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Role of Manganese Efflux for Signaling and Pathogenesis in Streptococcus pneumonia

ABSTRACT: Microarray analysis of Streptococcus pneumoniae TIGR4 transcriptome in response to manganese as the transcriptome changes in response to intracellular manganese accumulation via a mutation in sp1552/mntE a manganese efflux protein.

ORGANISM(S): Streptococcus pneumoniae TIGR4

PROVIDER: GSE14324 | GEO | 2009/03/01

SECONDARY ACCESSION(S): PRJNA111435

REPOSITORIES: GEO

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Role of Manganese Efflux for Signaling and Pathogenesis in Streptococcus pneumonia

Project description:Microarray analysis of Streptococcus pneumoniae TIGR4 transcriptome in response to manganese as the transcriptome changes in response to intracellular manganese accumulation via a mutation in sp1552/mntE a manganese efflux protein. Investigating role of manganese efflux and accumulation in S. pneumoniae: 3 TIGR4 in ThyB vs. TIGR4 in Mn and 3 TIGR4 in Mn vs mntE1 in Mn replicate 3

2010-05-22 | E-GEOD-14324 | biostudies-arrayexpress

Streptococcus pneumoniae. Two-color microarray bases Gene Expression Analysis v.6.5

Project description:TIGR4 and R6 bacterial strains of Streptococcus pneumoniae treated and not treated with the iron chelator deferoxamine mesylate (DFO)

2018-01-27 | GSE109693 | GEO

Transcriptomic analysis of Streptococcus suis in response to excess manganese

Project description:We explored the transcriptome change of Streptococcus suis in the presence of manganese by RNA sequencing. The data revealed that the genes in the troABCD operon were significantly downregulated in response to manganese.

2021-01-11 | GSE164206 | GEO

Transcription profiling of S. pneumonia strain TIGR4 early response to human A549 lung epithelial cells

Project description:Transcriptional responses of Streptococcus pneumoniae strain TIGR4 to human lung epithelial cells (A549) were investigated at the early stages of interactions (0.5 h and 1 h).

2008-09-30 | E-FPMI-15 | biostudies-arrayexpress

Proteomic Analysis on the Mechanism of Iron-Compensation Substitute for Manganese Deficiency of Streptococcus pneumoniae

Project description:Iron (Fe) and Manganese (Mn) are essential for bacterial survival and virulence as they are involved in catalysis, infection and biofilm formation. The basal metabolism of pathogenic bacteria would be disturbed by the deficiency of metal ions in the host environment. In this study, we found that Streptococcus pneumoniae (S. pneumoniae) can still grow slowly in the medium without manganese ions. Further ICP-MS determination showed that the iron concentration in the bacterium was increased when the manganese content was decreased. The supplement of iron in the manganese deficient culture medium (MDCM) can recovery the bacterial growth. The quantitative proteome using stable-isotope dimethyl labeling was performed to investigate the adaptive growth mechanism of S. pneumoniae in Mn-deficiency condition. Compared with the bacteria cultured in the normal medium, 25 proteins were down-regulated and 54 proteins were up-expressed with more than 1.2-fold alteration (P < 0.05) in S. pneumoniae cultured with MDCM. A large number of depressed proteins are participated in cell energy metabolism, amino acid synthesis process and oxidation products reduction process. The subsequent detection indicated that both intracellar and extracellular hydrogen peroxide levels of in cells were significantly elevated, and the intracellular ATP levels of were evidently decreased in cells cultured in the absence of manganese, meaning that Mn-deficiency can cause multiple metabolic disorders. More importantly, several iron ABC transporters, such as PiuA/PiaA/PitA/SPD_1609, etc, were over-expressed to uptake more iron from the medium. These results suggest that lacking of manganese only disturbed multiple metabolic processes of S. pneumoniae, but also caused the compensatory effect of iron for manganese Mn which is beneficial to the survival of bacteria in extreme environments.

2023-09-30 | PXD008652 | Pride

Transcription profiling of S. pneumonia early response to to THP-1 human macrophages

Project description:Transcriptional responses of an unencapsulated Streptococcus pneumoniae strain derived from TIGR4 to human macrophages THP-1 were investigated at the early stages of interactions (0.5 h, 1 h and 3h).

2008-10-21 | E-FPMI-16 | biostudies-arrayexpress

Anatomical Site-Specific Carbohydrate Availability Impacts Streptococcus pneumoniae Virulence and Fitness during Colonization and Disease

Project description:Transcriptomic analysis of Streptococcus pneumoniae TIGR4 wildtype and it's isogenic ccpA mutant, grown in chemically defined media supplemented with physiological levels of carbohydrates to mimic the human nasopharynx and bloodstream. The goal is to examine how anatomical site-specific carbohydrate availability impacts S. pneumoniae physiology and virulence.

2021-11-18 | GSE189057 | GEO

Impact of impaired polyamine biosynthesis on Streptococcus pneumoniae TIGR4 gene expression

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

Inducible expression of macrolide efflux in Streptococcus pneumoniae is controlled by transcriptional attenuation of the mef(E)/mel operon

Project description:Macrolide resistance, increasingly identified in Streptococcus pneumoniae and a wide range of other Gram-positive bacteria, is often due to efflux pumps encoded by the mef/mel(msr) operon found on discrete mobile genetic elements. The regulation of mef/mel(msr) in these elements is not well understood. We defined the promoter controlling the mef(E)/mel operon in S. pneumoniae, identified cis-acting 5′ regulatory elements and determined the mechanism of macrolide-inducible expression of the efflux pump. The mef(E)/mel transcriptional start site was a guanine 327 bp upstream of the mef(E) start codon. Consensus pneumococcal promoter -10 (5′-TATACT-3′) and -35 (5′-TTGAAC-3′) boxes separated by a 17 bp spacer were identified 7 bp upstream of the start site. Analysis of the predicted secondary structure of the 327 bp 5’ region identified four pairs of inverted repeats R1-R8 predicted to fold into stem-loops, a small leader peptide (MTASMRLR) required for macrolide induction and a Rho-independent transcription terminator involving the R5/R6 stem loop. Mutational analyses of the regulatory region identified transcriptional attenuation as the model for the inducible expression of macrolide efflux, which was confirmed by RNA-Seq expression data. The 327 bp region 5’ of mef(E) was highly conserved in other mef/mel(msr)-containing genetic elements complexes including Tn1207.1 and the 5612IQ complex in pneumococci and Tn1207.3 in Group A streptococci. Induction of the mef(E)/mel operon and macrolide efflux occurs by anti-attenuation in the presence of inducing macrolides and appears to be a mechanism RNA-seq was performed on wild type and mutant cultures of four strains of Streptococcus pneumoniae untreated, or treated with spiramycin, LL-37 or erythromycin

2014-02-01 | E-GEOD-54176 | biostudies-arrayexpress

Role of PsaR of Streptococcus pneumoniae D39 and TIGR4 in global gene expression and virulence

Project description:Previous studies have indicated that PsaR of Streptococcus pneumoniae is a manganese-dependent regulator, negatively affecting the expression of at least seven genes. Here, we extended these observations by transcriptome and proteome analysis of psaR mutants in strains D39 and TIGR4. The microarray analysis identified three shared PsaR targets: the psa-operon, pcpA, and prtA. Additionally, we found 31 genes to be regulated by PsaR in D39 only, most strikingly a cellobiose-specific PTS and a putative bacteriocin operon (sp0141-sp0146). In TIGR4, 14 PsaR gene targets were detected, with the rlrA pathogenicity islet being the most pronounced. Proteomics confirmed most of the shared gene targets. To examine the contribution of PsaR to pneumococcal virulence, we compared D39 and TIGR4 wild-type (wt) and psaR-mutants in three murine infection models. During colonization, no clear effect was observed of the psaR mutation in either D39 or TIGR4. In the pneumonia model, small but significant differences were observed in the lungs of mice infected with either D39wt or ∆psaR: D39∆psaR had an initial advantage in survival in the lungs. Conversely, TIGR4∆psaR-infected mice had significantly lower bacterial loads at 24h only. Finally, during experimental bacteremia, D39∆psaR-infected mice had significantly lower bacterial loads in the blood stream than wt-infected mice for the first 24h of infection. TIGR4∆psaR showed attenuation at 36h only. In conclusion, our results show that PsaR of D39 and TIGR4 has a strain-specific role in global gene expression and in the development of bacteremia in mice.

2008-11-19 | GSE13505 | GEO

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