Bacillus anthracis
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ABSTRACT:
PROVIDER: PRJNA248224 | ENA |
REPOSITORIES: ENA
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Project description:Spx, a member of the ArsC (arsenate reductase) protein family, is highly conserved in Gram-positive bacteria, where it interacts with RNA polymerase to activate transcription in response to toxic oxidants. In Bacillus anthracis, resistance to oxidative stress requires the activity of two paralogous forms of Spx, SpxA1 and SpxA2. Suppressor mutations were identified in spxA1 mutant cells that conferred resistance to hydrogen peroxide. The mutations, which reside in saiR within the operon that also contains the spxA2 gene, caused derepression of spxA2 transcription. The product of saiR is a member of the Rrf2 family of transcriptional repressors. Derepression of spxA2 in a saiR mutant required SpxA2, indicating an autoregulatory mechanism of spxA2 transcriptional activation. Reconstruction of SaiR-dependent control of spxA2 was accomplished in Bacillus subtilis, where deletion analysis uncovered two cis-elements within the spxA2 regulatory region that are required for repression. Both sites bear sequences of dyad symmetry, mutations in which abolished SaiR binding and SaiR-dependent repression of transcription from the spxA2 promoter in vitro. Previous studies have provided evidence that spxA2 is one of the most highly induced genes in a macrophage infected with B. anthracis. The work reported herein uncovered a key regulator, SaiR, which controls spxA2 transcriptional activation.
2014-05-21 | GSE57851 | GEO
Project description:Spx, a member of the ArsC (arsenate reductase) protein family, is highly conserved in Gram-positive bacteria, where it interacts with RNA polymerase to activate transcription in response to toxic oxidants. In Bacillus anthracis, resistance to oxidative stress requires the activity of two paralogous forms of Spx, SpxA1 and SpxA2.  Suppressor mutations were identified in spxA1 mutant cells that conferred resistance to hydrogen peroxide.  The mutations, which reside in saiR within the operon that also contains the spxA2 gene, caused derepression of spxA2 transcription. The product of saiR is a member of the Rrf2 family of transcriptional repressors.  Derepression of spxA2 in a saiR mutant required SpxA2, indicating an autoregulatory mechanism of spxA2 transcriptional activation.  Reconstruction of SaiR-dependent control of spxA2 was accomplished in Bacillus subtilis, where deletion analysis uncovered two cis-elements within the spxA2 regulatory region that are required for repression. Both sites bear sequences of dyad symmetry, mutations in which abolished SaiR binding and SaiR-dependent repression of transcription from the spxA2 promoter in vitro. Previous studies have provided evidence that spxA2 is one of the most highly induced genes in a macrophage infected with B. anthracis. The work reported herein uncovered a key regulator, SaiR, which controls spxA2 transcriptional activation. Direct comparison of experimental samples to control samples in a two-color hybridization. Two experimental samples were compared against two control samples in triplicate for each.
2014-05-21 | E-GEOD-57851 | biostudies-arrayexpress
Project description:The High Temperature Requirement (HtrA) chaperone/protease is involved in the stress-response of the anthrax-causing pathogen Bacillus anthracis. Resilience to oxidative stress is essential for manifestation of B. anthracis pathogenicity. We submitt transcriptome data sets detailing global gene expression in B. anthracis wild-type and htrA-disrupted strains following H2O2-induced oxidative stress.
2020-05-27 | GSE151208 | GEO
Project description:AtxA, the master virulence regulator of Bacillus anthracis, regulates the expression of three toxins that are required for the pathogenicity of Bacillus anthracis. Recent transcriptome analyses also showed that AtxA affects a large number of genes on both chromosome and plasmid, suggesting its role as a global regulator. Its mechanism of gene regulation nor binding target in vivo was, however, not well understood. In this work, we conducted ChIP-seq for cataloging binding sites of AtxA in vivo and Cappable-seq for catalogging the transcription start sites on the B. anthracis genome. For detected regulons, single knockout strains were constructed and RNA-seq was conducted for each strain.
2021-06-28 | GSE167871 | GEO
Project description:Bacillus anthracis causes anthrax infections in mammals. Large-scale mortality resulting from the intentional release of B. anthracis spores represents a potential bioterrorism threat. Inhalational anthrax almost invariably proceeds to fatal systemic infection, characterized by massive bacteremia. A better understanding of host-pathogen interactions is urgently needed for effective treatment of this lethal disease. However, virulence mechanisms used by B. anthracis to survive and multiply in human blood are not completely understood. Identification of genes that are differentially expressed during the growth of B. anthracis in human serum can elucidate how this pathogen successfully colonizes the bloodstream. We compared the transcriptional profile of B. anthracis growing in heat-inactivated human serum to that in LB medium. Genes involved in the biosynthesis of purines, certain amino acids and riboflavin and lipid metabolism, genes encoding ABC transporters, respiratory enzymes and several genes with hypothetical function were identified as being upregulated during growth in serum.
2022-12-01 | GSE97567 | GEO
Project description:B. anthracis 7702 and the codY mutant 7CodYS were grown in R-medium (Ristroph, J.D. & Ivins, B.E. (1983). Elaboration of Bacillus anthracis antigens in a new, defined culture medium. Infect. Immun. 39:483-486) with 0.6% sodium bicarbonate until A600 = 0.2 or 1.0. The transcriptome of both strains was compared at both time-points.
2008-11-15 | E-MEXP-1706 | biostudies-arrayexpress
Project description:Timecourse from log phase growth to sporulation in Bacillus anthracis Stern 34F2 Keywords: time-course
2004-01-08 | GSE840 | GEO
Project description:Bacillus anthracis is a gram-positive, aerobic, spore-forming, rod-shaped bacterium which has recently been used as an agent of bioterrorism. Because there is a significant delay between the initial contact of the spore with the host and clinical evidence of disease, there appears to be temporary containment of the pathogen by the innate immune system. Contact with the human alveolar macrophage (HAM) plays a key role in the innate immune response to B. anthracis spores. Therefore, the early macrophage response to anthrax exposure is important in understanding the pathogenesis of this disease. The majority of genes modulated by spores were upregulated, and a lesser number were downregulated. The data was subjected to Ingenuity Pathway analysis, the Database for Annotation, Visualization and Integrated Discovery (DAVID) analysis, and the Promoter Analysis and Interaction Network Toolset (PAINT). Among the upregulated genes, we identified a group of chemokine ligands, apoptosis genes and, interestingly, keratin filament genes. Central hubs regulating the activated genes were TNF-ï¡, NF-κB and their ligands/receptors. Other activated genes included IL-1ï¡ and IL-18. RNA for these, and several additional cytokines including IL-6, IL-1ï¢, IP-10 and GM-CSF, were differentially expressed from 1.6- to 27-fold. The microarray cytokine data is consistent with our previously published findings which demonstrated that there was 4- to 43-fold induction of these cytokines at the transcriptional and translational levels as determined by RNase protection assays and ELISA. The PAINT analysis revealed that the majority of the genes affected by spores contain the binding site for c-Rel, a member of the NF-κB family of transcription factors. Other transcription regulatory elements contained in many of the upregulated genes were c-Myb, CP2, Barbie Box, E2F and CRE-BP1. This study is the first detailed microarray analysis to describe the HAM response to B. anthracis. Experiment Overall Design: In this paper, we exposed HAM to B. anthracis Sterne spores at an MOI of 1 for 6 hours. RNA was extracted from HAM and analyzed by the Affymetrix Human Genome U133 Plus 2.0 Array. The transcriptional profile of Bacillus anthracis spore-treated HAM was compared with mock infected cells, and differentially expressed genes were identified.
2009-10-16 | E-GEOD-14390 | biostudies-arrayexpress
Project description:The spore forming pathogen Bacillus anthracis is the etiologic agent of anthrax in humans and animals. It cycles through infected hosts as vegetative cells and is eventually introduced into the environment where it generates an endospore resistant to many harsh conditions. The endospores are subsequently ingested by the next host to begin the next cycle. Outbreaks of anthrax occur regularly worldwide in wildlife and livestock, and the potential for human infection exists whenever humans encounter infected animals. It is also possible to encounter intentional releases of anthrax spores, as was the case in October 2001. Consequently, it is important to be able to rapidly establish the provenance of infectious strains of B. anthracis. Here, we compare protein expression in seven low-passage wild isolates and four laboratory strains of B. anthracis grown under identical conditions using LC-MS/MS proteomic analysis. Of the 1,023 total identified proteins, 96 had significant abundance differences between wild and laboratory strains. Of those, 28 proteins directly related to sporulation were upregulated in wild isolates, with expression driven by Spo0A, CodY, and AbrB/ScoC. In addition, we observed evidence of changes in cell division and fatty acid biosynthesis between the two classes of strains, despite being grown under identical experimental conditions. These results suggest wild B. anthracis cells are more highly tuned to sporulate than their laboratory cousins, and this difference should be exploited as a method to differentiate between laboratory adapted cultures and low passage wild strains isolated during an anthrax outbreak. This knowledge should distinguish between intentional releases and exposure to strains in nature providing a basis for the type of response by public health officials and investigators.
2018-12-04 | PXD010120 | Pride
Project description:Bacillus anthracis is a gram-positive, aerobic, spore-forming, rod-shaped bacterium which has recently been used as an agent of bioterrorism. Because there is a significant delay between the initial contact of the spore with the host and clinical evidence of disease, there appears to be temporary containment of the pathogen by the innate immune system. Contact with the human alveolar macrophage (HAM) plays a key role in the innate immune response to B. anthracis spores. Therefore, the early macrophage response to anthrax exposure is important in understanding the pathogenesis of this disease. The majority of genes modulated by spores were upregulated, and a lesser number were downregulated. The data was subjected to Ingenuity Pathway analysis, the Database for Annotation, Visualization and Integrated Discovery (DAVID) analysis, and the Promoter Analysis and Interaction Network Toolset (PAINT). Among the upregulated genes, we identified a group of chemokine ligands, apoptosis genes and, interestingly, keratin filament genes. Central hubs regulating the activated genes were TNF-alpha, NF-κB and their ligands/receptors. Other activated genes included IL-1alpha and IL-18. RNA for these, and several additional cytokines including IL-6, IL-1gamma, IP-10 and GM-CSF, were differentially expressed from 1.6- to 27-fold. The microarray cytokine data is consistent with our previously published findings which demonstrated that there was 4- to 43-fold induction of these cytokines at the transcriptional and translational levels as determined by RNase protection assays and ELISA. The PAINT analysis revealed that the majority of the genes affected by spores contain the binding site for c-Rel, a member of the NF-κB family of transcription factors. Other transcription regulatory elements contained in many of the upregulated genes were c-Myb, CP2, Barbie Box, E2F and CRE-BP1. This study is the first detailed microarray analysis to describe the HAM response to B. anthracis.
2009-09-07 | GSE14390 | GEO