Cr(VI) exposure, but retain a high level of Cr(VI)-induced DNA damage and silence the expression of DNA damage and cancer progression genes. We conclude that the combined effect of these two toxicants appears to be neither synergistic nor cumulative, generating a toxic/adaptive condition that cannot be predicted from the effect of each toxicant alone. Mouse Hepa-1 cells treated with Cr, Bap, Cr+Bap and untreated were profiled using RNAseq in duplicates.
2013-08-07 | E-GEOD-49571 | biostudies-arrayexpress
Project description:Hexavalent chromium (Cr(VI)) is a highly toxic contaminant, some bacteria are able to transform it to less toxic and less soluble trivalent chromium (Cr(III)). Klebsiella sp. strain AqSCr, isolated from Cr(VI)-polluted groundwater, reduces Cr(VI) both aerobically and anaerobically, and resists up 35 mM of Cr(VI); Subculturing of AqSCr in the presence of Cr(VI) conduces to adaptation. In this study, we performed RNA-Seq of Cr(VI) adapted stage, finding 255 genes upregulated and 240 downregulated with respect to controls without Cr(VI). Genes differentially expressed are mostly associated with oxidative stress response, DNA repair and replication, sulfur starvation response, envelope-osmotic stress response, fatty acid metabolism, ribosomal subunits and energy metabolism. Among them, genes not previously associated with chromium resistance as cybB, encoding a putative superoxide oxidase, gltA2, encoding an alternative citrate synthase, and des, encoding a fatty acid desaturase were upregulated. The alternative sigma factors fecl, rpoE and rpoS were upredgulated in Cr(VI) adapted cells, then they participate in orchestate the Cr(VI)-resistance mechanisms in AqSCr strain
2021-05-20 | GSE160968 | GEO
Project description:Living organisms are exposed on a daily basis to widespread mixtures of toxic compounds. Mixtures pose a major problem in the assessment of health effects because they often generate substance-specific effects that cannot be attributed to a single mechanism. Two compounds often found together in the environment are the heavy metal chromium and the polycyclic aromatic hydrocarbon benzo[a]pyrene (B[a]P). We have examined how long-term exposure to a low concentration of Cr(VI) affects the transcriptional response to B[a]P, a second toxicant with an unrelated mechanism of action. Growth of mouse hepatoma cells for 20 passages in medium with 0.1 or 0.5 uM Cr(VI) increases DNA damage and apoptosis and decreases clonogenic ability. These cells also show transcriptome changes indicative of increased expression of DNA damage response and repair genes. In them, B[a]P activates cancer progression pathways, unlike cells never exposed to Cr(VI), where B[a]P activates mostly xenobiotic metabolism pathways. Cells grown in Cr(VI) for 20 passages and then cultured for an additional 5 passages in the absence of Cr(VI) recover from some but not all the chromium effects. They show B[a]P-dependent transcriptome changes strongly weighted towards xenobiotic metabolism, similar to those in B[a]P-treated cells that had no previous Cr(VI) exposure, but retain a high level of Cr(VI)-induced DNA damage and silence the expression of DNA damage and cancer progression genes. We conclude that the combined effect of these two toxicants appears to be neither synergistic nor cumulative, generating a toxic/adaptive condition that cannot be predicted from the effect of each toxicant alone.
2013-08-07 | GSE49571 | GEO
Project description:Chromium (Cr) is a non-essential metal for normal plants and is toxic to plants at high concentration. In spite of many previous studies having been conducted on the effects of Cr stress, the precise molecular mechanisms and signaling pathways of action of Cr remain poorly understood. In this study, the transcriptome at the early of Cr (VI) stress were assayed in rice roots. To gain more insight into these cellular responses, we analyzed whole-genome transcriptome of rice expose to Cr (VI) for 1 and 3 h. Analysis revealed 1,261 and 267 up and down-regulated genes by Cr (VI). Cr (VI) stress triggered changes in transcript levels of genes related to secondary metabolism process, biosynthetic process, specially jasmonic acid biosynthetic process, response to abiotic stress, specially response to toxin, transcription regulator activity, specially transcription factors activity. The most predominant transcription factor families were WRKY, AP2/ERF, NAC, C2H2, MYB. In addition, many protein kinase, including eight MAPKKK, two CDPK, and one MAPK, showed significant increase in transcriptional level under Cr (VI) stress. Molecular mechanisms for the excess Cr(VI) in rice roots Comparison of mock control and rice seedlings treated with 200 M-NM-<M Cr(VI); Biological replicates: 3 control replicates, 3 Cr(VI)-treated replicates.
2013-10-31 | E-GEOD-33376 | biostudies-arrayexpress
Project description:Chromium (Cr) is an important environmental contaminant and also a genotoxic metal ion at high concentration, but its molecular mechanisms and signalling pathways of action in plants is still poorly unraveled. To help characterize the mechanism of molecular and signalling of rice, we present the large-scale, transcriptomic analysis of rice root responses to Cr(VI). We examined the possible involvement of reactive of reactive oxygen species (ROS) and calcium in Cr(VI) signaling transduction pathways, as well as the effect of Cr (VI) on CDPK and MAPK activity. Specially, we used the microarray assay to assess different stage Cr (VI) induced alteration in rice gene expression. This gene discovery effort will help expand our understanding of cellular responses to Cr (VI) treatment, and will identify candidate genes for enhancement of Cr resistance in crop.
2014-12-21 | GSE41733 | GEO
Project description:Chromium (Cr) is an important environmental contaminant and also a genotoxic metal ion at high concentration, but its molecular mechanisms and signalling pathways of action in plants is still poorly unraveled. To help characterize the mechanism of molecular and signalling of rice, we present the large-scale, transcriptomic analysis of rice root responses to Cr(VI). We examined the possible involvement of reactive of reactive oxygen species (ROS) and calcium in Cr(VI) signaling transduction pathways, as well as the effect of Cr (VI) on CDPK and MAPK activity. Specially, we used the microarray assay to assess different stage Cr (VI) induced alteration in rice gene expression. This gene discovery effort will help expand our understanding of cellular responses to Cr (VI) treatment, and will identify candidate genes for enhancement of Cr resistance in crop. Two-condition experiment, short exposures and long exposures. Comparison of mock control and rice seedlings treated with 50 μM Cr(VI) during short (pooled from 1- and 3-h treatments), as compared to long (24 h) exposures.; Biological replicates: 3 control replicates (short and long exposures), 3 Cr(VI)-treated replicates (short and long exposures).
2014-12-21 | E-GEOD-41733 | biostudies-arrayexpress
Project description:Hexavalent Chromium, Cr(VI), exposure is known to cause cancer and is a significant human health concern. While the effect of Cr(VI) exposure on exposed individuals is well studied, long-term effects of the same on the progeny of exposed individual are not known. In this study, using Drosophila model system, we show that Cr(VI) exposure of mothers leads to phenotypic variations in the progeny who have never been exposed to Cr(VI). These phenotypic variations arise due to epigenetic instability in the somatic tissues of the progeny rather than novel genetic mutations. Using a Drosophila cancer model system, we also show that maternal Cr(VI) exposure can lead to cancer phenotypes in the progeny and the propensity to cause cancer phenotypes in the progeny is fixed in the population for at least three generations. Thus, we show for the first time that effects of Cr(VI) exposure can last for several generations. This study also lays the foundation to use Drosophila model system to provide novel insights into Cr(VI) and other heavy metal toxicity.
2019-01-01 | GSE111834 | GEO
Project description:Hexavalent chromium compounds are well-established respiratory carcinogens utilized in industrial processes. While inhalation exposure constitutes an occupational risk affecting mostly chromium workers, environmental exposure from drinking water is a widespread gastrointestinal carcinogen, affecting millions of people throughout the world. Cr(VI) is genotoxic, by forming protein-Cr-DNA adducts and silencing tumor suppressor genes, but its mechanism of action at the molecular level is poorly understood. We have used FAIRE to show that Cr(VI) elicits broad changes in chromatin accessibility resulting from disruption of the binding of transcription factors CTCF and AP-1 to their cognate sites in chromatin. Here, we have used two complementary approaches to test the hypothesis that chromium perturbs chromatin organization and dynamics. DANPOS2 analyses of MNase.seq data identified several chromatin alterations induced by Cr(VI) affecting nucleosome architecture, including occupancy changes at specific genome locations; position shifts of 10 nucleotides or more; and fuzziness, or changes in signal amplitude. Using ATAC to analyze changes in chromatin accessibility, we found that Cr(VI) opened differentially accessible chromatin domains in a dose-dependent manner. These domains were enriched for the previously identified binding motifs for CTCF and AP-1, many located in promoters of differentially expressed genes. Cr(VI)-enriched CTCF sites were confirmed by ChIP.seq and, when compared with ENCODE-validated CTCF site datasets from mouse liver, correlated with evolutionarily conserved similar sites occupied in vivo. Our results show that Cr(VI) exposure promotes broad changes in chromatin accessibility and suggest that the subsequent dysregulation of transcription may result from the disruption of CTCF binding and nucleosome spacing, suggesting that transcription regulatory mechanisms are primary Cr(VI) targets.
2018-01-01 | GSE104565 | GEO