Stp1 regulated genes in Streptococcus agalactiae strain A909
Ontology highlight
ABSTRACT:
ORGANISM(S): Streptococcus agalactiae A909 Streptococcus agalactiae
PROVIDER: GSE21564 | GEO | 2010/04/29
SECONDARY ACCESSION(S): PRJNA126189
REPOSITORIES: GEO
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Project description:Genes that showed altered expression between wild type A909 and isogenic rgfC/A mutant were identified. A strain with a deletion in RgfC/A (SAK_1917/SAK_1918) was derived and microarray analysis was performed to identify genes regulated by the RgfC/A two component system. strain comparison, global regulation, two component system
2010-04-29 | GSE21563 | GEO
Project description:Genes that showed altered expression between wild type A909 and the isogenic Stp1 mutant were identified by microarray analysis Deletion mutants were examined for changes in gene expression
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Project description:Genes that showed altered expression between wild type A909 and isogenic rgfC/A mutant were identified. A strain with a deletion in RgfC/A (SAK_1917/SAK_1918) was derived and microarray analysis was performed to identify genes regulated by the RgfC/A two component system. strain comparison, global regulation, two component system Deletion mutant was compared to the wild type strain A909 for changes in gene expression
2010-04-28 | E-GEOD-21563 | biostudies-arrayexpress
Project description:The commensal bacterium Streptococcus agalactiae is responsible for various infections in a wide variety of hosts including humans. Its broad spectrum of hosts shows its ability to acquire nutrients in variable conditions. The carbon catabolite repression allows bacteria to prioritize the uptake and the catabolism of the environmental sugars. In Gram-positive bacteria, CcpA (catabolite control protein A), a pleiotropic transcriptional regulator, plays a key role in catabolite repression. Studies have shown the involvement of carbon catabolite repression in the adaptation and stress resistance of pathogenic bacteria. The goal of this study is to determine the regulon and the role(s) of CcpA in the physiology and adaptation of S. agalactiae. To this aim, Streptococcus agalactiae strain A909 WT and its isogenic mutant ∆ccpA, obtained by allelic exchange were grown in filter-sterilized chemically defined medium (CDM) supplemented with 0,25% or 1% (w/v) of glucose. Their transcriptomes were compared under these two conditions by using RNA-seq.
2022-07-12 | E-MTAB-11639 | biostudies-arrayexpress
Project description:Streptococcus agalactiae (Group B Streptococcus, GBS) is a leading cause of early-onset neonatal bacterial infection. Evasion of innate immune defenses is critical to neonatal GBS disease pathogenesis. Effectors of the innate immune system such as antimicrobial peptides, as well as numerous antibiotics, target the peptidoglycan layer of the gram positive bacterial cell wall. The intramembrane-sensing histidine kinase class of two-component regulatory systems has recently been identified as important to the gram-positive response to cell wall stress. We identified and characterized the GBS homolog of LiaR, the response regulator component of the LiaFSR system and constructed site-directed, non-polar deletion mutations in the regulator gene liaR. GBS LiaR deletion mutant strains are more susceptible to cell wall active antibiotics (vancomycin and bacitracin) as well as antimicrobial peptides (colistin, nisin and the human cathelicidin LL-37) compared to isogenic wild-type GBS. LiaR mutant GBS are significantly attenuated in mouse models of both GBS sepsis and GBS pneumonia. To determine the genes regulated by LiaR that account for these defects, transcriptional profiling was performed using DNA microarray analysis, comparing wild-type GBS to LiaR mutant GBS under non-stressed conditions.
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Project description:Regulation of gene expression in response to variable and often adverse environmental conditions is an essential component of microbial pathogenesis. We identified the two-component regulatory system CiaRH in a screen for genes essential for the survival of Streptococcus agalactiae (Group B Streptococcus, GBS) on exposure to in vitro models of environmental stress. We constructed site-directed, non-polar deletion mutations in the regulator gene ciaR and compared the growth of CiaR mutant GBS to wild-type GBS under stressed conditions. CiaR mutant GBS are more sensitive than wild-type GBS to elevated temperature, low pH, chemical mutagens and ultraviolet light; the mutants are also more sensitive to cell-wall active antibiotics and antimicrobial peptides. CiaR mutant strains are markedly attenuated in a mouse model of GBS sepsis. To determine the genes regulated by CiaR that account for these defects, transcriptional profiling was performed using DNA microarray analysis, comparing wild-type GBS to CiaR mutant GBS under non-stressed conditions.
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Project description:Gene expression-based global role of CovR in GBS A909 using stk1 deletion mutant
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Project description:The purpose of this study was to determine what S. agalactiae genes are under the control of the MtaR regulatory protein. Inactivation of the Streptococcus agalactiae mtaR gene resulted in the downregulation of 11 genes and the upregulation of 1 gene in the mtaR mutant. Genes involved in the uptake of methionine and a gene involved in the degradation of peptides were downregulated. Also, genes involved in the transport and biosynthesis of arginine were downregulated. The gene encoding the virulence factor cspA was downregulated, as well as a gene showing similarity to plasminogen activators. Thus, the expression of genes involved in both metabolic functions and virulence are under the influence of mtaR. Three cultures of an mtaR insertional mutant (DS101) and three cultures of the isogenic wild-type strain (COH1) were grown in a chemically-defined medium. Cells were disrupted with glass-bead and RNA was isolated by a Trizol method. A custom Affymetrix chip was utilized for microarray analysis. Genes were considered differentially-expressed if they showed a >2.0-fold difference in expression between the strains and a Bayesian (Cyber-T) t-test value of <0.001. The posterior probability of differential expression (PPDE) (< p) value for the genes identified was >0.964.
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Project description:Streptococcus agalactiae (Group B Streptococcus, GBS) is a leading cause of early-onset neonatal bacterial infection. Evasion of innate immune defenses is critical to neonatal GBS disease pathogenesis. Effectors of the innate immune system such as antimicrobial peptides, as well as numerous antibiotics, target the peptidoglycan layer of the gram positive bacterial cell wall. The intramembrane-sensing histidine kinase class of two-component regulatory systems has recently been identified as important to the gram-positive response to cell wall stress. We identified and characterized the GBS homolog of LiaR, the response regulator component of the LiaFSR system and constructed site-directed, non-polar deletion mutations in the regulator gene liaR. GBS LiaR deletion mutant strains are more susceptible to cell wall active antibiotics (vancomycin and bacitracin) as well as antimicrobial peptides (colistin, nisin and the human cathelicidin LL-37) compared to isogenic wild-type GBS. LiaR mutant GBS are significantly attenuated in mouse models of both GBS sepsis and GBS pneumonia. To determine the genes regulated by LiaR that account for these defects, transcriptional profiling was performed using DNA microarray analysis, comparing wild-type GBS to LiaR mutant GBS under non-stressed conditions. Two separate RNA samples were extracted for each condition. One flip-dye replicate (2 hybridizations) was obtained for each pair of RNA samples for 4 hybridizations total.
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Project description:The goal of the study was to identify subsets of the genes, which are up-regulated and down-regulated by CovR regulator in UA159 strain. Two independently isolated RNA samples from each of the wild-type UA159 strain and its covR mutant strain grown until mid-exponential phase were analyzed. Each sample was hybridized with 5 blocks of NimbleGen arrays.
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