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ABSTRACT:
PROVIDER: PRJNA556140 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Our group recently transcriptomically characterized coculture growth between Streptococcus mutans and several species of commensal streptococci (Rose et al, 2023; Choi et al 2024). One interaction that stood out was with Streptococcus mitis ATCC 49456, which completely inhibited the growth of S. mutans during biofilm formation. This is due to abudant hydrogen peroxide production by S. mitis ATCC 49456, 3-5x higher than other oral commensal streptococci we have worked with. To understand how the transcriptome of S. mutans is modified in coculture with a high hydrogen peroxide producer, we evaluated the transcriptome during monoculture or coculture growth between the two strains. Our results show differential gene expression (DEGs) in S. mutans that follows other trends we have documented previously with other commensal Streptococcus species, as well as DEGs specific to the interaction with S. mitis.
2024-08-02 | GSE273140 | GEO
Project description:Antibiotic resistance in Streptococcus pneumoniae is often the result of horizontal gene transfer events involving closely related streptococcal species. Laboratory experiments confirmed that S. mitis DNA functions as donor in transformation experiments, using the laboratory strain S. pneumoniae R6 as recipient and chromosomal DNA of a high level penicillin resistant S. mitis B6 strain. After four transformation steps, alterations in five penicillin-binding proteins (PBP) were observed, and sequence analysis confirmed recombination events in the corresponding PBP genes. In order to detect regions where recombination with S. mitis DNA has occurred we analyzed the S. pneumoniae transformants by microarray analyses, using oligonucleotide microarrays designed for the S. pneumoniae genome and the S. mitis B6 genome as well.
2011-04-21 | E-MEXP-3170 | biostudies-arrayexpress
Project description:Human bronchial epithelial cell line Beas-2B were infected with Streptococcus pneumoniae at Multiplicity of Infection (MOI) of 0.5 and 1 or treated with lipoteichonic acid (LTA) for 9 and 16 h. The mRNA profile changes upon infection shall be determined to investigate Streptococci pathogenesis.
2023-02-01 | GSE195778 | GEO
Project description:Genomic comparison of Streptococcus mitis B6 and other Streptococcus mitis strains.
2010-01-21 | E-MEXP-2497 | biostudies-arrayexpress
Project description:Our group recently transcriptomically characterized coculture growth between Streptococcus mutans and several species of commensal streptococci (Rose et al, 2023). However, these experiments were carried out in our lab-based experimental medium, tryptone and yeast extract (TY-). To understand whether culturing these species within a medium that more closely mimics their natural environment alters the interaction, we evaluated both monoculture and coculture growth between the dental caries pathogen Streptococcus mutans and oral commensal species Streptococcus oralis in a half TY- / half human saliva mix that was optimally chosen based on our initial characterization of oral streptococci behaviors in medium mixes containing saliva. Our results surprising show that inclusion of saliva enhances the competition of Streptococcus mutans against commensal streptococci through upregulation of carbohydrate uptake and glycolytic pathways.
2023-08-22 | GSE239483 | GEO
Project description:Treatment of pneumococcal infections is limited by antibiotic resistance and exacerbation of disease by bacterial lysis releasing pneumolysin toxin and other inflammatory factors. We identified a novel peptide in the Klebsiella pneumoniae secretome, which enters Streptococcus pneumoniae via its AmiA-AliA/AliB permease. Subsequent downregulation of genes for amino acid biosynthesis and peptide uptake was associated with reduction of pneumococcal growth in defined medium and human cerebrospinal fluid, irregular cell shape, decreased chain length and decreased genetic transformation. The bacteriostatic effect was specific to S. pneumoniae and Streptococcus pseudopneumoniae with no effect on Streptococcus mitis, Haemophilus influenzae, Staphylococcus aureus or K. pneumoniae. Peptide sequence and length were crucial to growth suppression. The peptide reduced pneumococcal adherence to primary human airway epithelial cell cultures and colonization of rat nasopharynx, without toxicity. We also analysed the effect of peptide on the proteome of S. pneumoniae. We found alteration of the proteome by the peptide with some proteins turned on or off in line with the transcriptomic changes. We therefore identified a peptide with potential as a therapeutic for pneumococcal diseases suppressing growth of multiple clinical isolates, including antibiotic resistant strains, while avoiding bacterial lysis and dysbiosis.
2024-04-08 | PXD050408 | Pride
Project description:We explored the regulatory mechanism of Leloir pathway genes in Streptococcus pneumoniae D39. Here, we demonstrate that the expression of galKT is galactose dependent. By microarray analysis and quantitative RT-PCR, we further show the role of the transcriptional regulator GalR, present upstream of galKT, as a transcriptional activator of galKT in the presence of galactose. Moreover, we predict a 19-bp regulatory site (5'-GATAGTTTAGTAAAATTTT-3' ) for the transcriptional regulator GalR in the promoter region of galK, which is also highly conserved in other streptococci. Growth comparison of Î galK with the D39 wildtype strain grown in the presence of galactose shows that galK is required for the proper growth of S. pneumoniae on galactose. Comparison of the Streptococcus pneumoniae D39 galR mutant compared to D39 wild type in M17 medium+ 0.5% (w/v) galactose (GalM17). One condition design comparison of two strains including a dye swap.
2015-10-30 | E-GEOD-74501 | biostudies-arrayexpress
Project description:We explored the regulatory mechanism of Leloir pathway genes in Streptococcus pneumoniae D39. Here, we demonstrate that the expression of galKT is galactose dependent. By microarray analysis and quantitative RT-PCR, we further show the role of the transcriptional regulator GalR, present upstream of galKT, as a transcriptional activator of galKT in the presence of galactose. Moreover, we predict a 19-bp regulatory site (5'-GATAGTTTAGTAAAATTTT-3' ) for the transcriptional regulator GalR in the promoter region of galK, which is also highly conserved in other streptococci. Growth comparison of Î galK with the D39 wildtype strain grown in the presence of galactose shows that galK is required for the proper growth of S. pneumoniae on galactose. Comparison of the Streptococcus pneumoniae D39 galR mutant compared to D39 wild type in M17 medium+ 0.5% (w/v) glucose (GM17). One condition design comparison of two strains including a dye swap.
2015-10-30 | E-GEOD-74500 | biostudies-arrayexpress
Project description:Small distortions in transcriptional networks might lead to drastic phenotypical changes, especially in cellular developmental programs such as competence for natural transformation. Here, we report a pervasive circuitry rewiring for competence and predation interplay in commensal streptococci. Canonically, in model species of streptococci such as Streptococcus pneumoniae and Streptococcus mutans, the pheromone-based two-component system BlpRH is a central node that orchestrates the production of antimicrobial compounds (bacteriocins) and incorporates signal from the competence activation cascade. However, the human commensal Streptococcus salivarius does not contain a functional BlpRH pair and in this species, the competence signaling system ComRS directly couples bacteriocin production and competence commitment. This network shortcut might account for an optimal reaction against microbial competitors and could explain the high prevalence of S. salivarius in the human digestive tract. Moreover, the broad spectrum of bacteriocin activity against pathogenic bacteria showcases the commensal and genetically tractable S. salivarius species as a user-friendly model for natural transformation and bacterial predation.
2018-01-10 | GSE100416 | GEO