Sodium fluoride exposure leads to ATP depletion and altered RNA decay in Escherichia coli under anaerobic conditions
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PROVIDER: PRJNA870936 | ENA |
REPOSITORIES: ENA
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Project description:We report genome-wide transcriptome profiles of E. coli obtained in the absence (control) and presence of 20 mM and 70 mM sodium fluoride (NaF) under anaerobic conditions, and assess the impact of fluoride-dependent ATP depletion on RNA turnover. We found that transcripts with increased abundance in response to NaF treatment correspond to genes that control cell envelope and osmotic stress adaptation, signal transduction systems, lipid biosynthesis, amine and polyamine degradation as well as acquisition of iron and iron homeostasis. In contrast, downregulated genes are involved in glycolysis, fatty acid metabolism, amino acid biosynthesis, energy production, cytochrome c biogenesis, protein translocation, translation, translation factors, protein folding/processing factors, transport for amino acid, sugar, or ion, and RNA metabolism. By using a quantile-based K-means clustering approach to identify gene clusters with similar expression profiles, we identified subset (100 genes) of transcriptome whose gene expression was up- and down-regulated under fluoride and diluted fluoride conditions, respectively. In addition, we found that about 40% of the highly abundant transcripts carry repetitive extragenic palindromes (REPs). By determining the mRNA stability of osmC as well as yghA, and addressing their ribonucleases/enzymes required for RNA degradation under anaerobic conditions, we found that fluoride ions slow down RNA degradation by increasing RNA stability, in turn increasing the steady-state level of RNA. Furthermore, our results show that turnover of these REP-containing transcripts is dependent on RNase E. Collectively, our study not only reveal the effects of NaF at the whole transcriptome level under hypoxic growth conditions, but also shows that fluoride can affect gene expression post-transcriptionally by slowing down the ATP-dependent degradation of structured RNAs.
2023-03-10 | GSE211579 | GEO
Project description: Not available
| S-EPMC10100675 | biostudies-literature
Project description:Although an appropriate range of fluoride is thought to be safe and effective, excessive fluoride intake results in toxic effects in either hard tissues of teeth and skeleton or soft tissues of kidney, lung and brain. It is also well known that fluoride at a millimolar range elicits the complex cellular responses such as enzyme activity, signal transduction and apoptosis in many kinds of cells. However, its toxic effects are still unclear. In this study, to identify genes involved in cell death induced by sodium fluoride (NaF) in rat oral epithelial ROE2 cells, global-scale gene expression analysis was carried out using a GeneChip® system.
2014-01-09 | GSE53937 | GEO
Project description:Fluorosis is caused due to excess of fluoride intake over a long period of time. Aberrant change in RUNX2-mediated signaling cascade is one of the decisive steps during the pathogenesis of fluorosis. Till date, role of fluoride on the epigenetic alterations is not studied. In the present study, global expression profiling ofshort non-coding RNAs, in particular miRNAs and snoRNAs was carried out in NaF treated HOS cells to understand their possible role in the development of fluorosis. RT-PCR and insilico hybridization revealed that miR-124 and miR-155 can be directly involved in the transcriptional regulation of RUNX2 and RANKL genes. Compare to control, C/D box analysis revealed mark elevation in the number of UG dinucleotides and D-box sequences in NaF exposed HOS cells. Herein, we report miR-124 and miR-155 as the new possible players involved in the development of fluorosis. We also state that the alterations in UG dinucleotides and D-box sequences of snoRNAs could be due to NaF exposure. HOS cells grown on MEM media were treated with sodium fluoride and total RNA was isolated from cells after one month of chronic exposure; Cells grown on six 25mm flask. two replicates of control and two different concentration of exposed samples; two replicate are served as control
2015-01-01 | E-GEOD-57550 | biostudies-arrayexpress
Project description:Although an appropriate range of fluoride is thought to be safe and effective, excessive fluoride intake results in toxic effects in either hard tissues of teeth and skeleton or soft tissues of kidney, lung and brain. It is also well known that fluoride at a millimolar range elicits the complex cellular responses such as enzyme activity, signal transduction and apoptosis in many kinds of cells. However, its toxic effects are still unclear. In this study, to identify genes involved in apoptosis induced by sodium fluoride (NaF) in rat oral epithelial ROE2 cells, global-scale gene expression analysis was carried out using a GeneChipM-BM-. system. NaF (2 mM) significantly induced apoptosis accompaning chromatin condensation and caspase-3 activation. Total RNA samples were prepared from the NaF-treated cells, and quality of the RNA was analyzed using a Bioanalyzer 2100. Gene expression was monitored by an Affymetrix GeneChipM-BM-. system with a Rat Genome 230 2.0 array. Sample preparation for array hybridization was carried out as described in the manufacturerM-bM-^@M-^Ys instructions.
2014-01-09 | E-GEOD-53937 | biostudies-arrayexpress
Project description:EFFECTS OF SODIUM FLUORIDE OVER ORAL BACTERIAL BIOFILMS COMPOSITION AND ACTIVITY
| PRJEB35662 | ENA
Project description:Fluorosis is caused due to excess of fluoride intake over a long period of time. Aberrant change in RUNX2-mediated signaling cascade is one of the decisive steps during the pathogenesis of fluorosis. Till date, role of fluoride on the epigenetic alterations is not studied. In the present study, global expression profiling ofshort non-coding RNAs, in particular miRNAs and snoRNAs was carried out in NaF treated HOS cells to understand their possible role in the development of fluorosis. RT-PCR and insilico hybridization revealed that miR-124 and miR-155 can be directly involved in the transcriptional regulation of RUNX2 and RANKL genes. Compare to control, C/D box analysis revealed mark elevation in the number of UG dinucleotides and D-box sequences in NaF exposed HOS cells. Herein, we report miR-124 and miR-155 as the new possible players involved in the development of fluorosis. We also state that the alterations in UG dinucleotides and D-box sequences of snoRNAs could be due to NaF exposure.
2015-01-01 | GSE57550 | GEO
Project description:Fluoride is a highly abundant, naturally occurring toxicant that causes oxidative stress, cell cycle arrest, and apoptosis at high concentrations. Our lab has created a fluoride-sensitized yeast model lacking fluoride exporters, FEX1 and FEX2. These yeast undergo cell cycle arrest and apoptosis at over 1000-fold less fluoride concentration than in wild type, and oxidative stress within four hours. To determine the mechanism by which fluoride triggers oxidative stress, we grew cells in 25 mL YPD media at starting O.D. 0.1 in +/- 50 uM NaF. After four hours, the cells were washed twice with sterile water, and RNA was harvested and treated with DNAse. RNA was then sent to the the Yale Center for Genome Analysis for quality analysis with a Bioanalyzer and subsequent poly-A sequencing.
2021-12-02 | E-MTAB-8061 | biostudies-arrayexpress
Project description:Fluoride toxicity in multiple organs has been extensively reported in several decades of research. In-depth study coverage is available on teeth and bone tissues. But studies addressing skeletal muscle fluorosis are scanty. C57BL/6 mice were provided with sodium fluoride in drinking water for 60 days. Histological analysis, primary culture of skeletal muscle was performed. Protein expressions were analyzed by Immunocytochemistry, qRT-PCR, and western blotting techniques. Proteomic approach was considered to overview the entire proteome response. Exposure to sodium fluoride resulted in the loss of body weight in C57BL/6 mice. The compactness of the myofibre arrangement was distorted due to the treatment. Major reduction of contractile proteins such as actinin, troponin, and myosin further loss of mitochondrial proteins were confirmed by proteomic approach. Sodium fluoride treatment altered mitochondrial function. Further, loss of contractile proteins triggered skeletal muscle weakness.
2023-03-11 | PXD035014 | Pride
Project description:Though fluoride is considered an essential trace element, chronic exposure to fluoride is known to cause toxic effects. Chronic exposure of high concentration of fluoride may leads to fluorosis. To understand the molecular mechanism of fluoride induced toxicity gene expression profiling was performed on osteosarcoma cells (HOS). Cells were exposed to sub-lethal concentration of fluoride (8 ppm) for 30 days. Our result demonstrates that fluoride alters multiple biological pathways including bone development, osteoblast differentiation and apoptotic pathways.
2016-06-30 | GSE70719 | GEO