CC2_Navarre_14028srpoSlowhns-_IP_pHNStagged_antiHA
Ontology highlight
ABSTRACT:
ORGANISM(S): Salmonella enterica Salmonella enterica subsp. enterica serovar Typhimurium
PROVIDER: GSE4881 | GEO | 2006/05/24
SECONDARY ACCESSION(S): PRJNA95769
REPOSITORIES: GEO
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Project description:array analysis of immunoprecipitated DNA from tagged HNS proteins in 14028s mutant strain (rpoS low, hns minus) four slides, FLAG-tagged HNS versus gDNA and HA-tagged HNS versus gDNA IP'd using anti-HA, including dye-swaps
2010-07-01 | E-GEOD-4881 | biostudies-arrayexpress
Project description:Transcriptome analysis of two independently derived hns mutants compared to an isogenic wild-type Salmonella (strain 14028s - lab ID# WN153). Note: both the wild-type and hns strains carry an additional mutation in the rpoS locus (encoding the stationary phase sigma factor) resulting in a deletion of amino acids 61-65 that diminish its activity. Keywords: cell type comparison
2006-06-08 | GSE4931 | GEO
Project description:HilD is a regulator of Salmonella pathogenicity island 1 (SPI-1) virulence genes in Salmonella enterica serovar Typhimurium. To identify novel HilD-regulated genes, we mapped the genome-wide association of HilD in S. Typhimurium under SPI-1-inducing conditions (high salt, low aeration) using ChIP-seq. HilD was C-terminally tagged with 3 FLAG tags in strain 14028s.
2013-09-19 | E-MTAB-1848 | biostudies-arrayexpress
Project description:We mapped the genome-wide binding of C-terminally FLAG-tagged AraC in S. enterica subsp. enterica serovar Typhimurium strain 14028s using ChIP coupled with deep sequencing (ChIP-seq). We identified five putative target loci for AraC: upstream of araB/araC, araE, araJ, STM14_0178, and within sseD.
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Project description:Transcriptional profiles of wt and dksA minus Salmonella enterica sv Typhimurium 14028S in E salts minimal medium in response to 5 mM DETANONOate for 30 min
2014-03-31 | GSE33529 | GEO
Project description:To determine sites where RpoS binds (and hence likely plays a direct role in transcription), we used ChIP-seq to map the association of RpoS across the Escherichia coli chromosome during stationary phase growth in minimal medium. To facilitate ChIP, RpoS was C-terminally SPA-tagged at its native locus.
2016-12-23 | E-MTAB-5339 | biostudies-arrayexpress
Project description:The transcriptional factor Zur plays a key role in regulating zinc homeostasis in Bacillus subtilis. The genomic sites bound by Zur were mapped using a chromatine immunoprecipitation approach. This allowed the identification of 80 inter- and intragenic chromosomal sites bound by Zur. This data set contains 2 samples. Immunoprecipitated (IP) DNA from Bacillus subtilis BSAS36 strain (BSB1, a tryptophan-prototrophic derivative 168 strain expressing a SPA-tagged Zur protein) were extracted from bacterial cells in the exponential growth phase. IP and whole-cell extract DNA were hybridized on tiling array to generate ChIP-on-chip profiles. Two biological replicates were anlyzed.
2015-01-06 | E-GEOD-64671 | biostudies-arrayexpress
Project description:RpoS is a conserved stress regulator that plays a critical role in survival under stress conditions in Escherichia coli and other γ-proteobacteria. RpoS is also involved in virulence of many pathogens including Salmonella and Vibrio species. Though well characterized in non-pathogenic E. coli K12 strains, the effect of RpoS on transcriptome expression has not been examined in pathogenic isolates. E. coli O157:H7 is a serious human enteropathogen, possessing a genome 20% larger than that of E. coli K12, and many of the additional genes are required for virulence. The genomic difference may result in substantial changes in RpoS-regulated gene expression. To test this, we compared the transcriptional profile of wild type and rpoS mutants of the E. coli O157:H7 EDL933 type strain. The rpoS mutation had a pronounced effect on gene expression in stationary phase, and more than 1,000 genes were differentially expressed (two-fold, p<0.05). By contrast, we found 11 genes expressed differently in exponential phase. Western blot analysis revealed that, as expected, RpoS level was low in exponential phase and substantially increased in stationary phase. The defect in rpoS resulted in impaired expression of genes responsible for stress response (e.g., gadA, katE and osmY), arginine degradation (astCADBE), putrescine degradation (puuABCD), fatty acid oxidation (fadBA and fadE), and virulence (ler, espI and cesF). For EDL933-specific genes on O-islands, we found 50 genes expressed higher in wild type EDL933 and 49 genes expressed higher in the rpoS mutants. The protein levels of Tir and EspA, two LEE-encoded virulence factors, were elevated in the rpoS mutants under LEE induction conditions. Our results show that RpoS has a profound effect on global gene expression in the pathogenic strain O157:H7 EDL933, and the identified RpoS regulon, including many EDL933-specific genes, differs substantially from that of laboratory K12 strains. In this study, we characterized the RpoS regulon of E. coli O157:H7 strain EDL933 using microarray analysis.
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Project description:Transcriptional profiles of wt and dksA minus Salmonella enterica sv Typhimurium 14028S in E salts minimal medium in response to 5 mM DETANONOate for 30 min Total RNA was harvested from three biological replicates of wt and dksA mutant cultures exposed or unexposed to 5mM DETANONOate for 30min in E salts minimal medium.
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Project description:Our study is the first to demonstrate BadR as a repressor of rpoS and thus facilitates spirocheteM-bM-^@M-^Ys transition back into ticks. BadR binds upstream and represses rpoS in unfed ticks. GLcNA-6P, an abundant nutrient of blood and released by subsequent remodeling of the tick peritrophic membrane, relieves repression of BadR on rpoS facilitating vertebrate host adaptation. BadR regulates chitobiose utilization genes and activates genes critical for spirochetes residence of ticks (lp28-4 genes) badR-deficient strain (Gene BB0693) compared to B31-A3 parental wild-type B. burgdorferi strains Two separate but identically designed microarrays were performed and thus two chips were used. Each chip contained two replicates of B31-A3 WT and badR-deficient strains, and thus the overall array analysis of both chips corresponds to n=4 for both WT and badR-deficient strains. Hierarchical clustering and correlation analysis was used to verify quality of the normalized array data. The expression data from biological replicates 1 and 2 (chip 1 and 2) were both pooled and analyzed individually. We used LIMMA R package to test contrasts between WT and badR-deficient strain (Smyth GK.2004. Stat Appl Genet Mol Biol 3:Article3 .)
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