Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24423100.fastq.gz | Fastqsanger.gz | |||
| SRR24423200.fastq.gz | Fastqsanger.gz | |||
| SRR24423101.fastq.gz | Fastqsanger.gz | |||
| SRR24423201.fastq.gz | Fastqsanger.gz | |||
| SRR24423102.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:In the present study, genomic binding sites of glucocorticoid receptors (GR) were identified in vivo in the rat hippocampus applying chromatin immunoprecipitation followed by next-generation sequencing. We identified 2470 significant GR-binding sites (GBS) and were able to confirm GR binding to a random selection of these GBS covering a wide range of P values. Analysis of the genomic distribution of the significant GBS revealed a high prevalence of intragenic GBS. Gene ontology clusters involved in neuronal plasticity and other essential neuronal processes were overrepresented among the genes harboring a GBS or located in the vicinity of a GBS. Male adrenalectomized rats were challenged with increasing doses of the GR agonist corticosterone (CORT) ranging from 3 to 3000 μg/kg, resulting in clear differences in the GR-binding profile to individual GBS. Two groups of GBS could be distinguished: a low-CORT group that displayed GR binding across the full range of CORT concentrations, and a second high-CORT group that displayed significant GR binding only after administering the highest concentration of CORT. All validated GBS, in both the low-CORT and high-CORT groups, displayed mineralocorticoid receptor binding, which remained relatively constant from 30 μg/kg CORT upward. Motif analysis revealed that almost all GBS contained a glucocorticoid response element resembling the consensus motif in literature. In addition, motifs corresponding with new potential GR-interacting proteins were identified, such as zinc finger and BTB domain containing 3 (Zbtb3) and CUP (CG11181 gene product from transcript CG11181-RB), which may be involved in GR-dependent transactivation and transrepression, respectively. In conclusion, our results highlight the existence of 2 populations of GBS in the rat hippocampal genome. - See more at: http://press.endocrine.org/doi/10.1210/en.2012-2187?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed#sthash.LqK088DP.dpuf
2016-07-09 | GSE84202 | GEO
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:The CiaRH and LiaFSR two-component regulatory systems in Streptococcus agalactiae (Group B Streptococcus, GBS) are essential mediators of the organism s response to biologically important sources of environmental stress, and positive regulators of GBS virulence. Transcriptional profiling of CiaR mutant GBS and LiaR mutant GBS reveals that LiaR is positively-regulated by CiaR, and the individual mutant transcriptomes share a number of commonly-regulated genes. To determine the GBS response to loss of both of these key regulatory systems, we constructed a GBS mutant strain with non-polar deletions in both ciaR and liaR, and performed transcriptional profiling using DNA microarray analysis, comparing wild-type GBS to CiaR/LiaR double mutant GBS under non-stressed conditions.
2012-11-18 | GSE14572 | GEO
Project description:Group B Streptococcus (GBS) is a pervasive perinatal pathogen, yet factors driving GBS dissemination in utero are poorly defined. Gestational diabetes mellitus (GDM), a complication marked by dysregulated immunity and maternal microbial dysbiosis, increases risk for GBS perinatal disease. We interrogated host-pathogen dynamics in a novel murine GDM model of GBS colonization and perinatal transmission. GDM mice had greater GBS in utero dissemination and subsequently worse neonatal outcomes. Dual-RNA sequencing revealed differential GBS adaptation to the GDM reproductive tract, including a putative glycosyltransferase (yfhO), and altered host responses. GDM disruption of immunity included reduced uterine natural killer cell activation, impaired recruitment to placentae, and altered vaginal cytokines. Lastly, we observed distinct vaginal microbial taxa associated with GDM status and GBS invasive disease status. Our translational model of GBS perinatal transmission in GDM hosts recapitulates several clinical aspects and enables discovery of host and bacterial drivers of GBS perinatal disease.
2023-07-05 | GSE236335 | GEO
Project description:Streptococcus agalactiae (Group B Streptococcus, GBS) is a leading cause of early-onset neonatal bacterial infection. Evasion of innate immune defenses is critical to neonatal GBS disease pathogenesis. Effectors of the innate immune system such as antimicrobial peptides, as well as numerous antibiotics, target the peptidoglycan layer of the gram positive bacterial cell wall. The intramembrane-sensing histidine kinase class of two-component regulatory systems has recently been identified as important to the gram-positive response to cell wall stress. We identified and characterized the GBS homolog of LiaR, the response regulator component of the LiaFSR system and constructed site-directed, non-polar deletion mutations in the regulator gene liaR. GBS LiaR deletion mutant strains are more susceptible to cell wall active antibiotics (vancomycin and bacitracin) as well as antimicrobial peptides (colistin, nisin and the human cathelicidin LL-37) compared to isogenic wild-type GBS. LiaR mutant GBS are significantly attenuated in mouse models of both GBS sepsis and GBS pneumonia. To determine the genes regulated by LiaR that account for these defects, transcriptional profiling was performed using DNA microarray analysis, comparing wild-type GBS to LiaR mutant GBS under non-stressed conditions.
2012-11-18 | GSE14571 | GEO
Project description:GBS data of 3 mapping families used to cluster scaffolds into linkage groups (Timema cristinae genome draft)
| PRJNA356911 | ENA
Project description:CsrRS is a two-component regulatory system that controls expression of multiple genes and affects virulence in group B Streptococcus (GBS), a major cause of neonatal sepsis and of invasive infection in chronically ill adults. To better understand the CsrRS regulon and its importance in GBS pathogenicity, we used GBS genomic microarrays to compare global gene expression in GBS strains 2603V/R and 515 with that in CsrR or CsrS isogenic mutants. These results and comparison with data reported previously for GBS strain NEM316 demonstrated a conserved CsrRS regulon of approximately 30 genes including those encoding beta-hemolysin, CAMP factor, and C5a-peptidase, as well as a variable repertoire of genes regulated in one or two of the three strains. Inactivation of CsrS had a similar but weaker effect at most regulated loci, but, in some cases, resulted in more pronounced or divergent regulation compared to CsrR. We conclude that CsrRS regulates a core group of genes including important virulence factors in diverse strains of GBS, but also displays marked variability in the repertoire of regulated genes and in the relative effects of CsrS signaling on CsrR-mediated gene regulation. Such variation is likely to play an important role in strain-specific adaptation of GBS to particular host environments and pathogenic potential in susceptible hosts.
2008-11-25 | E-TIGR-131 | biostudies-arrayexpress
Project description:Regulation of gene expression in response to variable and often adverse environmental conditions is an essential component of microbial pathogenesis. We identified the two-component regulatory system CiaRH in a screen for genes essential for the survival of Streptococcus agalactiae (Group B Streptococcus, GBS) on exposure to in vitro models of environmental stress. We constructed site-directed, non-polar deletion mutations in the regulator gene ciaR and compared the growth of CiaR mutant GBS to wild-type GBS under stressed conditions. CiaR mutant GBS are more sensitive than wild-type GBS to elevated temperature, low pH, chemical mutagens and ultraviolet light; the mutants are also more sensitive to cell-wall active antibiotics and antimicrobial peptides. CiaR mutant strains are markedly attenuated in a mouse model of GBS sepsis. To determine the genes regulated by CiaR that account for these defects, transcriptional profiling was performed using DNA microarray analysis, comparing wild-type GBS to CiaR mutant GBS under non-stressed conditions.
2012-11-18 | GSE14569 | GEO
Project description:Streptococcus agalactiae (Group B Streptococcus, GBS) can colonize the human vaginal tract leading to both superficial and serious infections in adults and neonates. To study bacterial colonization of the reproductive tract in a mammalian system, we employed a murine vaginal carriage model. Using RNASeq, the transcriptome of GBS growing in vivo during vaginal carriage was determined. Over one-quarter of the genes in GBS were found to be differentially regulated during in vivo colonization as compared to laboratory cultures. A two-component system (TCS) homologous to the staphylococcal virulence regulator SaeRS was identified as being up-regulated in vivo. One of the SaeRS targets, pbsP, a proposed GBS vaccine candidate, was shown to be important for colonization of the vaginal tract. A component of vaginal lavage fluid acted as a signal to turn on pbsP expression via SaeRS. These data demonstrate the ability to quantify RNA expression directly from the murine vaginal tract and identify novel genes involved in vaginal colonization by GBS. They also provide more information about the regulation of an important virulence and colonization factor of GBS, pbsP, by the TCS SaeRS.
2018-02-06 | GSE109680 | GEO