Project description:To investigate the subspecies level differences in the expression profiles of Streptococcus salivarius strains, we conducted the RNA sequencing analysis of Streptococcus salivarius strains.
Project description:Identification of proteins from extracellular vesicles isolated from Streptococcus salivarius. This work was financially supported by the National Science Centre, Poland (grant number 2021/43/D/NZ6/01464).
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.
Project description:NIP and NrpR forms a pair for the transcriptional regulator in Streptococcus salivarius K12 (SAL). To explore the target genes regulated by the NIP-NrpR pair in Streptococcus salivarius K12 (SAL), we generated mutants in which the NIP or NrpR gene has been knocked down through complement recombination. Comparative transcriptome profiling of WT, ▲nrpR, and nip* mutant strains revealed that the sar BGC is the major regulatory target controlled by the NIP signaling pathway in SAL.
