Active 2,4-DCP degraders in drilosphere and agricultural soil
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR092269.fastq.gz | Fastqsanger.gz | |||
| ERR092270.fastq.gz | Fastqsanger.gz | |||
| ERR092271.fastq.gz | Fastqsanger.gz | |||
| ERR092272.fastq.gz | Fastqsanger.gz | |||
| ERR092273.fastq.gz | Fastqsanger.gz |
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Project description:2,4-dinitrotoluene (2,4-DNT), a nitroaromatic used in industrial and explosive manufacturing processes, is known to contaminate artillery ranges, demilitarization areas and munitions manufacturing facilities. Previous transcriptomic and lipidomic studies identified energy metabolism as a principle biochemical process affected by 2,4-DNT where up-stream effects on PPARα signaling were hypothesized as themolecular initiating event for these effects. Here, the validity of this hypothetical adverse outcome pathway (AOP) was assessed by testing the hypothesis that 2,4-DNT-induced perturbations in PPARα signaling and resultant downstream deficits in energy metabolism, especially from lipids, would result in organism-level impacts on exercise endurance. PPARα knock-out (-/-) and wild-type (WT) mice were exposed for 14 days to vehicle or 2,4-DNT at a dose (134 mg/kg/day) that did not exhibit overt systemic toxicity. Mice performed an exercise challenge (forced swim) 1 day after the last dose. 2,4-DNT decreased swim times in WT and PPARα (-/-) mice, but the effect was significantly less in PPARα (-/-) mice indicating the critical of PPARα in mediating 2,4-DNT-induced energy metabolism deficits. 2,4-DNT caused down-regulation of transcripts involved in fatty acid metabolism, gluconeogenesis, triacylglycerol catabolism, and the pentose phosphate pathway, and 2,4-DNT treated wild-type mice had decreased serum trigylcerides and increased serum glucose versus 2,4-DNT treated PPARα (-/-) mice. Our results support the hypothesis that 2,4-DNT perturbs PPARα signaling as a molecular initiating event therefore impacting energy metabolism, especially lipid metabolism, producing reduced exercise endurance in mice.
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Project description:2,4-dinitrotoluene (2,4-DNT), a nitroaromatic used in industrial and explosive manufacturing processes, is known to contaminate artillery ranges, demilitarization areas and munitions manufacturing facilities. Previous transcriptomic and lipidomic studies identified energy metabolism as a principle biochemical process affected by 2,4-DNT where up-stream effects on PPARα signaling were hypothesized as themolecular initiating event for these effects. Here, the validity of this hypothetical adverse outcome pathway (AOP) was assessed by testing the hypothesis that 2,4-DNT-induced perturbations in PPARα signaling and resultant downstream deficits in energy metabolism, especially from lipids, would result in organism-level impacts on exercise endurance. PPARα knock-out (-/-) and wild-type (WT) mice were exposed for 14 days to vehicle or 2,4-DNT at a dose (134 mg/kg/day) that did not exhibit overt systemic toxicity. Mice performed an exercise challenge (forced swim) 1 day after the last dose. 2,4-DNT decreased swim times in WT and PPARα (-/-) mice, but the effect was significantly less in PPARα (-/-) mice indicating the critical of PPARα in mediating 2,4-DNT-induced energy metabolism deficits. 2,4-DNT caused down-regulation of transcripts involved in fatty acid metabolism, gluconeogenesis, triacylglycerol catabolism, and the pentose phosphate pathway, and 2,4-DNT treated wild-type mice had decreased serum trigylcerides and increased serum glucose versus 2,4-DNT treated PPARα (-/-) mice. Our results support the hypothesis that 2,4-DNT perturbs PPARα signaling as a molecular initiating event therefore impacting energy metabolism, especially lipid metabolism, producing reduced exercise endurance in mice.
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Project description:Resistance to agricultural fungicides in the field has created a need for discovering fungicides with new modes of action. DNA microarrays, because they provide information on expression of many genes simultaneously, could help to identify the modes of action. To begin an expression pattern database for agricultural fungicides, transcriptional patterns of Saccharomyces cerevisiae strain S288C genes were analysed following 2-h treatments with I50 concentrations of ergosterol biosynthesis inhibitors commonly used against plant pathogenic fungi. Eight fungicides, representing three classes of ergosterol biosynthesis inhibitors, were tested. To compare gene expression in response to a fungicide with a completely different mode of action, a putative methionine biosynthesis inhibitor (MBI) was also tested. Expression patterns of ergosterol biosynthetic genes supported the roles of Class I and Class II inhibitors in affecting ergosterol biosynthesis, confirmed that the putative MBI did not affect ergosterol biosynthesis, and strongly suggested that in yeast, the Class III inhibitor did not affect ergosterol biosynthesis. The MBI affected transcription of three genes involved in methionine metabolism, whereas there were essentially no effects of ergosterol synthesis inhibitors on methionine metabolism genes. There were no consistent patterns in other up- or downregulated genes between fungicides. These results suggest that inspection of gene response patterns within a given pathway may serve as a useful first step in identifying possible modes of action of fungicides. agricultural sterol biosynthesis inhibitor fungicides. Keywords = agriculture Keywords = ergosterol Keywords = methionine Keywords = fungicide Keywords = Saccharomyces cerevisiae S288C Keywords = biosynthesis
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Project description:2,4-dinitrotoluene (2,4-DNT), a nitroaromatic used in industrial and explosive manufacturing processes, is known to contaminate artillery ranges, demilitarization areas and munitions manufacturing facilities. Previous transcriptomic and lipidomic studies identified energy metabolism as a principle biochemical process affected by 2,4-DNT where up-stream effects on PPARα signaling were hypothesized as themolecular initiating event for these effects. Here, the validity of this hypothetical adverse outcome pathway (AOP) was assessed by testing the hypothesis that 2,4-DNT-induced perturbations in PPARα signaling and resultant downstream deficits in energy metabolism, especially from lipids, would result in organism-level impacts on exercise endurance. PPARα knock-out (-/-) and wild-type (WT) mice were exposed for 14 days to vehicle or 2,4-DNT at a dose (134 mg/kg/day) that did not exhibit overt systemic toxicity. Mice performed an exercise challenge (forced swim) 1 day after the last dose. 2,4-DNT decreased swim times in WT and PPARα (-/-) mice, but the effect was significantly less in PPARα (-/-) mice indicating the critical of PPARα in mediating 2,4-DNT-induced energy metabolism deficits. 2,4-DNT caused down-regulation of transcripts involved in fatty acid metabolism, gluconeogenesis, triacylglycerol catabolism, and the pentose phosphate pathway, and 2,4-DNT treated wild-type mice had decreased serum trigylcerides and increased serum glucose versus 2,4-DNT treated PPARα (-/-) mice. Our results support the hypothesis that 2,4-DNT perturbs PPARα signaling as a molecular initiating event therefore impacting energy metabolism, especially lipid metabolism, producing reduced exercise endurance in mice. RNA was isolated from liver tissue of vehicle or 2,4-DNT treated wild-type or PPARα (-/-) mice (n=6) and RT-PCR performed to analyze genes involved in fatty acid metabolism
2014-06-30 | E-GEOD-50167 | biostudies-arrayexpress