Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1193780 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31602059_1.fastq.gz | Fastqsanger.gz | |||
| SRR31602059_2.fastq.gz | Fastqsanger.gz | |||
| SRR31602060_1.fastq.gz | Fastqsanger.gz | |||
| SRR31602060_2.fastq.gz | Fastqsanger.gz | |||
| SRR31602061_1.fastq.gz | Fastqsanger.gz |
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Project description:Increasing concern about pollution of our environment calls for advanced and rapid methods to estimate ecological toxicity. The use of gene expression microarrays in environmental studies can potentially meet this challenge. We present a novel method to examine soil toxicity. We exposed the collembolan Folsomia candida to soil containing an ecologically relevant cadmium concentration, and found a cumulative total of 1586 differentially expressed transcripts across three exposure durations, including transcripts involved in stress response, detoxification, and hypoxia. Additional enrichment analysis of gene ontology (GO) terms revealed that antibiotic biosynthesis is important at all time points examined. Interestingly, genes involved in the "penicillin and cephalosporin biosynthesis pathway" have never been identified in animals before, but are expressed in F. candida’s tissue. The synthesis of antibiotics can possibly be a response to increased cadmium-induced susceptibility to invading pathogens, which might be caused by repression of genes involved in the immune-system (C-type lectins and Toll receptor). This study presents a first global view on the environmental stress response of an arthropod species exposed to contaminated soil,and provides a mechanistic basis for the development of a gene expression soil quality test. Keywords: cadmium, soil, Collembola, environmental genomics
2008-08-08 | GSE11122 | GEO
Project description:Ecotoxicological tests may be biased by the use of laboratory strains that usually contain very limited genetic diversity. It is therefore essential to study how genetic variation influences stress tolerance relevant for toxicity outcomes. To that end we studied sensitivity to cadmium in two distinct genotypes of the parthogenetic soil ecotoxicological model organism Folsomia candida. Clonal lines of both genotypes (TO1 and TO2) showed divergent fitness responses to cadmium exposure; TO2 reproduction was 20% less affected by cadmium. Statistical analyses revealed significant differences between the cadmium-affected transcriptomes; i) the number of genes affected by cadmium in TO2 was only minor (~22%) compared to TO1; ii) 97 genes showed a genotype M-CM-^W cadmium interaction and their response to cadmium showed globally larger fold changes in TO1 when compared to TO2; iii) the interaction genes showed a concerted manner of expression in TO1 while a less coordinated pattern was observed in TO2. We conclude that (1) there is genetic variation in parthenogenetic populations of F. candida, and (2) this variation affects life-history and molecular endpoints relative to cadmium toxicity. This sheds new light on the sources of biological variability in test results, even when the test organisms are thought to be genetically homogeneous because of their parthenogenetic reproduction. Gene expression was measured in two different clones (TO1 and TO2) of the springtail Folsomia candida, after exposure of 2 days to soil containing cadmium (Cd+) and non-spiked (Cd-) soil. A 2 x 2 factorial analysis was performed, to examine the effect of clone (TO1, TO2), of treatment (Cd+, Cd-), and the clone x treatment interaction.
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Project description:The stress response of the soil bacterium Sinorhizobium meliloti towards elevated concentrations of the heavy metals cadmium and zinc was analyzed via transcriptional profiling.
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Project description:Ecotoxicological tests may be biased by the use of laboratory strains that usually contain very limited genetic diversity. It is therefore essential to study how genetic variation influences stress tolerance relevant for toxicity outcomes. To that end we studied sensitivity to cadmium in two distinct genotypes of the parthogenetic soil ecotoxicological model organism Folsomia candida. Clonal lines of both genotypes (TO1 and TO2) showed divergent fitness responses to cadmium exposure; TO2 reproduction was 20% less affected by cadmium. Statistical analyses revealed significant differences between the cadmium-affected transcriptomes; i) the number of genes affected by cadmium in TO2 was only minor (~22%) compared to TO1; ii) 97 genes showed a genotype × cadmium interaction and their response to cadmium showed globally larger fold changes in TO1 when compared to TO2; iii) the interaction genes showed a concerted manner of expression in TO1 while a less coordinated pattern was observed in TO2. We conclude that (1) there is genetic variation in parthenogenetic populations of F. candida, and (2) this variation affects life-history and molecular endpoints relative to cadmium toxicity. This sheds new light on the sources of biological variability in test results, even when the test organisms are thought to be genetically homogeneous because of their parthenogenetic reproduction.
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Project description:Opioid analgesics are frequently prescribed in the United States and worldwide. However, serious side effects such as addiction, immunosuppression and gastrointestinal symptoms limit long term use. In the current study using a chronic morphine-murine model a longitudinal approach was undertaken to investigate the role of morphine modulation of gut microbiome as a mechanism contributing to the negative consequences associated with opioids use. The results revealed a significant shift in the gut microbiome and metabolome within 24 hours following morphine treatment when compared to placebo. Morphine induced gut microbial dysbiosis exhibited distinct characteristic signatures profiles including significant increase in communities associated with pathogenic function, decrease in communities associated with stress tolerance. Collectively, these results reveal opioids-induced distinct alteration of gut microbiome, may contribute to opioids-induced pathogenesis. Therapeutics directed at these targets may prolong the efficacy long term opioid use with fewer side effects.
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