Bacteria
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA976120 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24735640_1.fastq.gz | Fastqsanger.gz | |||
| SRR24735640_2.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 2 of 2 |
Similar Datasets
Project description:Isolation and identification of phenol degrading bacteria
| PRJEB31471 | ENA
Project description:This dataset holds three runs of our new Atrandi-SPC based single-cell WGS protocol, applied to human saliva. The files are Bascet-FASTQ-format, i.e. barcodes are part of read names, reads are trimmed, and human DNA has been filtered out
2026-07-31 | E-MTAB-15285 | biostudies-arrayexpress
Project description:Two nitrile-metabolizing bacteria isolated from two major landfills in Lagos, Nigeria Genome sequencing and assembly
| PRJNA1043449 | ENA
Project description:WGS: Florfenicol-resistant lactic acid bacteria from cattle at slaughter
| PRJNA783265 | ENA
Project description:The aim of this experiment was to determine if the development of resistance to antibiotics can be driven by the concentration and speciation of Cu. Experimental setup was designed to investigate two hypotheses for which two strains of Gram- bacteria have been selected: - Do TE enhance AR in resistant bacteria? Resistant strain: Bioluminescent Pseudomonas aeruginosa PAO1 (Xen41, Tetracycline resistant) - Do TE induce AR in sensitive bacteria? Sensitive strain: Pseudomonas aeruginosa PAO1 (Wild Type)
2020-10-28 | GSE160188 | GEO
Project description:Widespread organic pollutants such as BTEX (benzene, toluene, ethylbenzene, and xylene) are traditionally considered to enhance soil carbon loss through mineralization and ecotoxicity. Challenging this paradigm, we reveal that BTEX can stimulate microbial carbon chain elongation (CE)—a previously overlooked carbon fixation pathway—thereby reshaping soil carbon dynamics. Through phased amplicon sequencing, metagenomics, and metaproteomics, we demonstrate that BTEX exerts bidirectional regulation on CE at both taxonomic and molecular levels. Specifically, BTEX selectively enriches Clostridium_sensu_stricto_12 and Rummelibacillus, while suppressing Acinetobacter, a key CE contributor in natural soils. BTEX also inhibits Petrimonas, a syntrophic degrader of medium-chain fatty acids (MCFAs), promoting MCFAs accumulation. Moreover, BTEX-degrading bacteria establish cooperative interactions with CE bacteria, facilitating the sequestration of carbon as MCFAs rather than complete mineralization to CO₂, with Bacillus bridging both metabolic roles. At the molecular level, BTEX enhances CE by accelerating substrate uptake and acetyl-CoA flux into the reverse β-oxidation (RBO) pathway. Multi-omics analysis revealed that BTEX downregulates fatty acid biosynthesis (FAB), another pathway of CE, through fabR, acrR, and fadR while maintaining NADH availability to relieve Rex-mediated inhibition of the key RBO enzyme gene bcd. However, excessive BTEX disrupts metabolic homeostasis and suppresses CE activity. Collectively, our findings redefine the ecological implications of aromatic hydrocarbon contamination by uncovering its capacity to modulate anaerobic carbon fixation and retention in soil microbial communities. This work highlights a previously unrecognized link between pollutant degradation and biogenic carbon sequestration, with broader implications for understanding soil biogeochemical resilience under anthropogenic pressure.
| PXD064805 |
Project description:<p>Individuals vary widely in their drug responses, which can be dangerous and expensive due to treatment delays and adverse effects. Growing evidence implicates the gut microbiome in this variability, however the molecular mechanisms remain largely unknown. We measured the ability of 76 diverse human gut bacteria to metabolize 271 oral drugs and found that many of these drugs are chemically modified by microbes. We combined high-throughput genetics with mass spectrometry to systematically identify drug-metabolizing microbial gene products. These microbiome-encoded enzymes can directly and significantly impact intestinal and systemic drug metabolism in mice, and can explain drug-metabolizing activities of human gut bacteria and communities based on their genomic contents. These causal links between microbiota gene content and metabolic activities connect interpersonal microbiome variability to interpersonal differences in drug metabolism, which has implications for medical therapy and drug development across multiple disease indications.</p><p><br></p><p>Additional data related to this study can also be found by the following links;</p><p>- Raw sequencing data; <a href='https://www.ebi.ac.uk/ena/data/view/PRJEB31790' rel='noopener noreferrer' target='_blank'>ENA (accession no. PRJEB31790)</a></p><p>- Data for Figures; <a href='https://doi.org/10.6084/m9.figshare.8119058' rel='noopener noreferrer' target='_blank'>FigShare</a> </p><p>- Analysis pipeline schemes, scripts and input files for analzing data and generating figures; <a href='https://github.com/mszimmermann/drug-bacteria-gene_mapping' rel='noopener noreferrer' target='_blank'>GitHub</a> and archived <a href='https://doi.org/10.5281/zenodo.2827640' rel='noopener noreferrer' target='_blank'>Zenodo</a></p>
2019-07-10 | MTBLS896 | MetaboLights