Ontology highlight
ABSTRACT:
PROVIDER: PRJNA926651 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:A wheat–Thinopyrum chromosome substitution line (GLA3) was characterized at the genomic level using genotyping-by-sequencing (GBS). In the GLA3 line, a Thinopyrum-derived group 3 chromosome (3J) replaces wheat chromosome 3D. To confirm the chromosomal composition, identify the homoeologous relationships of the alien chromosome, and detect potential chromosomal rearrangements or deletions, GBS read coverage analysis was performed. Short reads from the GLA3 introgression line were aligned to the wheat (Triticum aestivum IWGSC RefSeq v2.1) and Thinopyrum intermedium (v3.1) reference genomes, revealing the absence of chromosome 3D and the presence of Thinopyrum group 3 chromatin predominantly of J-genome origin.
2026-05-19 | E-MTAB-17093 | biostudies-arrayexpress
Project description:To define the transcriptional response associated to a CovR inactivation we performed RNA-Seq in GBS strains BM110 and NEM316. We used mutants in which CovR is inactivated following a two base-pairs chromosomal substitution (AT->CC) resulting in the translation of a CovRD53A variant unable to be phosphorylated by the histidine kinase CovS. We also used a ∆covR mutant in strain BM110 in which the covR sequence is deleted from the chromosome.
2021-08-23 | GSE158047 | GEO
Project description:We report the characterization of the major regulator of virulence gene expression (CovR) in Group B Streptococcus. The ChIP-seq experiments define the binding of CovR on the chromosome of the BM110 strain, a representative of the hypervirulent GBS lineage responsible of neonatal meningitis. Regulatory evolution of CovR signaling was investigated by comparing ChIP-seq done in parallel in a second GBS clinical isolate (NEM316) not belonging to the hypervirulent lineage.
2021-08-23 | GSE158046 | GEO
Project description:One of the strongest associated type 2 diabetes (T2D) loci reported to date resides within the TCF7L2 gene. Previous studies point to the T allele of rs7903146 in intron 3 as the causal variant at this locus. To aid in the identification of the actual gene(s) under the influence of this variant, we first generated a CRISPR/Cas9 mediated 1.4kb deletion of the genomic region harboring rs7903146 in the HCT116 cell line followed by global gene expression analysis (see experiment E-MTAB-4839). We then carried out high-throughput chromosome conformation capture assays in the HCT116 and NCM460 cell lines and in colon tissue in order to ascertain which of these perturbed genes promoters made consistent physical contact with the genomic region harboring the variant. To assess consistency and reproducibility we utilized two different techniques: Circularized Chromosome Conformation Capture (4C) and Capture C. In both types of assays, after preparing 3C libraries, our bait of interest was the region harboring rs7903146. Loci interacting with such bait are enriched for by inverse PCR in 4C and by oligonucleotide capture in capture C. 4C assays were carried out in the following samples: two on NCM460 cells (using different primer sets), one on HCT116 cells, one on HCT116 cells with a CRISPR/Cas9 mediated 1.4kb deletion of the genomic region harboring the SNP rs7903146, and one on colon tissue. Capture C assays were carried out in one sample each of the cell lines NCM 460 and HCT116. This experiment, coupled with the associated E-MTAB-4839, revealed just one gene, ACSL5, which resides in the same topologically associating domain as TCF7L2.
2016-08-15 | E-MTAB-4845 | biostudies-arrayexpress
Project description:Guillain-Barré syndrome (GBS) is an autoimmune disorder that causes sensory loss, motor deficits, autonomic dysfunction, and chronic neuropathic pain. The most common GBS variant, acute inflammatory demyelinating polyradiculoneuropathy (AIDP), primarily results from immune attack against myelin surrounding cranial and peripheral axons and associated Schwann cells. Pathogenic peripheral myelin-specific antibodies are hypothesized to contribute to pathogenesis; however, the specific immune mediators responsible for driving autoimmune injury in early disease stages remain incompletely understood. We performed bulk and single-cell RNA sequencing on peripheral blood mononuclear cells collected from early untreated AIDP-variant GBS patients and healthy controls to comprehensively deduce leukocyte transcript and signaling pathway alterations and predict interactions between pathogenic leukocytes and peripheral nervous system cells that could drive disease. Bulk transcriptomics showed a type I and II interferon- and JAK/STAT-driven proinflammatory signature in myeloid cells, while CD8+ T-cells were highly proliferative and expressed axon guidance genes. Single-cell transcriptomics revealed dysregulation of regulatory and CD4+ effector memory T-cells indicative of poorly controlled type 1 and type 17 immune response. A subset of intermediate CD14+CD16+ intermediate monocytes with a highly activated phenotype uniquely upregulated genes related to angiogenesis and the interleukin (IL)-6 family cytokine oncostatin M. Interactome analysis between GBS leukocytes, Schwann cells, and sensory neurons predicted increased engagement of ligand-receptor pairs with nerve integrity and pain functions. These included epiregulin, interferon-beta, adrenomedullin, clusterin, IL-6, and IL-15. Activated intermediate monocytes participated in a CCL4 to CCR1/CCR5 interaction toward both sensory neurons and Schwann cells. These results unearth specific molecular interactions by which specific leukocyte populations in AIDP-variant GBS may induce peripheral nerve injury and drive associated neuropathic pain.
2026-02-19 | GSE304872 | GEO
Project description:Guillain-Barré syndrome (GBS) is an autoimmune disorder that causes sensory loss, motor deficits, autonomic dysfunction, and chronic neuropathic pain. The most common GBS variant, acute inflammatory demyelinating polyradiculoneuropathy (AIDP), primarily results from immune attack against myelin surrounding cranial and peripheral axons and associated Schwann cells. Pathogenic peripheral myelin-specific antibodies are hypothesized to contribute to pathogenesis; however, the specific immune mediators responsible for driving autoimmune injury in early disease stages remain incompletely understood. We performed bulk and single-cell RNA sequencing on peripheral blood mononuclear cells collected from early untreated AIDP-variant GBS patients and healthy controls to comprehensively deduce leukocyte transcript and signaling pathway alterations and predict interactions between pathogenic leukocytes and peripheral nervous system cells that could drive disease. Bulk transcriptomics showed a type I and II interferon- and JAK/STAT-driven proinflammatory signature in myeloid cells, while CD8+ T-cells were highly proliferative and expressed axon guidance genes. Single-cell transcriptomics revealed dysregulation of regulatory and CD4+ effector memory T-cells indicative of poorly controlled type 1 and type 17 immune response. A subset of intermediate CD14+CD16+ intermediate monocytes with a highly activated phenotype uniquely upregulated genes related to angiogenesis and the interleukin (IL)-6 family cytokine oncostatin M. Interactome analysis between GBS leukocytes, Schwann cells, and sensory neurons predicted increased engagement of ligand-receptor pairs with nerve integrity and pain functions. These included epiregulin, interferon-beta, adrenomedullin, clusterin, IL-6, and IL-15. Activated intermediate monocytes participated in a CCL4 to CCR1/CCR5 interaction toward both sensory neurons and Schwann cells. These results unearth specific molecular interactions by which specific leukocyte populations in AIDP-variant GBS may induce peripheral nerve injury and drive associated neuropathic pain.
2026-02-19 | GSE304871 | GEO
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:Group B Streptococcus (GBS) is an opportunistic pathogen that colonizes the vaginal tract and can be transmitted to the fetus or newborn resulting in infection. Previously we identified that Akkermansia muciniphila alters the dynamics of GBS vaginal colonization. Here we determine that A. muciniphila promotes GBS aggregation and attachment to human vaginal epithelial cells (hVECs). RNA-sequencing analysis revealed that A. muciniphila changed expression of 258 unique GBS genes during hVEC colonization, with many involved in cell wall/membrane/envelope biogenesis. We demonstrate that A. muciniphila-mediated increases in GBS aggregation and attachment to hVECs are dependent on GBS capsule and pili, respectively. Lastly, we found that A. muciniphila promoted GBS aggregation in the murine vaginal lumen and continual treatment with A. muciniphila reduced GBS vaginal persistence. Our results highlight the dynamic impact of a commensal organism on GBS colonization, as well as demonstrate the probiotic potential of A. muciniphila in the vaginal environment.
2026-04-15 | GSE306314 | GEO