Project description:We report the characterization of the major regulator of virulence gene expression (CovR) in Group B Streptococcus. The ChIP-seq experiments define the binding of CovR on the chromosome of the BM110 strain, a representative of the hypervirulent GBS lineage responsible of neonatal meningitis. Regulatory evolution of CovR signaling was investigated by comparing ChIP-seq done in parallel in a second GBS clinical isolate (NEM316) not belonging to the hypervirulent lineage.
Project description:Global regulatory roles of the TCS response regulator CovR in GBS serotype 1a A909 Keywords: Strain comparison; global regulation Deletion mutant was examined for alterations in gene expression
Project description:Global regulatory roles of the TCS response regulator CovR in GBS serotype 1a A909 Keywords: Strain comparison; global regulation Deletion mutant was examined for alterations in gene expression
Project description:The goal of this study were to compare the transcriptoms of CcpA and CovR in group A Streptococcus. Isogenic mutant strains were created in which CcpA and CovR were inactivated alone and in combination. The transcriptomes of the four strains (wild-type, CcpA mutant, CovR mutant, and ccpA-covR double mutant) were then compared.
Project description:To define the transcriptional response associated to a CovR inactivation we performed RNA-Seq in GBS strains BM110 and NEM316. We used mutants in which CovR is inactivated following a two base-pairs chromosomal substitution (AT->CC) resulting in the translation of a CovRD53A variant unable to be phosphorylated by the histidine kinase CovS. We also used a ∆covR mutant in strain BM110 in which the covR sequence is deleted from the chromosome.
Project description:We sought to determine how CovRS mutations varying CovR phosphorylation levels affect the gene expression profile of group A streptococcus
Project description:The aim of this study was to investigate the response of human brain endothelial cells to bacterial (group B streptococcus, GBS) infection. Results: GBS WT strain infection results in a specific gene induction pattern that is different from the pilA mutant, but not other mutants such as pilB and srr-1. Conclusion: These findings suggest that the GBS PilA protein contributes to gene induction in brain endothelium.
Project description:The goal of this study were to compare the transcriptoms of CcpA and CovR in group A Streptococcus. Isogenic mutant strains were created in which CcpA and CovR were inactivated alone and in combination. The transcriptomes of the four strains (wild-type, CcpA mutant, CovR mutant, and ccpA-covR double mutant) were then compared. Four biological replicates of each strain were grown to the mid-exponential and stationary phases of growth in THY. Cells were harvested, RNA isolated, and converted to cDNA. cDNA was hybridized to a custom-made Affymetrix GeneChip that contains 100% of the ORFs of the wild-type strain MGAS2221.