Ontology highlight
ABSTRACT:
PROVIDER: PRJNA833488 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19095547_1.fastq.gz | Fastqsanger.gz | |||
| SRR19095547_2.fastq.gz | Fastqsanger.gz | |||
| SRR19095548_1.fastq.gz | Fastqsanger.gz | |||
| SRR19095548_2.fastq.gz | Fastqsanger.gz | |||
| SRR19095549_1.fastq.gz | Fastqsanger.gz |
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Project description:We used Affymetrix microarrays to profile the Dapnia pulex miRNA expression under Cadmium exposure and identified Cadmium-responsive miRNAs
2015-10-15 | GSE68481 | GEO
Project description:Exposure to cadmium is associated with a variety of human diseases. At low concentrations, cadmium activates the transcription of stress-responsive genes, which can prevent or repair the adverse effects caused by this metal. Using C. elegans, 290 genes were identified that are differentially expressed (≥1.5-fold) following a 4 or 24 hour exposure to cadmium. Several of these genes are known to be involved in metal detoxification, including mtl-1, mtl-2, cdr-1 and ttm-1, confirming the efficacy of the study. The majority, however, were not previously associated with metal-responsiveness and are novel. Gene Ontology analysis mapped these genes to cellular/ion trafficking, metabolic enzymes and proteolysis categories. RNAi-mediated inhibition of 50 cadmium-responsive genes resulted in an increased sensitivity to cadmium toxicity, demonstrating that these genes are involved in the resistance to cadmium toxicity. Several functional protein interacting networks were identified by interactome analysis. Within one network, the signaling protein KEL-8 was identified. Kel-8 protects C. elegans from cadmium toxicity in a mek-1 (MAPKK)-dependent manner. Because many C. elegans genes and signal transduction pathways are evolutionarily conserved, these results may contribute to the understanding of the functional roles of various genes in cadmium toxicity in higher organisms. Keywords: gene expression time course
2008-03-26 | GSE7535 | GEO
Project description:Purpose: Cadmium is a nonessential heavy metal and a well known toxic agent. Cadmium is known to alter the gene expression and signaling but the role of miRNAs during Cadmium exposure is not understood. Methods: Mice were treated with 100 mg/ ml cadmium chloride for 120 days and accumulation of cadmium in blood and organs are confirmed by GFAAS. Subsequently, the total RNA was isolated from the whole blood and small RNA sequencing was executed in Illumina HiSeq 1000. Results: The reads were annotated to the mice genome and miRNAs in miRbase using miRDeep* and novel miRNAs were also predicted. The differential expression was studied by DeSeq Conclusions: This is the first report to reveal the cadmium responsive miRNome. These candidate miRNAs can serve as biomarkers for cadmium
2015-11-01 | GSE73744 | GEO
Project description:Field-selected tolerance to heavy metals has been reported for Orchesella cincta (Arthropoda: Collembola) populations occurring at metal-contaminated mining sites. This tolerance is correlated with heritable increase of metal excretion efficiency; less pronounce cadmium induced growth reduction and, over-expression of the metallothionein gene. We applied transcriptomics to determine differential gene expression caused by this abiotic stress in reference and cadmium tolerant populations. Many cDNAs responded to cadmium exposure in a reference population. Significantly fewer clones were cadmium responsive in tolerant animals. Analysis of variance revealed transcripts that interact between cadmium exposure and population. Hierarchical clustering of these clones revealed two major groups. The first one contained cDNAs that were up regulated by cadmium in the reference culture, but non-responsive or down regulated in tolerant animals. This cluster was also characterized by elevated constitutive expression in the tolerant population. Gene ontology analysis revealed that these cDNAs were involved in structural integrity of the cuticle, anti-microbial defense, calcium-channel blocking, neurotransmitter transport, chromatin remodeling and, endoplasmatic vesicle activity. The second group consisted of cDNAs down regulated in reference animals but not responding or slightly up regulated in tolerant animals. Their functions involved carbohydrate metabolic processes, Ca2+ dependent stress signaling, proteolysis and digestion. The reference population showed a strong signature of stress-induced genome-wide perturbation of gene expression, whereas the tolerant animals maintained normal gene expression upon cadmium exposure. We confirmed the micro-evolutionary processes occurring in soil arthropod populations and suggest a major contribution of gene regulation to the evolution of a stress-adapted phenotype.
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Project description:Cadmium is a naturally occurring heavy metal, and it is widely used in industry. Due to its persistent toxic effect, cadmium is classified as a category one human carcinogen. Its toxicity has been extensively studied in different organisms, including the nematode Caenorhabditis elegans. To investigate the transcriptomic responses following cadmium during early life exposure, C. elegans larval were exposed either from L1 to L3 stage or L1 to L4 stage to 20 µM cadmium chloride. RNAseq was applied to identified the changes of the transcriptome and the pathways which are specific to each stage. Overall, the result revealed that the highest responsive genes in both exposure scenario were linked to oxidative stress, lipid metabolism and ion binding. Additionally, some of these genes are well characterized and linked to specific functions, but some have no known function, however these uncharacterized genes are differentially expressed in both stages as a result of cadmium toxicity.Numerous transcripts were identified in one stage but not at the other. Furthermore, a general trend was observed where a larger number of genes were differentially expressed at L3 stage compared to L4, which suggest stage specific sensitivity in response to cadmium exposure.
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Project description:This study reports the impact of cadmium toxicity on the transcriptome of S. pneumoniae. The most transcriptionally-responsive pathways were found to be carbon source metabolism, fatty acid biosynthesis, cellular metal homeostasis and competence. This data provides a global overview of how the pneumococcus responds to metal ion intoxication, and subsequently, how it maintains viability during this stress.
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Project description:Plant growth is severely affected by toxic concentrations of the non-essential heavy metal cadmium (Cd). Comprehensive transcriptome analysis by RNA-Seq following cadmium exposure is required to further understand plant responses to Cd and facilitate future systems-based analyses of the underlying regulatory networks. In this study, rice plants were hydroponically treated with 50 µM Cd for 24 hours. In total, ~60,000 transcripts, including transcripts that could not be characterized by microarray-based approaches, were evaluated and ~36,000 transcripts were responsive to Cd exposure. Among multigenic families that may protect cells from generated ROS and reduce Cd toxicity, prominently upregulated antioxidant enzyme genes were identified. Furthermore, 168 different metal ion transporter genes, which might mediate the transport of transition Cd, responded to Cd exposure. qRT-PCR analysis of randomly selected genes indicated that their expression changed obviously after exposure to various heavy metal stresses. The Cd responsive genes included many abiotic stress (drought, high-salinity, low temperature) responsive genes. Based on further investigation into the expression patterns of abiotic stress regulatory genes such as DREB, part of the signal transduction pathway for Cd exposure was determined to cross-talk with abiotic stress signaling pathways. Our results provide useful information for further studies of the molecular mechanisms of plant adaptation to Cd exposure and the improvement of Cd tolerance in crop species.
2014-08-07 | E-MTAB-4306 | biostudies-arrayexpress
Project description:Increasing evidences have shown that cadmium could caused male infertility. However, the exhaustive mechanisms have not been elucidated in mammals. Here, the mice testes and sperm RNA were used to investigate lncRNA expression profiles by stranded-specific RNA-seq on the transcriptome levels after exposure to cadmium. More LncRNA expression have been changed than mRNA genes by cadmium. Furthermore, many novel LncRNA were inducible expression, suggesting that LncRNA might be a good candidate for indicating the reproductive toxicity of cadmium. The present study provides a preliminary database for further exploring the mechanisms of reproductive toxicity caused by cadmium in mammalians.
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Project description:Repetitive CdCl2 exposure resulted in cadmium accumulation and remarkable renal injuries in the animals. In the present study, we established an animal model to mimic chronic cadmium exposure-induced renal injury and performed whole transcriptome profiling studies. RNA-Seq data analysis showed that cadmium treatment induced dramatic gene expression changes in kidneys in a dose-dependent manner and higher severity of injury in ob/ob mice.
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