Epigenetic gene regulation by type I restriction modification systems in Streptococcus pneumoniae and Escherichia coli
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ABSTRACT:
ORGANISM(S): Streptococcus pneumoniae
PROVIDER: GSE293985 | GEO | 2026/04/01
REPOSITORIES: GEO
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Project description:Streptococcus pneumoniae (pneumococcus) is a major human respiratory pathogen and the leading cause of bacterial pneumonia worldwide. Small regulatory RNAs (sRNAs), which often act by post-transcriptionally regulating gene expression, have been shown to be crucial for the virulence of S. pneumoniae and other bacterial pathogens. Over 170 putative sRNAs have been identified in S. pneumoniae TIGR4 strain (serotype 4) through transcriptomic studies, and a subset of these sRNAs have been further implicated in regulating pneumococcal pathogenesis. However, there was little overlap in the sRNAs identified among these studies, which indicated that the approaches used for sRNA identification were not sufficiently sensitive and robust and that there were likely many more undiscovered sRNAs encoded in the S. pneumoniae genome. Here, we sought to comprehensively identify sRNAs in Avery's virulent S. pneumoniae strain D39 using two independent RNA-seq based approaches. We developed an unbiased method for identifying novel sRNAs from bacterial RNA-seq data and have further tested the specificity of our analysis program towards identifying sRNAs encoded by both strains D39 and TIGR4. Interestingly, the genes for 15% of the putative sRNAs identified in strain TIGR4 including ones previously implicated in virulence were not present in strain D39 genome suggesting that the differences in sRNA repertoires between these two serotypes may contribute to their strain-specific virulence properties. Finally, this study has identified 67 new sRNA candidates in strain D39, 28 out of which have been further validated, raising the total number of sRNAs that have been identified in strain D39 to 112.
2019-03-11 | GSE123437 | GEO
Project description:Streptococcus pneumoniae (pneumococcus) is a major human respiratory pathogen and a leading cause of bacterial pneumonia worldwide. Small regulatory RNAs (sRNAs), which often act by post-transcriptionally regulating gene expression, have been shown to be crucial for the virulence of S. pneumoniae and other bacterial pathogens. Over 170 putative sRNAs have been identified in S. pneumoniae TIGR4 strain (serotype 4) through transcriptomic studies, and a subset of these sRNAs have been further implicated in regulating pneumococcal pathogenesis. However, there is little overlap in the sRNAs identified among these studies, which indicates that the approaches used for sRNA identification were not sufficiently sensitive and robust and that there are likely many more undiscovered sRNAs encoded in the S. pneumoniae genome. Here, we sought to comprehensively identify sRNAs in Avery's virulent S. pneumoniae strain D39 using two independent RNA-seq based approaches. We developed an unbiased method for identifying novel sRNAs from bacterial RNA-seq data and have further tested the specificity of our analysis program towards identifying sRNAs encoded by both strains D39 and TIGR4. Interestingly, the genes for 15% of the putative sRNAs identified in strain TIGR4 including ones previously implicated in virulence are not present in strain D39 genome suggesting that the differences in sRNA repertoires between these two serotypes may contribute to their strain-specific virulence properties. Finally, this study has identified 67 new sRNA candidates in strain D39, 28 out of which have been further validated, raising the total number of sRNAs that have been identified in strain D39 to 112.
2019-05-13 | GSE124170 | GEO
Project description:We report the mRNA expression profile of Streptococcus pneumoniae Type 2 D39 strain-derived mutant lacking the phpP gene encoding eukaryote-type ser/thr phosphatase . Measuring transcriptome profiling in D39Î?phpP mutants vs D39-WT pneumococcus wild-type strain
2016-10-27 | E-GEOD-74421 | biostudies-arrayexpress
Project description:Streptococcus pneumoniae is an opportunistic pathogen that colonizes the mucosal surfaces of the human upper respiratory tract. To the exception of very few studies, all previous transcriptomic analyses on the pneumococcus were carried out using lab-adapted strains such as D39 or TIGR4. Our study is one of the first to investigate the transcriptomes of serotype 1 (S1) pneumococci. We took the most basic approach of growing S. pneumoniae in brain heart infusion medium using three distinct strains, i.e. sequence type ST306, ST217 and ST615, as representative isolates of the European, African and South American S1 clusters. As a follow-up to our recent studies on these three lineages, we sought to investigate their respective in vitro transcriptomic profiles in comparison to D39. In total, 292 genes showed significant differential expression in the exponential growth phases of all three S1 isolates compared to D39. A total of 151 genes showed higher transcription levels while 141 genes presented lower expression. The most prominent functional groups showing higher expression included the competence pathway and purine metabolism, while lactose metabolism and iron/amino acid transport presented lower expression in serotype 1 strains. Our study provides novel insight into the signature gene expression associated with hypervirulent pneumococci S1 and highlight the need to perform transcriptomic analysis on pneumococcal strains other than lab-adapted strains.
2025-07-11 | GSE279694 | GEO
Project description:Comparison of the Streptococcus pneumoniae D39 spxB- mutant vs D39. For DNA microarray analysis, D39 wild-type and two independently obtained D39spxB- mutants were grown as four, two and two biological replicates, respectively, in Glc-M17 under semi-aerobic conditions and harvested at an OD595 of approximately 0.25 (mid-exponential). The RNA of both D39spxB- strains was compared to D39 and the combined data was analyzed. All other procedures regarding microarray analyses were done as described before. A gene was considered differentially expressed when the fold change was ≥ 2, ≤ 0.5, with a Bayes p ≤ 0.00001 and when at least 7 measurements were available.
2013-08-08 | GSE45971 | GEO
Project description:Our understanding of the synergism between S. pneumoniae and influenza virus remains incomplete. The classic dogma has been that influenza attenuates the host innate immunity and increase the susceptibility to subsequent bacterial infection. Therefore, the majority of current studies have been focusing on the interaction of S. pneumoniae and influenza in the context of host cells. By contrast, in this study, we set out to investigate the response of pneumococcus alone to virus infection. Our hypothesis was that prior to causing any damages to host cells, influenza may have induced (lethal) changes to pneumococcus cell itself. Indeed, a very recent evidence has shown that direct viral treatment to pneumococcus will increase its adhesion to macrophage cells. Here, using quantitative phosphoproteomic approach, we attempt to investigate the global alterations of S. pneumoniae phosphorylation by influenza virus challenge, and provide a landscape of synergism between the IAV and pneumococcus.
2022-12-09 | PXD016214 | Pride
Project description:Streptococcus pneumoniae (pneumococcus) is a leading human pathogen that can cause serious localized and invasive diseases. Pneumococci can undergo a spontaneous and reversible phase variation that is reflected in colony opacity, which allows the population to adapt to different host environments. Generally, transparent variants are adapted for nasopharyngeal colonization whereas opaque variants are associated with invasive disease. In recent work, colony phase variation was shown to occur by means of recombination events to generate multiple alleles of the hsdS targeting domain of a DNA methylase complex, which mediates epigenetic changes in gene expression. A panel of isogenic strains were created in the well-studied S. pneumoniae TIGR4 background that are “locked” in the transparent (n=4) or opaque (n=2) colony phenotype. The strains had significant differences in colony size which were stable over multiple passages in vitro and in vivo. While there were no significant differences in adherence for the phase-locked mutant strains to immortalized epithelial cells, biofilm formation and viability was reduced for opaque variants in static assays. Nasopharyngeal colonization was stable for all strains, but the mortality rate differed between them. Transcript profiling by RNA-seq analyses revealed that expression of certain virulence factors were increased in a phase-specific manner. As epigenetic regulation of phase variation (often referred to as phasevarion) is emerging as a common theme for mucosal pathogens, these studies serve as a model for future studies of host-pathogen interactions.
2017-09-21 | GSE103364 | GEO
Project description:Toxin-antitoxin loci belonging to the yefM-yoeB family are located in the chromosome or in some plasmids of several bacteria. We cloned the yefM-yoeB locus of Streptococcus pneumoniae, and these genes encode bona fide antitoxin (YefM(Spn)) and toxin (YoeB(Spn)) products. We showed that overproduction of YoeB(Spn) is toxic to Escherichia coli cells, leading to severe inhibition of cell growth and to a reduction in cell viability; this toxicity was more pronounced in an E. coli B strain than in two E. coli K-12 strains. The YoeB(Spn)-mediated toxicity could be reversed by the cognate antitoxin, YefM(Spn), but not by overproduction of the E. coli YefM antitoxin. The pneumococcal proteins were purified and were shown to interact with each other both in vitro and in vivo. Far-UV circular dichroism analyses indicated that the pneumococcal antitoxin was partially, but not totally, unfolded and was different than its E. coli counterpart. Molecular modeling showed that the toxins belonging to the family were homologous, whereas the antitoxins appeared to be specifically designed for each bacterial locus; thus, the toxin-antitoxin interactions were adapted to the different bacterial environmental conditions. Both structural features, folding and the molecular modeled structure, could explain the lack of cross-complementation between the pneumococcal and E. coli antitoxins.
| S-EPMC1797350 | biostudies-literature
Project description:Transcriptome comparison of the Streptococcus pneumoniae D39 ΔnaiR to D39 wild type grown in CDM
2017-02-24 | GSE94511 | GEO