Streptococcus pneumoniae
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ABSTRACT:
PROVIDER: PRJNA96343 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Investigation of pneumococcal two-component signal transduction system RR/HK06 in D39
| PRJNA96331 | ENA
Project description:We wanted to identify genes regulated by the two-component signal transduction system RR/HK06 in Streptococcus pneumoniae. We used microarray in order to discover regulated genes, investigating the effects of the over-expression of RR06 in TIGR4 (serotype 4). Keywords: Gene Regulation
2006-12-17 | GSE5330 | GEO
Project description:We wanted to identify genes regulated by the two-component signal transduction system RR/HK06 in Streptococcus pneumoniae. We used microarray in order to discover regulated genes, investigating the effects of the over-expression of RR06 in D39 (serotype 2). Keywords: Gene Regulation
2006-12-23 | GSE5322 | GEO
Project description:The polyamine biosynthesis gene, speE, in Streptococcus pneumoniae TIGR4 is necessary for survival in murine models of pneumococcal pneumonia. To date, there is no description of polyamine biosynthesis dependent pneumococcal gene expression. In this study, we compared gene expression between the wild-type and biosynthesis deficient (speE) TIGR4 by RNA-Seq analysis.
2023-01-01 | E-MTAB-6070 | biostudies-arrayexpress
Project description:We used a combination of adherence assays, mutagenesis and functional genomics to identify novel factors involved in adherence. This work identifies a list of novel potential pneumococcal adherence determinants. S. pneumoniae TIGR4 transcriptome was sequenced using RNA-Seq on the Illumina GA. High-quality, single ended, 36bp reads were mapped to the TIGR4 genome.
2013-09-30 | E-GEOD-44947 | biostudies-arrayexpress
Project description:Recent murine studies have demonstrated that the role of response regulator 09 (RR09) of S. pneumoniae in virulence varies between strains. In the present study, we used a murine pneumonia model of infection to assess the virulence of a TIGR4 rr09-mutant, and found that TIGR4Δrr09 was attenuated after intranasal infection. Further, we investigated the in vitro transcriptional changes in pneumococcal rr09 mutants of two strains, D39 and TIGR4, by microarray analysis. The transcriptional profiles of the rr09 mutants in both strains displayed clear differences compared to their parental wild-type. In D39Δrr09 but not TIGR4Δrr09, genes involved in competence (e.g. comAB) were upregulated. In TIGR4, genes located on the rlrA pathogenicity islet, absent in the D39 genome, appeared to be regulated by RR09. Furthermore, several phosphotransferase systems (PTSs), believed to be involved in sugar uptake (e.g., sp0060-sp0066), were strongly downregulated in D39Δrr09, while not regulated by RR09 in TIGR4. To address the role of one of these PTS in virulence, D39Δsp0063 was constructed and tested in a murine infection model. No difference in virulence compared to the wild-type was found, indicating that downregulation of this gene alone is not the cause of the avirulent phenotype of D39Δrr09. Finally, expression of rr09 and three of our identified RR09 targets were assessed during infection in mice. This in vivo experiment confirmed differences in expression between TIGR4 wild-type and rr09-mutant, as well as between wild-type D39 and TIGR4. In conclusion, our results indicate strain specific regulation of pneumococcal gene expression by RR09. Keywords: Genetic modification
2006-10-28 | GSE6139 | GEO
Project description:Recent murine studies have demonstrated that the role of response regulator 09 (RR09) of S. pneumoniae in virulence varies between strains. In the present study, we used a murine pneumonia model of infection to assess the virulence of a TIGR4 rr09-mutant, and found that TIGR4Δrr09 was attenuated after intranasal infection. Further, we investigated the in vitro transcriptional changes in pneumococcal rr09 mutants of two strains, D39 and TIGR4, by microarray analysis. The transcriptional profiles of the rr09 mutants in both strains displayed clear differences compared to their parental wild-type. In D39Δrr09 but not TIGR4Δrr09, genes involved in competence (e.g. comAB) were upregulated. In TIGR4, genes located on the rlrA pathogenicity islet, absent in the D39 genome, appeared to be regulated by RR09. Furthermore, several phosphotransferase systems (PTSs), believed to be involved in sugar uptake (e.g., sp0060-sp0066), were strongly downregulated in D39Δrr09, while not regulated by RR09 in TIGR4. To address the role of one of these PTS in virulence, D39Δsp0063 was constructed and tested in a murine infection model. No difference in virulence compared to the wild-type was found, indicating that downregulation of this gene alone is not the cause of the avirulent phenotype of D39Δrr09. Finally, expression of rr09 and three of our identified RR09 targets were assessed during infection in mice. This in vivo experiment confirmed differences in expression between TIGR4 wild-type and rr09-mutant, as well as between wild-type D39 and TIGR4. In conclusion, our results indicate strain-specific regulation of pneumococcal gene expression by RR09. Keywords: genetic modification
2006-12-24 | GSE6137 | GEO
Project description:Two-component signal transduction systems in Streptomyces and related organisms
| PRJNA110647 | ENA
Project description:Refutation: Structure and mechanism of the essential two-component signal-transduction system WalKR in Staphylococcus aureus.
| PRJEB14381 | ENA
Project description:RNases perform indispensable functions in regulating gene expression in many bacterial pathogens by processing and/or degrading RNAs. Despite the pivotal role of RNases in regulating bacterial virulence factors, the functions of RNases have not yet been studied in the major human respiratory pathogen Streptococcus pneumoniae (pneumococcus). Here, we sought to determine the impact of two conserved RNases, the endoribonuclease RNase Y and exoribonuclease polynucleotide phosphorylase (PNPase), on the physiology and virulence of S. pneumoniae serotype 2 strain D39. We report that RNase Y and PNPase are essential for pneumococcal pathogenesis as both deletion mutants showed strong attenuation of virulence in murine models of invasive pneumonia. Genome-wide transcriptomic analysis revealed that nearly 200 mRNA transcripts were significantly up-regulated, whereas the abundance of several pneumococcal sRNAs, including the Ccn (CiaR Controlled Noncoding RNA) sRNAs, were altered in the ∆rny mutant relative to the wild-type strain. Additionally, lack of RNase Y resulted in pleiotropic phenotypes that included defects in pneumococcal cell morphology and growth in vitro. In contrast, Dpnp mutants showed no growth defect in vitro, but differentially expressed a total of 40 transcripts including the tryptophan biosynthesis operon genes and numerous 5’-cis-acting regulatory RNAs, a majority of which were previously shown to impact pneumococcal disease progression in mice using the serotype 4 strain TIGR4. Altogether our data suggest that RNase Y exerts a global impact on pneumococcal physiology, while PNPase-mediates virulence phenotypes, likely through sRNA regulation.
2021-09-02 | GSE173392 | GEO