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PROVIDER: PRJEB52424 | ENA |
REPOSITORIES: ENA
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Project description:Whole genome sequencing of bacterial isolates (Neisseria, Campylobacter, Haemophilus and Streptococcus)
| PRJEB51219 | ENA
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: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:Microarray comparative genome hybridization (mCGH) data was collected from one Neisseria cinerea, two Neisseria lactamica, two Neisseria gonorrhoeae, and 48 Neisseria meningitidis isolates. For N. meningitidis, these isolates are from diverse clonal complexes, invasive and carriage strains, and all major serogroups. The microarray platform represented N. meningitidis strains MC58, Z2491, and FAM18 and N. gonorrhoeae FA1090.
2007-04-04 | E-TIGR-129 | 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 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:In a transcriptome based trail, we figured out that the deletion of luxS has a massive influence to cell growth and metabolism of Streptococcus sanguinis SK36. The biofilm defective luxS deletion mutant was comlemented by transgenic sahH from Pseudomonas aeruginosa. Thus 209 of 216 influenced genes of the luxS mutant compared to the isogenic wildype were restored in their expression (fold change of n M-bM-^IM-% 3; p M-bM-^IM-$ 0.05), including genes involved in cell division processes, stress response and catabolite control. Phenotypically, the reduced biofilm depth of S. sanguinis SR DELTAluxS was elevated to wild type level by the complementation with sahH. Neither the addition of physiological concentrated artificial autoinducer 2 (AI-2) to the culture of S. sanguinis SR DELTAluxS nor the presence of the wild type strain in a trans-well assay had a cumulative effect on biofilm thickness of the luxS mutant. Furthermore, we identified 9 genes in the sahH complemented luxS mutant, which were regulated directly by AI-2 (fold change M-bM-^IM-% 3; p M-bM-^IM-$ 0.05), amongst them genes involved in competence development. So we concluded that AI-2 has no influence on biofilm growth, but regulative functions in competence development in S. sanguinis. Further, we figured out the suitability of transgenic sahH for the complementation of the interrupted Pfs/LuxS pathway without restoration of AI-2 release acquiring an essential tool for further investigations on AI-2. Aim: Is the presence of AI-2 necessary for the biofilm formation of S. sanguinis SK36? What is the impact of a deletion of luxS, is a disrupted activated methionine cycle the reason for the hampered biofilm depth causes by its inactivation? Materials and Methods: S. sanguinis SK36, S. sanguinis SR M-NM-^TluxS, and S. sanguinis SR M-NM-^TluxS/sahH were grown in CDM/sucrose for 24 h anaerobically; biofilm depth was measured by safranine and crystal violet stain. Biofilm morphology was investigated by scanning electron microscopy. The AI-2 release was monitored hourly to identify the time period of its release. For transcriptome analysis total RNA was isolated after 8 hours of growth and used for microarray analysis. The chip study used total RNA recovered from S. sanguinis SK36, its luxS mutant, and the sahH complementated luxS mutant. Gene expression analysis was done with three independent replicates, each. Chip content: 10186 genes (1883 genes of P. gingivalis W83, 1964 genes of F. nucleatum DSMZ 25586, 2244 genes of S. sanguinis SK36, 2168 genes of A. actinomycetemcomitans HK1651, 1927 genes of S. mutans UA159) with up to thirteen 60-mer probes per gene, with three-fold technical redundancy and additionally 3510 random sequence probe. In this study only the S. sanguinis and RANDOM probes were used for analysis.
2012-04-03 | E-GEOD-37007 | biostudies-arrayexpress
Project description:Baart2007 - Genome-scale metabolic network of
Neisseria meningitidis (iGB555)
This model is described in the article:
Modeling Neisseria
meningitidis metabolism: from genome to metabolic fluxes.
Baart GJ, Zomer B, de Haan A, van
der Pol LA, Beuvery EC, Tramper J, Martens DE.
Genome Biol. 2007; 8(7): R136
Abstract:
BACKGROUND: Neisseria meningitidis is a human pathogen that
can infect diverse sites within the human host. The major
diseases caused by N. meningitidis are responsible for death
and disability, especially in young infants. In general, most
of the recent work on N. meningitidis focuses on potential
antigens and their functions, immunogenicity, and pathogenicity
mechanisms. Very little work has been carried out on Neisseria
primary metabolism over the past 25 years. RESULTS: Using the
genomic database of N. meningitidis serogroup B together with
biochemical and physiological information in the literature we
constructed a genome-scale flux model for the primary
metabolism of N. meningitidis. The validity of a simplified
metabolic network derived from the genome-scale metabolic
network was checked using flux-balance analysis in chemostat
cultures. Several useful predictions were obtained from in
silico experiments, including substrate preference. A minimal
medium for growth of N. meningitidis was designed and tested
successfully in batch and chemostat cultures. CONCLUSION: The
verified metabolic model describes the primary metabolism of N.
meningitidis in a chemostat in steady state. The genome-scale
model is valuable because it offers a framework to study N.
meningitidis metabolism as a whole, or certain aspects of it,
and it can also be used for the purpose of vaccine process
development (for example, the design of growth media). The flux
distribution of the main metabolic pathways (that is, the
pentose phosphate pathway and the Entner-Douderoff pathway)
indicates that the major part of pyruvate (69%) is synthesized
through the ED-cleavage, a finding that is in good agreement
with literature.
This model is hosted on
BioModels Database
and identified by:
MODEL1507180069.
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2015-07-30 | MODEL1507180069 | BioModels
Project description:Whole genome DNA microarray of Neisseria meningitidis serogroup B strain MC58 and the isogenic mutant strain deficient of the transcriptional regulator FarR, MC58 ∆farR.
2011-02-11 | GSE20643 | GEO
Project description:In a transcriptome based trail, we figured out that the deletion of luxS has a massive influence to cell growth and metabolism of Streptococcus sanguinis SK36. The biofilm defective luxS deletion mutant was comlemented by transgenic sahH from Pseudomonas aeruginosa. Thus 209 of 216 influenced genes of the luxS mutant compared to the isogenic wildype were restored in their expression (fold change of n ≥ 3; p ≤ 0.05), including genes involved in cell division processes, stress response and catabolite control. Phenotypically, the reduced biofilm depth of S. sanguinis SR DELTAluxS was elevated to wild type level by the complementation with sahH. Neither the addition of physiological concentrated artificial autoinducer 2 (AI-2) to the culture of S. sanguinis SR DELTAluxS nor the presence of the wild type strain in a trans-well assay had a cumulative effect on biofilm thickness of the luxS mutant. Furthermore, we identified 9 genes in the sahH complemented luxS mutant, which were regulated directly by AI-2 (fold change ≥ 3; p ≤ 0.05), amongst them genes involved in competence development. So we concluded that AI-2 has no influence on biofilm growth, but regulative functions in competence development in S. sanguinis. Further, we figured out the suitability of transgenic sahH for the complementation of the interrupted Pfs/LuxS pathway without restoration of AI-2 release acquiring an essential tool for further investigations on AI-2. Aim: Is the presence of AI-2 necessary for the biofilm formation of S. sanguinis SK36? What is the impact of a deletion of luxS, is a disrupted activated methionine cycle the reason for the hampered biofilm depth causes by its inactivation? Materials and Methods: S. sanguinis SK36, S. sanguinis SR ΔluxS, and S. sanguinis SR ΔluxS/sahH were grown in CDM/sucrose for 24 h anaerobically; biofilm depth was measured by safranine and crystal violet stain. Biofilm morphology was investigated by scanning electron microscopy. The AI-2 release was monitored hourly to identify the time period of its release. For transcriptome analysis total RNA was isolated after 8 hours of growth and used for microarray analysis.
2012-04-04 | GSE37007 | GEO