Ontology highlight
ABSTRACT:
PROVIDER: PRJNA761098 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15815700_1.fastq.gz | Fastqsanger.gz | |||
| SRR15815700_2.fastq.gz | Fastqsanger.gz | |||
| SRR15815800_1.fastq.gz | Fastqsanger.gz | |||
| SRR15815800_2.fastq.gz | Fastqsanger.gz | |||
| SRR15815900_1.fastq.gz | Fastqsanger.gz |
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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
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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.
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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.
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Project description:Group B Streptococcus (GBS) frequently colonizes the vagina asymptomatically where the bacterium interacts with a complex microbial community. During pregnancy, colonization can trigger adverse outcomes and neonatal invasive infection. Using an adapted murine model of vaginal colonization, we show that the human pathobiont Candida albicans supports GBS fitness in the vaginal tract and ascension to the uterus. C. albicans positively associates with GBS across several human studies, and C. albicans and GBS physically interact in a mouse co-colonization model. This co-colonization contributes to GBS persistence in the vagina, cervix, and uterus and facilitates antibiotic evasion. Across clinical isolates, the hyphal form of C. albicans promotes GBS aggregation and adhesion to host epithelial cells. Contact with GBS induces arginine biosynthesis in C. albicans, which drives bacterial virulence gene expression and primes GBS adhesion. These findings show that interkingdom nutrient exchange can increase GBS pathogenic potential and highlight targets for preventative therapies.
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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.
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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.
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