Ontology highlight
ABSTRACT:
PROVIDER: PRJNA665310 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12705453_1.fastq.gz | Fastqsanger.gz | |||
| SRR12705453_2.fastq.gz | Fastqsanger.gz | |||
| SRR12705454_1.fastq.gz | Fastqsanger.gz | |||
| SRR12705454_2.fastq.gz | Fastqsanger.gz | |||
| SRR12705455_1.fastq.gz | Fastqsanger.gz |
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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: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: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: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.
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