Ontology highlight
ABSTRACT:
PROVIDER: PRJNA392957 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5801550_1.fastq.gz | Fastqsanger.gz | |||
| SRR5801550_2.fastq.gz | Fastqsanger.gz | |||
| SRR5801560_1.fastq.gz | Fastqsanger.gz | |||
| SRR5801560_2.fastq.gz | Fastqsanger.gz | |||
| SRR5801570_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 288 |
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: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:The purpose of this study was to identify Group B Streptococcus (GBS) genes that are controlled by the CiaR response regulator. Deletion of the GBS ciaR gene resulted in a significant decrease in intracellular survival within neutrophils, murine macrophages, and human BMEC, which was linked to increased susceptibility to killing by antimicrobial peptides, lysozyme, and reactive oxygen species. Furthermore, competition experiments in mice showed that wild-type GBS had a significant survival advantage compared to the isogenic ciaR mutant. Microarray analysis comparing gene expression between the wild-type and ciaR mutant strains revealed several CiaR-regulated genes that may contribute to GBS stress tolerance and subversion of host defenses.
2009-01-22 | GSE14259 | GEO
Project description:The purpose of this study was to identify Group B Streptococcus (GBS) genes that are controlled by the CiaR response regulator. Deletion of the GBS ciaR gene resulted in a significant decrease in intracellular survival within neutrophils, murine macrophages, and human BMEC, which was linked to increased susceptibility to killing by antimicrobial peptides, lysozyme, and reactive oxygen species. Furthermore, competition experiments in mice showed that wild-type GBS had a significant survival advantage compared to the isogenic ciaR mutant. Microarray analysis comparing gene expression between the wild-type and ciaR mutant strains revealed several CiaR-regulated genes that may contribute to GBS stress tolerance and subversion of host defenses. Two cultures each of the wild-type GBS strain (COH1) and the isogenic ciaR mutant were grown in Todd-Hewitt broth to an optical density of 0.3. Cells were disrupted by shaking with glass beads and RNA was isolated by a Trizol method. A custom Affymetrix chip with a design based on the COH1 genomic sequence was used to analyze gene expression.
2009-01-22 | E-GEOD-14259 | biostudies-arrayexpress
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:GBS sequencing of canola from Northern European populations
| PRJNA835738 | ENA
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: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:The underlying change of gene network expression of Guillain-Barre syndrome (GBS) remains elusive. We sought to identify GBS-associated gene networks and signalling pathways by analyzing the transcriptional profile of leukocytes in the patients with GBS.
2011-07-28 | GSE31014 | GEO
Project description:Genome wide expression profiling was used to identify signifnificantly changed genes in fetal membranes after GBS treatment Genome-wide expression profiles in GBS-inoculated human extraplacental membranes in vitro were used to identify transcriptomic pathways altered by GBS . Using bioinformatics analysis of these expression profiles we aimed to test our hypothesis that GBS activates pathways related to inflammation and premature birth in human extraplacental membranes.
2018-01-18 | GSE96557 | GEO