Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8781990_1.fastq.gz | Fastqsanger.gz | |||
| SRR8781990_2.fastq.gz | Fastqsanger.gz | |||
| SRR8781991_1.fastq.gz | Fastqsanger.gz | |||
| SRR8781991_2.fastq.gz | Fastqsanger.gz | |||
| SRR8781992_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
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: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 | GSE104563 | 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 | GSE104564 | 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
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
2013-10-31 | GSE33376 | GEO
Project description:The ability of chromatin to switch back and forth from open euchromatin to closed heterochromatin is vital for transcriptional regulation and genomic stability, and subject to disruption by exposure to environmental agents such as hexavalent chromium. Cr(VI) exposure can cause chromosomal disruption through formation of Cr-DNA adducts, free radical-induced DNA damage, and DNA-Cr-protein and DNA-Cr-DNA cross-links, all of which may disrupt chromatin remodeling mechanisms responsible for maintenance or controlled modification of epigenetic homeostasis. In addition, dose-response analyses have shown that acute exposures to high-concentrations of Cr(VI) and chronic exposures to low-concentrations of the same agent lead to significantly different transcriptomic and genomic stability outcomes. To investigate how transcriptional responses to chromium exposure might correlate to structural changes in chromatin, we have used whole genome Formaldehyde-Assisted Isolation of Regulatory Elements (FAIRE) analysis coupled with deep sequencing to identify regions of the genome that switch from open to closed chromatin or vice versa in response to exposure to varying Cr(VI) concentrations. We find that the switch affects gene expression levels in the target areas that vary depending on Cr(VI) concentration. At either Cr(VI) concentration, chromatin domains surrounding binding sites for AP-1 transcription factors become significantly open, treatment whereas BACH2 and CTCF binding sites are open solely at the low and high concentrations, respectively. Our results suggest that FAIRE may be a useful technique to map chromatin elements targeted by DNA damaging agents for which there is no prior knowledge of their specificity, and to identify subsequent transcriptomic changes induced by those agents.
2014-04-10 | GSE56636 | GEO