Ontology highlight
ABSTRACT:
PROVIDER: PRJNA642007 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| JACAAL01.dat.gz | Other | |||
| JACAAL01.fasta.gz | Fasta.gz | |||
| JACAAL01.master.dat | Other | |||
| SRR12109700_1.fastq.gz | Fastqsanger.gz |
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Project description:Suspended cell studies were performed to document whole-genome transcriptional profiles as a function of Cr(VI) reduction under different electron accepting conditions. Cell suspension studies were performed in 250 mL serum bottles for two conditions: 1) under anoxic condition with lactate as carbon source and nitrate as electron acceptor, and 2) under aerobic condition with lactate as carbon source and oxygen as electron acceptor. The initial Cr(VI) and nitrate concentrations were 1000 μg/L and 40 mg N/L, respectively. Samples from both the conditions were collected after 5 hours and the cell pellet was saved at -80°C.
2021-08-11 | GSE181731 | 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.
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:Columns containing Hanford 100H aquifer sediment continuously infused with 5 mM lactate, 5 uM Cr(VI), and either 7.5 mM sulfate or 12 mM nitrate as an electron acceptor.
2014-04-08 | GSE56554 | GEO
Project description:Columns containing Hanford 100H aquifer sediment continuously infused with 5 mM lactate, 5 uM Cr(VI), and either 7.5 mM sulfate or 12 mM nitrate as an electron acceptor. A two-chip study using total RNA extracted from unfiltered effluent from columns (nitrate or sulfate infused).
2014-04-08 | E-GEOD-56554 | 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: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