Project description:Rgg-dependent transcriptional regulation in SF370 Streptococcus pyogenes strain was analyzed during post-exponential phase of growth Keywords: rgg mutant
Project description:Streptococcus agalactiae, also known as Group B streptococcus, emerged in the 1960s as a leading cause of septicemia and meningitis in neonates. It is also an increasing cause of infections in adults with underlying diseases. To characterize transcription start sites (TSS) in the hypervirulent ST17 lineage (strain BM110) we used a differential RNA-seq strategy, based on selective Tobacco Acid Pyrophosphatase (TAP) treatment and adapter ligation, which differentiates primary transcripts and processed RNAs
Project description:To investigate the effect of CodY mutation on the gene expression in Streptococcus suis serotype 2 SC19 strain, we have employed whole genome microarray expression profiling as a discovery platform to identify genes regulated by CodY mutation. DNA microarray analysis was performed using an Agilent custom-designed oligonucleotide microarray. Based upon the whole genome sequence of SC19 , specific 60-mer oligonucleotide probes were designed using eArray (https://earray.chem.agilent.com/earray/), to cover all annotated genes. Probes were printed seven times on microarray slides. Three biological replicates of total RNA from two wild type strains and from two codY mutant strains were amplified and labeled with Cy3-CTP using Low Input Quick Amp Labeling Kit, one-color(Agilent technologies, US), following the manufacturer’s instructions. Labeled cRNA was purified using the RNeasy mini kit (Qiagen). After fragmentation, microarray slides were hybridized with 600 ng Cy3-labeled cRNA. Hybridization was performed at 65 °C for 17 h with rotation at 10 rpm. Microarray slides were washed and scanned by an Agilent Microarray Scanner (G2565BA). Those genes with greater than two-fold change ratios were regarded as differentially expressed genes. codY mutation induced gene expression in Streptococcus suis serotype 2 SC19 was detected in two wild type and two codY mutated strain of Streptococcus suis serotype 2.
Project description:Two large-scale outbreaks of streptococcal toxic shock-like syndrome (STSLS) have revealed Streptococcus suis 2 (SS2) to be a severe, evolving pathogen in humans. We investigated the mechanism by which SS2 causes STSLS. The transcriptional regulator TstS up-regulated during experimental infection. Compared with the wild type 05ZY strain, the tstS deletion mutant (∆tstS) elicited reduced cytokine secretion in macrophages. In mice, tstS deletion decreased virulence, bacterial load, and cytokine production. Moreover, TstS expression in P1/7 strain led to induction of STSLS in the infected mice. This is noteworthy because although virulent, P1/7 does not normally induce STSLS. Through microarray-based comparative transcriptomics analysis, we found that TstS regulates multiple metabolism related genes and several virulence-related genes associated with immune evasion.