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Streptococcus pneumoniae TIGR4

ABSTRACT: Streptococcus pneumoniae TIGR4 Genome sequencing

PROVIDER: PRJNA750080 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15300800.fastq.gz	Fastqsanger.gz
	SRR15300801.fastq.gz	Fastqsanger.gz
	SRR15300802.fastq.gz	Fastqsanger.gz
	SRR15300803.fastq.gz	Fastqsanger.gz
	SRR15300804.fastq.gz	Fastqsanger.gz

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Streptococcus pneumoniae TIGR4

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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.

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Project description:Purpose: We recently reported that isogenic deletion of lysine decarboxylase (ΔcadA/SP_0916), an enzyme that catalyzes the biosynthesis of polyamine cadaverine in Streptococcus pneumoniae TIGR4 results in loss of capsular polysaccharide (CPS), which constitutes a novel mechanism of regulation of CPS. Here, we conducted RNA-Seq to elucidate molecular mechanisms of CPS regulation in polyamine synthesis impaired pneumococci. Result: Significantly differentially expressed genes in ΔcadA represent pneumococcal pathways involved in the biosynthesis of precursors for CPS and peptidoglycan. Conclusion: We establish a possible link and interchange between two cellular processes such as high energy demanding capsule production and oxidative stress responses in polyamine synthesis impaired pneumococci (ΔcadA).

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Differential transcription of small RNAs and mRNAs of Streptococcus pneumoniae TIGR4 when grown with the biofilm inhibitor Carolacton

Project description:Carolacton is a novel biofilm inhibitor that kills biofilm cells of Streptococcus mutans in nanomolar concentrations. Interestingly, Carolacton also inhibits growth of the clinically relevant and human pathogenic bacterium Streptococcus pneumoniae TIGR4. The cellular target of Carolacton is still unknown. Here, we adressed the differential transcription of cellular RNAs when S. pneumoniae TIGR4 was grown in the presence of Carolacton. This was done to identify transcriptional regulatory networks that are directly affected by treatment of the pneumococcus with Carolacton. In order to gain insights into the primary transcriptional response, early time-points were chosen for sampling, which should not reflect secondary responses (e.g. due to differences in growth phase, drop in pH etc.). To achieve a thorough overview over all affected cellular RNA species, such as mRNAs, small regulatory RNAs and tRNAs, and not to lose small transcripts during library preparation, RNAs were separated according to size and used to construct two separate libraries for sequencing.

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Project description:Streptococcus pneumoniae strain:TIGR4:19F Genome sequencing

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Project description:The polyamine transport operon in Streptococcus pneumoniae TIGR4 is necessary for survival in murine models of pneumococcal pneumonia. To date, there is no description of polyamine transport dependent pneumococcal gene expression. In this study, we compared gene expression between the wild-type and transport deficient (potABCD) TIGR4 by RNA-Seq analysis.

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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.

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