Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1078606 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28026291_1.fastq.gz | Fastqsanger.gz | |||
| SRR28026291_2.fastq.gz | Fastqsanger.gz |
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Project description:Enterocloster bolteae strain:AHG0001 Genome sequencing and assembly
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Project description:Urolithins are a class of bioactive metabolites derived from the metabolism of dietary ellagitannins by the human gut microbiota. In the gut, urolithins are dehydroxylated regioselectively based on microbiota composition and activity. A single 9-hydroxy urolithin dehydroxylase (ucd) operon in gut resident Enterocloster species has been described to date; however, most enzymes in the urolithin metabolic pathway remain uncharacterized. Here, we investigate urolithin cross-feeding between members of the gut microbiota and discover a novel urolithin dehydroxylase in a subset of Enterocloster species. We show that urolithin intermediates, released by gut resident Gordonibacter species during ellagic acid metabolism, are dehydroxylated at both the 9- and 10-positions by E. asparagiformis, E. citroniae, and E. pacaense, but not E. bolteae. Using untargeted proteomics, we uncover a 10-hydroxy urolithin dehydroxylase operon, termed uxd, responsible for these species-specific differences in urolithin metabolism. By inducing uxd expression with diverse urolithins, we show that 9-hydroxy urolithins are required for uxd transcription and 10-position dehydroxylation. Collectively, this study reveals some of the genes, proteins, and substrate features underlying differences in urolithin metabolism by the human gut microbiota.
2025-11-12 | PXD066865 | Pride
Project description:<p>Objective: Guillain barre syndrome (GBS) is a rare immune-mediated inflammatory disease of the complex peripheral nervous system. Long-term “silent infection” caused by changes in intestinal flora is potentially a contributing factor for immune-mediated inflammatory diseases, but the causative link between GBS and intestinal flora remains unclear. The present study aimed to characterize gut microbiome structure and estimate its association with the serum metabolic profile and in GBS. </p><p>Methods: Untargeted metabolomics profiling of serum, using liquid chromatography-mass spectrometry, and metagenomics sequencing of stool samples from a cohort of GBS and non-GBS subjects were performed to evaluate serum metabolic profiles and gut microbiome structure in GBS subjects relative to healthy controls. Pearson’s correlation analysis was used to estimate the correlations between the gut microbial abundance and serum metabolic profile. </p><p>Results: For intestinal microflora, Ligilactobacillus_salivarius, Klebsiella pneumonia, Enterocloster bolteae and Methanobrevibacter smithii were notably more abundant in GBS subjects, while Bacteroides sp., Roseburia hominis, and Paraprevotella xylaniphila decreased significantly. Metabolome data revealed that the gamma-aminobutyric acid (GABA) and secondary cholic acid metabolism were perturbed in GBS. GABA increased significantly, while secondary cholic acids as methyl deoxycholate, glycodeoxycholic acid, glycolithocholic acid, taurolithocholic acid and coprocholic acid, decreased significantly in GBS versus non-GBS controls. Metagenome data also revealed that GABA biosynthesis pathway was enriched, while secondary cholic acid metabolism pathways were decreased in gut microbes in GBS subjects. Correlation analysis revealed that changes in GABA were associated with altered gut microbes, such as Enterococcus species, Ligilactobacillus salivarius, Enterocloster bolteae and Methanobrevibacter smithii, and changes in secondary cholic acids were positively correlated with Bacteroides species and Roseburia species.</p><p>Conclusion: The well-known opportunistic pathogenic Klebsiella pneumonia and other special gut microbes significantly enriched in GBS. GABA and secondary cholic acid metabolism were significantly disturbed in GBS subjects and might be affected by the dysbiosis of gut microbial flora. These findings suggest that GABA may be a promising biomarker for the diagnosis of GBS and that modulation of gut microbiota might impact the clinical course of GBS.</p>
2025-02-20 | MTBLS10392 | MetaboLights
Project description:In Drosophila, defects in asymmetric cell division can result in the formation of stem cell derived tumors. Here, we reveal a different mechanism that can result in the formation of very similar terminal brain tumor phenotypes. We demonstrate that brain tumors in l(3)mbt mutants originate from overproliferation of neuroepithelial cells in the optic lobes caused by de-repression of target genes in the Salvador-Warts-Hippo (SWH) pathway. We use ChIP-seq to identify L(3)mbt-binding sites and show that L(3)mbt binds to chromatin insulator elements. Mutating l(3)mbt or inhibiting the insulator protein mod(mdg4) results in upregulation of SWH pathway reporters. As l(3)mbt tumors are rescued by mutations in bantam or yorkie or by overexpression of expanded the deregulation of SWH pathway target genes is an essential step in brain tumor formation. Our data reveal that very different primary defects can result in the formation of brain tumors, which behave quite similarly in their advanced stages. Examination of l(3)mbt binding in third instar larval brain and wing/haltere/third leg imaginal discs tissue.
2011-08-29 | E-GEOD-29206 | biostudies-arrayexpress
Project description:In Drosophila, defects in asymmetric cell division can result in the formation of stem cell derived tumors. Here, we reveal a different mechanism that can result in the formation of very similar terminal brain tumor phenotypes. We demonstrate that brain tumors in l(3)mbt mutants originate from overproliferation of neuroepithelial cells in the optic lobes caused by de-repression of target genes in the Salvador-Warts-Hippo (SWH) pathway. We use ChIP-seq to identify L(3)mbt-binding sites and show that L(3)mbt binds to chromatin insulator elements. Mutating l(3)mbt or inhibiting the insulator protein mod(mdg4) results in upregulation of SWH pathway reporters. As l(3)mbt tumors are rescued by mutations in bantam or yorkie or by overexpression of expanded the deregulation of SWH pathway target genes is an essential step in brain tumor formation. Our data reveal that very different primary defects can result in the formation of brain tumors, which behave quite similarly in their advanced stages.
2011-08-29 | GSE29206 | GEO
Project description:Early zebrafish embryo development proceeds first from a maternally transcribed and stored mRNAs, and zygotic gene activation (ZGA) is initiated at the mid-blastula transition (MBT; 1000-cell stage), 3.3 h post-fertilization. Very little is known on how the zygotic genome is programmed for transcriptional activation at the MBT. To start addressing this issue, we have mapped by ChIP-chip genome-wide promoter histone methylation (H3K4me3, H3K9me3, H3K27me3, H3K36me3) and RNA Pol II profiles before ZGA (256-cell stage; 2.5 hpf), during ZGA (MBT; 3.5 hpf)) and after ZGA (Post-MBT; 5.3 hpf) . We used a custom 2.1M probe HD promoter array (Nimblegen) for ChIP and input DNA hybridization. Peak detection was done using MA2C with P=10e-4 as cutoff.
2011-12-02 | GSE27314 | GEO
Project description:L(3)mbt regulate the transcription of germ-specific genes in somatic cells but the detailed mechanism remains unclear. We performed shotgun LC/MS/MS of L(3)mbt-IP samples and identified a new interactor in OSCs.
2022-08-15 | PXD026945 | Pride