Sequencing of endogenous mRNA from Caenorhabditis elegans at two time points in the presence and absence of arsenite
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ABSTRACT:
ORGANISM(S): Caenorhabditis elegans
PROVIDER: GSE110845 | GEO | 2021/10/19
REPOSITORIES: GEO
Similar Datasets
Project description:Background: Arsenite is one of the most toxic chemical substances known and is assumed to exert detrimental effects on viability even at lowest concentrations. By contrast and unlike higher concentrations, we here find that exposure to low-dose arsenite promotes growth of cultured mammalian cells. In the nematode C. elegans, low-dose arsenite promotes resistance against thermal and chemical stressors, and extends lifespan of this metazoan, whereas higher concentrations reduce longevity. While arsenite causes a transient increase in reactive oxygen species (ROS) levels in C. elegans, co-exposure to ROS scavengers prevents the lifespan-extending capabilities of arsenite, indicating that transiently increased ROS levels act as transducers of arsenite effects on lifespan, a process known as mitohormesis. The RNA-seq data comprises 2 biological replicates for worms exposed to 100nM Arsenite 48h after L4 and 2 biological replicates of the same age as controls 4 samples: 2 mRNA profiles of C.elegans 48h after L4 exposed to Arsenite; 2 mRNA profiles of C.elegans 48h after L4 as controls (H20). The N2 wild type (var. Bristol) strain was used.
2013-04-23 | E-GEOD-46257 | biostudies-arrayexpress
Project description:Background: Arsenite is one of the most toxic chemical substances known and is assumed to exert detrimental effects on viability even at lowest concentrations. By contrast and unlike higher concentrations, we here find that exposure to low-dose arsenite promotes growth of cultured mammalian cells. In the nematode C. elegans, low-dose arsenite promotes resistance against thermal and chemical stressors, and extends lifespan of this metazoan, whereas higher concentrations reduce longevity. While arsenite causes a transient increase in reactive oxygen species (ROS) levels in C. elegans, co-exposure to ROS scavengers prevents the lifespan-extending capabilities of arsenite, indicating that transiently increased ROS levels act as transducers of arsenite effects on lifespan, a process known as mitohormesis. The RNA-seq data comprises 2 biological replicates for worms exposed to 100nM Arsenite 48h after L4 and 2 biological replicates of the same age as controls Jena Centre for Systems Biology of Ageing - JenAge (www.jenage.de)
2013-04-23 | GSE46257 | GEO
Project description:Gebauer2016 - Genome-scale model of
Caenorhabditis elegans metabolism (without bacteria)
This model is one of the two versions
of ElegCyc presented in the paper. It describes the metabolism of a
worm raised in a medium without bacteria.
This model is described in the article:
A Genome-Scale Database and
Reconstruction of Caenorhabditis elegans Metabolism.
Gebauer J, Gentsch C, Mansfeld J,
Schmeißer K, Waschina S, Brandes S, Klimmasch L, Zamboni N,
Zarse K, Schuster S, Ristow M, Schäuble S, Kaleta C.
Cell Syst 2016 May; 2(5): 312-322
Abstract:
We present a genome-scale model of Caenorhabditis elegans
metabolism along with the public database ElegCyc
(http://elegcyc.bioinf.uni-jena.de:1100), which represents a
reference for metabolic pathways in the worm and allows for the
visualization as well as analysis of omics datasets.
Our model reflects the metabolic peculiarities of
C. elegans that make it distinct from other higher
eukaryotes and mammals, including mice and humans. We
experimentally verify one of these peculiarities by showing
that the lifespan-extending effect of L-tryptophan
supplementation is dose dependent (hormetic). Finally, we show
the utility of our model for analyzing omics datasets through
predicting changes in amino acid concentrations after genetic
perturbations and analyzing metabolic changes during normal
aging as well as during two distinct, reactive oxygen
species (ROS)-related lifespan-extending treatments. Our
analyses reveal a notable similarity in metabolic adaptation
between distinct lifespan-extending interventions and point to
key pathways affecting lifespan in nematodes.
This model is hosted on
BioModels Database
and identified by:
MODEL1704200000.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2017-04-20 | MODEL1704200000 | BioModels
Project description:Gebauer2016 - Genome-scale model of
Caenorhabditis elegans metabolism (with bacteria)
This model is one of the two versions
of ElegCyc presented in the paper. It describes the metabolism of a
worm raised in a medium with bacteria
This model is described in the article:
A Genome-Scale Database and
Reconstruction of Caenorhabditis elegans Metabolism.
Gebauer J, Gentsch C, Mansfeld J,
Schmeißer K, Waschina S, Brandes S, Klimmasch L, Zamboni N,
Zarse K, Schuster S, Ristow M, Schäuble S, Kaleta C.
Cell Syst 2016 May; 2(5): 312-322
Abstract:
We present a genome-scale model of Caenorhabditis elegans
metabolism along with the public database ElegCyc
(http://elegcyc.bioinf.uni-jena.de:1100), which represents a
reference for metabolic pathways in the worm and allows for the
visualization as well as analysis of omics datasets.
Our model reflects the metabolic peculiarities of
C. elegans that make it distinct from other higher
eukaryotes and mammals, including mice and humans. We
experimentally verify one of these peculiarities by showing
that the lifespan-extending effect of L-tryptophan
supplementation is dose dependent (hormetic). Finally, we show
the utility of our model for analyzing omics datasets through
predicting changes in amino acid concentrations after genetic
perturbations and analyzing metabolic changes during normal
aging as well as during two distinct, reactive oxygen
species (ROS)-related lifespan-extending treatments. Our
analyses reveal a notable similarity in metabolic adaptation
between distinct lifespan-extending interventions and point to
key pathways affecting lifespan in nematodes.
This model is hosted on
BioModels Database
and identified by:
MODEL1704200001.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2017-04-20 | MODEL1704200001 | BioModels
Project description:Arsenic is methylated during its metabolism, thereby depleting the intracellular methyl donor S-adenosyl-methionine, which may lead to disturbances in DNA methylation patterns Cells were exposed to sodium arsenite (NaAsO2, Sigma) at concentrations of 0.08 M-BM-5M, 0.4 M-BM-5M and 2 M-BM-5M for 1, 2 and 8 weeks. A549 arsenic dose time response study.
2014-09-17 | E-GEOD-44173 | biostudies-arrayexpress
Project description:Arsenic (As) exposure is a significant worldwide environmental health concern. Low dose, chronic arsenic exposure has been associated with higher risk of skin, lung, and bladder cancer, as well as cardiovascular disease and diabetes. While arsenic-induced biological changes play a role in disease pathology, little is known about the dynamic cellular changes due to arsenic exposure and withdrawal. In these studies, we seek to understand the molecular mechanisms behind the biological changes induced by chronic low doses of arsenic exposure. We used a comprehensive approach involving chromatin structural studies and mRNA microarray analyses to determine how chromatin structure and gene expression patterns change in response to chronic low dose arsenic exposure and its subsequent withdrawal. Our results show that cells exposed to low doses of sodium arsenite have distinct temporal and coordinated chromatin, gene expression and miRNA changes that are consistent with differentiation and activation of multiple biochemical pathways. Most of these temporal patterns in gene expression are reversed when arsenic was withdrawn. However, some of the gene expression patterns remained altered, plausibly as a result of an adaptive response by these cells. Additionally, these gene expression patterns correlated with changes in chromatin structure, further solidifying the role of chromatin structure in gene regulatory changes due to arsenite exposure. Lastly, we show that arsenite exposure influences gene regulation both at the transcription initiation as well as at the splicing level. Thus our results suggest that general patterns of alternative splicing, as well as expression of particular gene regulators, can be indicative of arsenite-induced cell transformation. A total of eight (8) samples with two biological replicates under four separate conditions: wild-type treated with deionized H2O for 36 days (NT); chronic low-dose arsenic exposure of 1 uM of sodium arsenite (iAs-T) for 36 days; chronic arsenic exposure of 1 uM of sodium arsenite for 26 days followed by removal of sodium arsenite for 10 days, measured at day 36 (iAs-Rev); and chronic arsenic exposure of 1 uM of sodium arsenite for 26 days, followed by removal of sodium arsenite exposure for 10 days, followed by 1 uM of chronic sodium arsenite exposure for 10 days (measured at day 46) (iAs-Rev-T).
2015-05-05 | E-GEOD-60760 | biostudies-arrayexpress
Project description:D-Glucosamine (2-amino-2-deoxy-D-glucose, C.A.S.# 3416-24-8) (GlcN) is a freely available and commonly used dietary supplement possibly promoting cartilage health in humans which also acts as an inhibitor of glycolysis. We here find that GlcN extends C. elegans lifespan by impairing glucose metabolism to activate AMP-activated protein kinase (AMPK/AAK2) leading to increased mitochondrial biogenesis. Consistent with the concept of mitohormesis, this promotes increased formation of mitochondrial reactive oxygen species (ROS) and p38/PMK-1-mediated stress signaling culminating in increased expression of the nematodal amino acid-transporter 1 (aat-1) gene. Ameliorating mitochondrial ROS formation as well as impairment of aat-1-expression abolishes GlcN-mediated lifespan extension in a NRF2/SKN-1-dependent fashion. Notably and unlike other calorie restriction mimetics (CRM) like 2-deoxy-D-glucose (2DG, DOG), GlcN extends lifespan of aging C57BL/6 mice (log-rank: p=0.002; cox regression: p=0.01) similarly paralleled by an induction of mitochondrial biogenesis, increased expression of several murine amino acid transporters, as well as increased amino-acid catabolism. Taken together, GlcN mimics a ketogenic diet to extend healthspan in evolutionary distinct species. 24 samples: 12 mRNA profiles of C.elegans: 6 without GlcN and 6 with GlcN supplementaion; 12 mRNA profiles of M.musculus: 6 without GlcN and 6 with GlcN supplementaion
2014-03-07 | E-GEOD-54853 | biostudies-arrayexpress
Project description:D-Glucosamine (2-amino-2-deoxy-D-glucose, C.A.S.# 3416-24-8) (GlcN) is a freely available and commonly used dietary supplement possibly promoting cartilage health in humans which also acts as an inhibitor of glycolysis. We here find that GlcN extends C. elegans lifespan by impairing glucose metabolism to activate AMP-activated protein kinase (AMPK/AAK2) leading to increased mitochondrial biogenesis. Consistent with the concept of mitohormesis, this promotes increased formation of mitochondrial reactive oxygen species (ROS) and p38/PMK-1-mediated stress signaling culminating in increased expression of the nematodal amino acid-transporter 1 (aat-1) gene. Ameliorating mitochondrial ROS formation as well as impairment of aat-1-expression abolishes GlcN-mediated lifespan extension in a NRF2/SKN-1-dependent fashion. Notably and unlike other calorie restriction mimetics (CRM) like 2-deoxy-D-glucose (2DG, DOG), GlcN extends lifespan of aging C57BL/6 mice (log-rank: p=0.002; cox regression: p=0.01) similarly paralleled by an induction of mitochondrial biogenesis, increased expression of several murine amino acid transporters, as well as increased amino-acid catabolism. Taken together, GlcN mimics a ketogenic diet to extend healthspan in evolutionary distinct species.
2014-03-07 | GSE54853 | GEO
Project description:Arsenic (As) exposure is a significant worldwide environmental health concern. Low dose, chronic arsenic exposure has been associated with higher risk of skin, lung, and bladder cancer, as well as cardiovascular disease and diabetes. While arsenic-induced biological changes play a role in disease pathology, little is known about the dynamic cellular changes due to arsenic exposure and withdrawal. In these studies, we seek to understand the molecular mechanisms behind the biological changes induced by chronic low doses of arsenic exposure. We used a comprehensive approach involving chromatin structural studies and mRNA microarray analyses to determine how chromatin structure and gene expression patterns change in response to chronic low dose arsenic exposure and its subsequent withdrawal. Our results show that cells exposed to low doses of sodium arsenite have distinct temporal and coordinated chromatin, gene expression and miRNA changes that are consistent with differentiation and activation of multiple biochemical pathways. Most of these temporal patterns in gene expression are reversed when arsenic was withdrawn. However, some of the gene expression patterns remained altered, plausibly as a result of an adaptive response by these cells. Additionally, these gene expression patterns correlated with changes in chromatin structure, further solidifying the role of chromatin structure in gene regulatory changes due to arsenite exposure. Lastly, we show that arsenite exposure influences gene regulation both at the transcription initiation as well as at the splicing level. Thus our results suggest that general patterns of alternative splicing, as well as expression of particular gene regulators, can be indicative of arsenite-induced cell transformation.
2015-05-05 | GSE60760 | GEO
Project description:Marine ingredients can contain relatively high levels of arsenic. The main aim of this study is to assess the hepatic toxicity of arsenic species in Atlantic salmon (Salmo salar) in vitro. Primary hepatocytes were isolated from six male Atlantic salmon and exposed for 48 h to establish dose-response curves for arsenite (AsIII) (0.1-3 μM) and for arsenosugar (AsSug) (5-250 μM). Regarding arsenite, results obtained indicated that the dose between 0.1 and 1 represented a marked threshold for effect. Very few genes were differentially expressed (N=5, p-adjust < 0.1) following AsIII 0.1 µM treatment compared to AsIII 1µM (N=2338 p-adjust < 0.01). Similar was observed for AsSug exposure where exposure to 50 µM resulted in 195 DEGs (p-adjust < 0.1) vs 6899 (p-adjust < 0.01) following AsSug 250µM exposure
2024-09-30 | GSE247189 | GEO