FliA regulon of Helicobacter hepaticus
Ontology highlight
ABSTRACT:
ORGANISM(S): Helicobacter hepaticus
PROVIDER: GSE12123 | GEO | 2009/07/14
SECONDARY ACCESSION(S): PRJNA113781
REPOSITORIES: GEO
Similar Datasets
Project description:Differential gene regulation in Helicobacter hepaticus between wild type bacteria and fliA mutant 3 biological experiments of both wild type and fliA mutant bacteria (1-3) and 2 replicates (dye flip) of each biological experiment
2009-07-14 | E-GEOD-12123 | biostudies-arrayexpress
Project description:fliA regulon of Helicobacter hepaticus
| PRJNA113781 | ENA
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Project description:The human gastric pathogen Helicobacter pylori is extremely well adapted to the highly acidic conditions encountered in the stomach. The pronounced acid resistance of H. pylori relies mainly on the ammonia-producing enzyme urease, however, urease-independent mechanisms are likely to contribute to acid adaptation. Acid-responsive gene regulation is mediated at least in part by the ArsRS two-component system consisting of the essential OmpR-like response regulator ArsR and the non-essential cognate histidine kinase ArsS whose autophosphorylation is triggered in response to low pH. In this study by global transcriptional profiling of an ArsS-deficient H. pylori mutant grown at pH 5.0 we define the ArsR~P- dependent regulon consisting of 110 genes including the urease gene cluster, the genes encoding the aliphatic amidases AmiE and AmiF and the rocF gene encoding arginase. Transcriptome analyses were performed using a whole-genome microarray containing 1649 PCR products generated with specific primer pairs derived from the genome sequences of H. pylori 26695 (Tomb et al., 1997. The complete genome sequence of the gastric pathogen Helicobacter pylori. Nature 388:539-547) and J99 (Alm et al., 1999. Genomic-sequence comparison of two unrelated isolates of the human gastric pathogen Helicobacter pylori. Nature 397:176-180) which were spotted in duplicate. Microarrays were produced as described by Gressmann et al. (Gressmann et al., 2005. Gain and loss of multiple genes during the evolution of Helicobacter pylori. PLoS Genet 1(4):e43). To determine genes which are differentially expressed in the ArsS-deficient mutant G27/HP165::km at pH 5.0, cDNA was prepared from RNA extracted from H. pylori G27 and G27/HP165::km after exposing the bacteria for one hour to acidic pH. A total of eight RNA samples from two independent RNA preparations from strain G27 and G27/HP165::km, respectively, was used for cDNA labelling und hybridisation. Dye reversal colour swaps were performed as follows: One cDNA sample was generated using Cy3-dCTP and the other using Cy5-dCTP resulting in four labelled cDNAs per colour swap. Cy5-dCTP and Cy3-dCTP labelled cDNAs were combined and hybridized to the H. pylori microarray. The slides were scanned using ScanArray HT and analysed by using the ScanArray express software (Perkin Elmer). Spots were flagged and eliminated from analysis when the signal to background ratio was less then three or in obvious instances of high background or stray fluorescent signals. Median intensities of spots were background corrected and differences in dye bias were normalized by using the LOWESS algorithm (Yang et al., 2002. Normalization for cDNA microarray data: a robuste composite method addressing single and multiple slide systematic variation. Nucleic Acid Res. 30:e15). The signal ratios as measure of differential expression between the red and green channels were obtained from processed signal intensities. Ratios were further analysed with Microsoft Excel (Microsoft) and SAM software for statistic significance (Tusher et al., 2001. Significance analysis of microarrays applied to the ionizing radiation response. Proc. Natl. Acad. Sci. USA 98:5116-5121). To determine the significance of differential expression RNA was isolated from the H. pylori G27 wild-type grown in BHI broth (pH 5.0), and 20 µg of this RNA were labelled either with Cy3-dCTP or with Cy5-dCTP. The two cDNA probes generated were hybridized onto the same slide, and the data were analysed as mentioned above. Signal ratios < 0.5 and > 2.0 were analyzed further.
2010-07-01 | E-GEOD-4293 | biostudies-arrayexpress
Project description:The genome of the gastric pathogen Helicobacter pylori harbors a remarkably low number of regulatory genes, including three and five open reading frames encoding two-component histidine kinases and response regulators, respectively, which are putatively involved in transcriptional regulation. Inactivation of the response regulator gene hp1021 resulted in a severe growth defect, as indicated by a small-colony phenotype. Recently we found that phosphorylation of the receiver domain HP1021 is not needed for its response regulator function and may not occur at all. No target genes have been identified so far. In this study we define the HP1021-dependent regulon consisting of 79 genes (51 activated, 28 repressed) by global transcriptional profiling of an HP1021-deficient H. pylori mutant. Keywords: Identification of an HP1021-Regulon
2007-04-01 | GSE5971 | GEO
Project description:The mammalian gastrointestinal tract harbors a diverse microbiota residing in intimate contact with the host immune system. Though most associations are symbiotic or commensal, some resident bacteria (termed pathobionts) have the potential to induce disease in immunocompromised hosts. Type VI secretion systems (T6SSs) have recently emerged as a novel mechanism for forging microbial-host interactions during infection. We reveal here a unique protective role for the T6SS of Helicobacter hepaticus, a Gram-negative bacterium of the murine intestinal microbiota. The T6SS of H. hepaticus targets effector substrates to intestinal epithelial cells (IECs). Mutants in T6SSs display higher intracellular and cell-associated numbers upon incubation with IECs, and exhibit increased bacterial colonization of the gastrointestinal tract compared to wild-type bacteria. The T6SS accordingly directs an anti-inflammatory gene expression profile in IECs co-cultured with H. hepaticus. Remarkably, T6SS mutants induce an exacerbated pro-inflammatory response in an experimental model of colitis. CD4+ T cells isolated from T6SS mutant-colonized animals produce increased T-helper 17 (Th17) cytokines in response to IECs presenting H. hepaticus antigens. These data demonstrate that H. hepaticus intimately interacts with IECs and employs type VI secretion to establish a balanced host relationship by limiting microbial colonization and intestinal inflammation. We propose that altering host-bacterial equilibriums that lead to dysbiosis of the microbiota contributes to human disorders such as inflammatory bowel disease and colon cancer.
2010-06-01 | GSE20434 | GEO
Project description:The genome of the gastric pathogen Helicobacter pylori harbors a remarkably low number of regulatory genes, including three and five open reading frames encoding two-component histidine kinases and response regulators, respectively, which are putatively involved in transcriptional regulation. Inactivation of the response regulator gene hp1021 resulted in a severe growth defect, as indicated by a small-colony phenotype. Recently we found that phosphorylation of the receiver domain HP1021 is not needed for its response regulator function and may not occur at all. No target genes have been identified so far. In this study we define the HP1021-dependent regulon consisting of 79 genes (51 activated, 28 repressed) by global transcriptional profiling of an HP1021-deficient H. pylori mutant. Transcriptome analyses were performed using a whole-genome microarray containing 1649 PCR products generated with specific primer pairs derived from the genome sequences of H. pylori 26695 (Tomb et al., 1997. The complete genome sequence of the gastric pathogen Helicobacter pylori. Nature 388:539-547) and J99 (Alm et al., 1999. Genomic-sequence comparison of two unrelated isolates of the human gastric pathogen Helicobacter pylori. Nature 397:176-180) which were spotted in duplicate. Microarrays were produced as described by Gressmann et al. (Gressmann et al., 2005. Gain and loss of multiple genes during the evolution of Helicobacter pylori. PLoS Genet 1(4):e43). To determine genes which are differentially expressed in the HP1021-deficient mutant 26695/1021::km, cDNA was prepared from RNA extracted from H. pylori 26695 WT and 26695/1021::km. A total of eight RNA samples from two independent RNA preparations from strain 26695 WT and 26695/HP1021::km, respectively, was used for cDNA labelling und hybridisation. Dye reversal colour swaps were performed as follows: one cDNA sample was generated using Cy3-dCTP and the other using Cy5-dCTP resulting in four labelled cDNAs per colour swap. Cy5-dCTP and Cy3-dCTP labelled cDNAs were combined and hybridized to the H. pylori microarray. The slides were scanned using ScanArray HT and analysed by using the ScanArray express software (Perkin Elmer, version 3.0). Spots were flagged and eliminated from analysis when the signal to background ratio was less then three or in obvious instances of high background or stray fluorescent signals. Median intensities of spots were background corrected and differences in dye bias were normalized by using the LOWESS algorithm (Yang et al., 2002. Normalization for cDNA microarray data: a robuste composite method addressing single and multiple slide systematic variation. Nucleic Acid Res. 30:e15). The signal ratios as measure of differential expression between the red and green channels were obtained from processed signal intensities. Ratios were further analysed with Microsoft Excel (Microsoft) and SAM software for statistic significance (Tusher et al., 2001. Significance analysis of microarrays applied to the ionizing radiation response. Proc. Natl. Acad. Sci. USA 98:5116-5121). To determine the significance of differential expression RNA was isolated from the H. pylori 26695 WT grown in BHI broth, and 20 µg of this RNA were labelled either with Cy3-dCTP or with Cy5-dCTP. The two cDNA probes generated were hybridized onto the same slide, and the data were analysed as mentioned above. Signal ratios < 0.5 and > 2.0 were analyzed further.
2010-07-01 | E-GEOD-5971 | biostudies-arrayexpress
Project description:The human gastric pathogen Helicobacter pylori is extremely well adapted to the highly acidic conditions encountered in the stomach. The pronounced acid resistance of H. pylori relies mainly on the ammonia-producing enzyme urease, however, urease-independent mechanisms are likely to contribute to acid adaptation. Acid-responsive gene regulation is mediated at least in part by the ArsRS two-component system consisting of the essential OmpR-like response regulator ArsR and the non-essential cognate histidine kinase ArsS whose autophosphorylation is triggered in response to low pH. In this study by global transcriptional profiling of an ArsS-deficient H. pylori mutant grown at pH 5.0 we define the ArsR~P- dependent regulon consisting of 110 genes including the urease gene cluster, the genes encoding the aliphatic amidases AmiE and AmiF and the rocF gene encoding arginase. Keywords: Identification of an ArsRS-Regulon
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Project description:We studied the differential gene expression in the gastric cell line AGS infected with wild type (WT) or arginase gene mutant (rocF) Helicobacter pylori (Hp). We found that the presence of the gene regulates the inflammatory responses in terms of IL8 and MIP-1B. We conclude that arginase may be involved in regulating inflammatory responses which improves the chances of survival against the human immune response.
2013-06-15 | GSE39919 | GEO
Project description:We are investigating hepatic transcriptional responses associated with castration and tumorigenic hepatitis induced by Helicobacter hepaticus infection in mature male A/JCr mice; Microarray data demonstrated a global loss of gender-dimorphic gene expression regulation in mice with chronic hepatitis and liver cancer Experiment Overall Design: Male A/JCr mice were inoculated with H. hepaticus or vehicle at 4 weeks; some underwent castration at 1 year, and all were necropsied at 21 months
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