Ontology highlight
ABSTRACT:
PROVIDER: PRJNA528849 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8781900.fastq.gz | Fastqsanger.gz | |||
| SRR8781910.fastq.gz | Fastqsanger.gz | |||
| SRR8781920.fastq.gz | Fastqsanger.gz | |||
| SRR8781930.fastq.gz | Fastqsanger.gz | |||
| SRR8781940.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Background: The uncontrolled and widespread use of (nano)silver compounds has led to the increased release of these compounds into the environment, raising concerns about their negative impact on ecosystems. Concomitantly, silver resistance determinants are widely spread among environmental and clinically relevant bacteria although the underlying mechanisms are not yet fully understood. Results: In this study, we show that Cupriavidus metallidurans is able to adapt to toxic silver concentrations and explicate the genetic circuit responsible for this adaptation. None of the known silver resistant determinants present in C. metallidurans are involved in the adapted response. Instead, increased silver resistance is achieved by the concerted action of a two-component system AgrR-AgrS, previously not associated with metal resistance, and two intrinsically disordered proteins PrsQ1 and PrsQ2. Both belong to an unique group of small, uncharacterized, extracellular proteins restricted to the genera Cupriavidus and Ralstonia. This system seems to be much more efficient as it gives C. metallidurans the ability to withstand much higher silver concentrations. The latter could be facilitated by the accumulation of silver ions and the formation of silver nanoparticles. Conclusions: Detailed knowledge and exploitation of this protein family could result in novel routes for metal nanoparticle formation and metal processing relevant for biotechnical and biomedical applications.
2018-12-31 | GSE107669 | GEO
Project description:Silver nanoparticles cause toxicity in exposed organisms and are an environmental health concern. The mechanisms of silver nanoparticle toxicity, however, remain unclear. We examined the effects of exposure to silver in nano-, bulk- and ionic forms on zebrafish embryos (Danio rerio) using a Next Generation Sequencing approach in an Illumina platform (High-Throughput SuperSAGE). Significant alterations in gene expression were found for all treatments and many of the gene pathways affected, most notably those associated with oxidative phosphorylation and protein synthesis, overlapped strongly between the three treatments indicating similar mechanisms of toxicity for the three forms of silver studied. Changes in oxidative phosphorylation indicated a down-regulation of this pathway at 24h of exposure, but with a recovery at 48h. This finding was consistent with a dose-dependent decrease in oxygen consumption at 24h, but not at 48h, following exposure to silver ions. Overall, our data provide support for the hypothesis that the toxicity caused by silver nanoparticles is principally associated with bioavailable silver ions in exposed zebrafish embryos. These findings are important in the evaluation of the risk that silver particles may pose to exposed vertebrate organisms. mRNA profiles of whole zebrafish embryos at 24 and 48 hours post-fertilisation (hpf) exposed to silver in nano, bulk and ionic forms were generated by deep sequencing using HT-SuperSAGE (Illumina GA2).
2013-06-17 | E-GEOD-38125 | biostudies-arrayexpress
Project description:The toxicity of silver and zinc oxide nanoparticles is hypothesised to be mediated by dissolved metal ions and cerium dioxide nanoparticles (CeO2 NPs) are hypothesised to induce toxicity specifically by oxidative stress dependant on their surface redox state. To test these hypotheses, RNAseq was applied to characterise the molecular responses of cells to metal nanoparticle and metal ion exposures. The human epithelial lung carcinoma cell line A549 was exposed to different CeO2 NPs with different surface charges, micron-sized and nano-sized silver particles and silver ions, micron-sized and nano-sized zinc oxide particles and zinc ions, or control conditions, for 1 hour, 6 hours and 24 hours. Concentrations were the lower of either EC20 or 128 micrograms/mL. Transcriptional responses were characterised by RNAseq transcriptomics using an Illumina HiSeq2500 .
2018-02-01 | E-MTAB-5734 | biostudies-arrayexpress
Project description:Decoding the Nano-Silver Resistance Mechanism Switch: Targeted Strategies for Control
| PRJNA1150138 | ENA
Project description:Silver nanoparticles cause toxicity in exposed organisms and are an environmental health concern. The mechanisms of silver nanoparticle toxicity, however, remain unclear. We examined the effects of exposure to silver in nano-, bulk- and ionic forms on zebrafish embryos (Danio rerio) using a Next Generation Sequencing approach in an Illumina platform (High-Throughput SuperSAGE). Significant alterations in gene expression were found for all treatments and many of the gene pathways affected, most notably those associated with oxidative phosphorylation and protein synthesis, overlapped strongly between the three treatments indicating similar mechanisms of toxicity for the three forms of silver studied. Changes in oxidative phosphorylation indicated a down-regulation of this pathway at 24h of exposure, but with a recovery at 48h. This finding was consistent with a dose-dependent decrease in oxygen consumption at 24h, but not at 48h, following exposure to silver ions. Overall, our data provide support for the hypothesis that the toxicity caused by silver nanoparticles is principally associated with bioavailable silver ions in exposed zebrafish embryos. These findings are important in the evaluation of the risk that silver particles may pose to exposed vertebrate organisms.
2013-06-17 | GSE38125 | GEO
Project description:The current study deals to decipher the antibacterial mechanism of lysozyme coated silver nanoparticles (L-Ag NPs) (coated with lysozyme) against a Gram negative modal organism Escherichia coli K12 (MTCC 1302). Hence, the whole transcriptome profiling of E. coli K12 was done by exposing it to the MIC75 concentration of L-Ag NPs for 5 and 30 min., by RNA sequencing (RNAseq) analysis. The obtained results were utilized to understand all the metabolic pathways, signaling and molecular functions in bacterial cells under the stress of L-Ag NPs. RNAseq showed a high number of total reads along with significant ratio of high-quality reads, which confirmed the excellent quality and quantity of the obtained RNAseq data. Controlled release of ions from the surface of L-Ag NPs allowed the bacterial cells to function normally till the accumulation of threshold amount of silver ions which triggered the action of defence system, thus, reducing the chances of resistance development in bacteria. In long term, such treatment may force the bacterial machinery to induce changes in their genome to counteract the situation and develop resistance against silver ions, similar to the well-known antibiotic resistance problem. The obtained results advocate that L-Ag NPs can be used as effective antibacterial agent.
2022-06-15 | GSE151954 | GEO
Project description:The rapid emergence of drug resistant Staphylococcus aureus (S. aureus), in particular, methicillin-resistant S. aureus (MRSA) poses a serious threat to public health globally. Reuse of metal-based antimicrobials stands for one of the most promising strategies to resensitize drug resistant bacteria to conventional antibiotics. Silver (Ag) has been used as an antimicrobial agent since antiquity, yet its molecular mechanism of action is elusive largely owing to technical challenges to identify the direct silver-binding protein targets accountable for its action. Herein, using an in-house developed hyphenated technique LC-GE-ICP-MS, we successfully separated and identified 38 authentic Ag+-binding proteins (Ag+-proteome) in S. aureus at the whole-cell scale for the first time. By integration with bioinformatic analysis and systematic biochemical characterizations, we captured the first snapshot on the dynamic action of Ag+ against S. aureus at the molecular level, i.e., Ag+ primarily targets glycolysis via inhibiting multiple enzymes and induces the elevation of ROS through functional disruption of redox homeostasis system at the late stage, leading to an upregulation of oxidative pentose phosphate pathway (oxPPP) to alleviate Ag+ stress. However, the activation of oxPPP is ultimately futile due to key oxPPP enzymes being inhibited by Ag+. We further validated that Ag+ could inhibit 6-phosphogluconate dehydrogenase, a key target from oxPPP through binding to His185 at the active site and morphing the shape of catalytic pocket by X-ray crystallography. Significantly, the multi-target mode of action of silver is accountable for its suppression of antibiotic selection effects towards S. aureus as well as its sustainable antimicrobial activity. Such a unique mode of action of Ag+ (and silver nanoparticles) led to enhanced efficacy of a broad range of antibiotics and resensitization of MRSA to antibiotics. Our study resolves the long-standing question of the molecular targets of silver in S. aureus and offers a novel insight into the sustainable bacterial susceptibility of silver, providing a potential approach for combating antimicrobial resistance.
2021-09-10 | PXD025106 | Pride
Project description:Silver-resistant Saccharomyces cerevisiae mutant was obtained by evolutionary engineering method. Briefly, genetic diversity in reference strain, CEN.PK.113-7D, was increased by ethyl methane sulfonate (EMS)-mutagenesis. The mutant population was passaged several times in gradually increasing silver stress. Several mutant individuals were selected from the final population. Among selected mutant individuals, one of them was much more resistant to silver stress than the reference strain, called as 2E. Whole-genome transcriptomic analysis was performed to identify the silver resistance mechanisms in the silver-resistant mutant strain.
2020-01-09 | GSE143335 | GEO
Project description:<p>The study of antimicrobial resistance (AMR) in infectious diarrhea has generally been limited to cultivation, antimicrobial susceptibility testing and targeted PCR assays. When individual strains of significance are identified, whole genome shotgun (WGS) sequencing of important clones and clades is performed. Genes that encode resistance to antibiotics have been detected in environmental, insect, human and animal metagenomes and are known as "resistomes". While metagenomic datasets have been mined to characterize the healthy human gut resistome in the Human Microbiome Project and MetaHIT and in a Yanomani Amerindian cohort, directed metagenomic sequencing has not been used to examine the epidemiology of AMR. Especially in developing countries where sanitation is poor, diarrhea and enteric pathogens likely serve to disseminate antibiotic resistance elements of clinical significance. Unregulated use of antibiotics further exacerbates the problem by selection for acquisition of resistance. This is exemplified by recent reports of multiple antibiotic resistance in Shigella strains in India, in Escherichia coli in India and Pakistan, and in nontyphoidal Salmonella (NTS) in South-East Asia. We propose to use deep metagenomic sequencing and genome level assembly to study the epidemiology of AMR in stools of children suffering from diarrhea. Here the epidemiology component will be surveillance and analysis of the microbial composition (to the bacterial species/strain level where possible) and its constituent antimicrobial resistance genetic elements (such as plasmids, integrons, transposons and other mobile genetic elements, or MGEs) in samples from a cohort where diarrhea is prevalent and antibiotic exposure is endemic. The goal will be to assess whether consortia of specific mobile antimicrobial resistance elements associate with species/strains and whether their presence is enhanced or amplified in diarrheal microbiomes and in the presence of antibiotic exposure. This work could potentially identify clonal complexes of organisms and MGEs with enhanced resistance and the potential to transfer this resistance to other enteric pathogens.</p> <p>We have performed WGS, metagenomic assembly and gene/protein mapping to examine and characterize the types of AMR genes and transfer elements (transposons, integrons, bacteriophage, plasmids) and their distribution in bacterial species and strains assembled from DNA isolated from diarrheal and non-diarrheal stools. The samples were acquired from a cohort of pediatric patients and controls from Colombia, South America where antibiotic use is prevalent. As a control, the distribution and abundance of AMR genes can be compared to published studies where resistome gene lists from healthy cohort sequences were compiled. Our approach is more epidemiologic in nature, as we plan to identify and catalogue antimicrobial elements on MGEs capable of spread through a local population and further we will, where possible, link mobile antimicrobial resistance elements with specific strains within the population.</p>
| phs001260 | dbGaP
Project description:The evolution of antibiotic resistance is a clear example of adaptation by natural selection. Although a number of mutations contributing to the resistance have been identified, the relationship between the mutations and the related phenotypic changes responsible for the resistance has yet to be fully elucidated. To better characterize phenotype-genotype mapping for drug resistance, we performed parallel laboratory evolution of Escherichia coli under the selection of single antibiotics and after 90 days propagation obtained resistant strains. We find that an acquisition of resistance to one drug drastically changes the resistance and susceptibility to other drugs. Based on transcriptome data of these strains, we demonstrated that the resistances could be quantitatively predicted by the expression changes of a small number of genes. Whole-genome resequencing analysis provided several candidate mutations contributing to the resistances, while phenotype-genotype mapping was suggested to be complex and included various mutations that caused similar phenotypic changes. The integration of transcriptome and genome data enables us to extract essential phenotypic changes for drug resistances. To examine the contribution of the gene expression changes to the antibiotic resistances, transcriptome of the parent strain (duplicated) and 40 resistant strains (4 parallel-evolved resistant strains for 10 antibiotics) were analyzed.
2014-09-17 | E-GEOD-59408 | biostudies-arrayexpress