Effect of 5-HT and fluoxetine on Turicibacter sanguinis gene expression in vitro
Ontology highlight
ABSTRACT:
ORGANISM(S): Turicibacter sanguinis
PROVIDER: GSE133810 | GEO | 2019/07/04
REPOSITORIES: GEO
Similar Datasets
Project description:Effect of 5-HT and fluoxetine on Turicibacter sanguinis gene expression in vitro
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Project description:Arid1b is a chromatin remodeler implicated in neurodevelopmental disorders. Arid1b mutant mice with haploinsufficiency (Arid1b HT) displayed persistent excitatory synaptic dysfunction from juvenile to adult stage, decreased synaptic density and transmission. Moreover, they showed autistic-like behaviors in both of early and adult stages, decreased sociability in pup USV calling and adult social interaction, and adult repetitive grooming. To investigate early transcriptomic changes in Arid1b mutant mice, RNAseq analysis of whole brain from wild-type and Arid1b mutant mice at postnatal day 10 was done. Transcriptomic changes support these electrophysiological and behavioral deficits. Arid1b HT mice at postnatal day 10 showed alterations in genes implicated in synaptic functions and ASD. Next, we found that early chronic fluoxetine treatment could carry out long-lasting restoration in electrophysiological and behavioral deficits in Arid1b HT mice. Whole brain transcriptomic analysis with mice at postnatal day 120 which underwent chronic fluoxetine treatment from postnatal day 3 to postnatal day 21 via mammillary milk was done to figure out transcriptomic reprogramming which contributes to this restoration. Comparing fluoxetine treated Arid1b HT mice and vehicle group, fluoxetine treated mice showed upregulation of synapse-related genes and disease related gene sets with reverse-ASD directions.
2022-07-21 | GSE189653 | GEO
Project description:The current project investigates the proteomic profiles of essential genes, mass spectrometric analysis respectively, under impact of sub-inhibitory concentration of ampicillin (0.125 micro gm/ml), to elucidate the S. sanguinis stress response mechanisms on a temporal basis and define “pathogenesis signatures” as potential therapeutic targets. We further believe that the current findings will help characterize a bacterial model for studying the dynamics of essential genes under clinically relevant stress factors (antibiotic treatment) and assist in designing evidence-based guidelines for treatment in clinical settings.
2018-01-09 | PXD006479 | Pride
Project description:Transcriptional profiling of ssa_1972-null mutant of Streptococcus sanguinis compared with wild type. The ssa_1972 gene was inactivated in Streptococcus sanguinis SK36 and transcriptional profile was compared with wild type SK36. More information can be found at http://www.people.vcu.edu/~pingxu One-condition experiment, M-NM-^Tssa_1972 vs S. sanguinis SK36 cells. Biological replicates: 3 wild type, 3 M-NM-^Tssa_1972, independently grown and harvested. One replicate (one wild type and one M-NM-^Tssa_1972 mixture) per array.
2013-07-17 | E-GEOD-48940 | biostudies-arrayexpress
Project description:Transcriptional profiling of ssa_1972-null mutant of Streptococcus sanguinis compared with wild type. The ssa_1972 gene was inactivated in Streptococcus sanguinis SK36 and transcriptional profile was compared with wild type SK36. More information can be found at http://www.people.vcu.edu/~pingxu
2013-07-17 | GSE48940 | GEO
Project description:Streptococcus sanguinis is a major component of the oral flora and an important cause of infective endocarditis. The genome sequence of S. sanguinis strain SK36 was recently determined. A number of foreign genes acquired by natural transformation were detected, as well as orthologs of competence genes previously identified in other species. However, significant differences in the S. sanguinis competence system relative to that of other streptococci were noted. We sought to examine S. sanguinis genetic competence, to characterize the global transcriptional response to competence induction, and to compare our results with those obtained from previous analyses of other streptococci. A mutant possessing an in-frame deletion in the comC gene encoding the competence-stimulating peptide was created and confirmed to have the expected phenotype. Studies indicated that competence could be induced in this strain by addition of competence-stimulating peptide, and determined the optimal conditions to employ for this purpose. Expression was monitored by microarray analysis at multiple time points from 2.5 to 30 min after induction. Over 200 genes were identified whose expression was altered at least two-fold in at least one time point, with the majority upregulated. The M-bM-^@M-^\lateM-bM-^@M-^] response was typical of that seen in previous studies. However, comparison of the M-bM-^@M-^\earlyM-bM-^@M-^] response in S. sanguinis with that of other streptococci revealed unexpected heterogeneity with regard to the number of genes induced, the nature of these genes, and their putative upstream regulatory sequences. S. sanguinis possesses a comparatively limited early response, which may define a minimal competence regulatory circuit. Transcriptional analysis of S. sanguinis strain JFP41 cells 0 to 30 min after treatment with CSP. Biological replicates: 3 replicates each independently grown and harvested. 4 technical replicates per array
2011-01-21 | E-GEOD-21619 | biostudies-arrayexpress
Project description:The neural embryonic stem cell test (ESTn) is in vitro test that mimics early neural differentiation. The aim of this study was to define the biological domain of ESTn based on gene expression of selective markers for certain cell types, and to investigate the effects of two antidepressants, fluoxetine (FLX) and venlafaxine (VNX), on neural differentiation.
2021-02-27 | GSE153836 | GEO
Project description:Streptococcus sanguinis is a major component of the oral flora and an important cause of infective endocarditis. The genome sequence of S. sanguinis strain SK36 was recently determined. A number of foreign genes acquired by natural transformation were detected, as well as orthologs of competence genes previously identified in other species. However, significant differences in the S. sanguinis competence system relative to that of other streptococci were noted. We sought to examine S. sanguinis genetic competence, to characterize the global transcriptional response to competence induction, and to compare our results with those obtained from previous analyses of other streptococci. A mutant possessing an in-frame deletion in the comC gene encoding the competence-stimulating peptide was created and confirmed to have the expected phenotype. Studies indicated that competence could be induced in this strain by addition of competence-stimulating peptide, and determined the optimal conditions to employ for this purpose. Expression was monitored by microarray analysis at multiple time points from 2.5 to 30 min after induction. Over 200 genes were identified whose expression was altered at least two-fold in at least one time point, with the majority upregulated. The “late” response was typical of that seen in previous studies. However, comparison of the “early” response in S. sanguinis with that of other streptococci revealed unexpected heterogeneity with regard to the number of genes induced, the nature of these genes, and their putative upstream regulatory sequences. S. sanguinis possesses a comparatively limited early response, which may define a minimal competence regulatory circuit.
2011-01-21 | GSE21619 | GEO
Project description:Transcriptional profiling of the spxA1-null mutant of Streptococcus sanguinis SK36 compared with wild type. The spxA1 gene was inactivated in Streptococcus sanguinis SK36, and the mutant demonstrated opaque colony morphology, reduced hydrogen peroxide (H2O2) production, and reduced antagonistic activity against Streptococcus S. mutans UA159 both on plates and in liquid media. The mutant also showed decreased tolerance to high temperature, and acidic and oxidative stresses. Complementation of the ΔspxA1 mutant with spxA1 restored colony morphology, H2O2 production and stress tolerance to the ΔspxA1 mutant. The mutant also exhibited an ~5-fold reduction in competitiveness in an animal model of endocarditis, indicating the involvement of SpxA1 in endocarditis virulence. Microarray studies revealed that a number of SpxA1-upregulated genes are involved in oxidative stress. The expression of spxB and nox (which encode pyruvate oxidase and NADH oxidase, respectively, and are involved in H2O2 production and nox involved virulence) significantly decreased in ΔspxA1 compared with the wild type. This may be at least partly responsible for the decreased H2O2 production and reduced virulence in the ΔspxA1 mutant because spxB and nox were involved in H2O2 production and nox involved virulence. One-condition experiment: ΔspxA1 vs. S. sanguinis SK36 cells. Biological replicates: 3 wild type, 3 ΔspxA1, independently grown and harvested. One replicate (one wild type and one ΔspxA1 mixture) per array.
2011-12-08 | E-GEOD-34203 | biostudies-arrayexpress
Project description:Gene expression profile of the Streptococcus sanguinis SSA_0351 deletion mutant, ssx_0351, compared to the wild-type strain SK36
2019-06-01 | GSE90021 | GEO