RNA-seq analyses of gene expression in Helicobacter pylori CrdRS two-component system deletion strains
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ABSTRACT:
PROVIDER: PRJNA913885 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22810285_1.fastq.gz | Fastqsanger.gz | |||
| SRR22810285_2.fastq.gz | Fastqsanger.gz | |||
| SRR22810286_1.fastq.gz | Fastqsanger.gz | |||
| SRR22810286_2.fastq.gz | Fastqsanger.gz | |||
| SRR22810287_1.fastq.gz | Fastqsanger.gz |
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Project description:Next-generation sequencing (NGS) was used to analyze gene expression in H. pylori CrdRS two-component system deletion strains. The goal of this study was to examine the role that the CrdRS two-component system plays in H. pylori gene expression through identification of regulon differences
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Project description:Helicobacter pylori colonizes the gastric epithelium and is the leading cause of gastric adenocarcinoma. There is increasing evidence that DNA methylation regulates gene expression in addition to its role in genome protection. In this study, we characterize the impact of acidity, the Two-Component System (TCS) ArsRS, Autoinducer-2, and the Type I m6A DNA methyltransferase HsdM1 (HP0463) on the Helicobacter pylori methylome. Transcription of hsdM1 increases at least 4-fold in the absence of the sensory histidine kinase ArsS, the major acid sensing protein of H. pylori. HsdM1 exists in the phase-variable operon hsdR1-hsdM1. Phase-locking hsdR1 (HP0464), the restriction endonuclease gene, has significant impacts on the transcription of hsdM1. To determine the impacts of methyltransferase transcription patterns on the methylome, we conducted methylome sequencing on samples that had undergone prolonged acid-exposure experiment. We found differentially methylated motifs between pH 7 and pH 5 growth conditions, and that deletions of arsS and hsdM1 interfere with the epigenetic acid response. Deletion of arsS leads to altered hsdM1 expression and alters the activity of multiple methyltransferases in both conditions indicating that the ArsRS TCS, in addition to its role in acid acclimation via direct effects on regulon member transcription, may also indirectly impact gene expression via regulation of the methylome. We characterized the target motif of HsdM1 (HP0463) to be (H)HTCAVN6TGY. HsdM1 may hierarchically regulate the Type II m5C DNA methyltransferase HP1121. This complex regulation of DNA methyltransferases, and thus differential methylation patterns, may have implications for the decades-long persistent infection by H. pylori.
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Project description:Helicobacter pylori encounters a wide range of pH within the human stomach. In a comparison of H. pylori cultured in vitro under neutral or acidic conditions, about 15% of genes are26 differentially expressed, and corresponding changes are detectable for many of the encoded proteins. The ArsRS two-component system (TCS), comprised of the sensor kinase ArsS and its cognate response regulator ArsR, has an important role in mediating pH-responsive changes in H. pylori gene expression. In this study, we sought to delineate the pH-responsive ArsRS regulon and further define the role of ArsR in pH-responsive gene expression. We compared H. pylori strains containing an intact ArsRS system with an arsS null mutant or strains containing site32 specific mutations of a conserved aspartate residue (D52) in ArsR, which is phosphorylated in response to signals relayed by the cognate sensor kinase ArsS. We identified 178 genes that were pH-responsive in strains containing an intact ArsRS system but not in ∆arsS or arsR mutants. These constituents of the pH-responsive ArsRS regulon include genes involved in acid acclimatization (ureAB, amidases), oxidative stress responses (katA, sodB), transcriptional regulation related to iron or nickel homeostasis (fur, nikR), and genes encoding outer membrane proteins [including sabA, alpA, alpB, hopD (labA), and horA]. When comparing H. pylori strains containing an intact ArsRS TCS with arsRS mutants, each cultured at neutral pH, relatively few genes are differentially expressed. Collectively, these data suggest that ArsRS41 mediated gene regulation has an important role in H. pylori adaptation to changing pH conditions.
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Project description:Helicobacter pylori genome is rich in restriction - modification (R-M) systems. Around 4 % of the genome codes for components of R-M systems. hpyAVIBM, which codes for a putative phase-variable C5 - cytosine methyltransferase (MTase) from H. pylori lacks a cognate restriction enzyme. To analysis the effect of deleting hpyAVIBM on the Helicobacter pylori transcriptome, microarray analysis was done with the wild type strains and corresponding hpyAVIBM deletion strains
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Project description:Helicobacter pylori genome is rich in restriction - modification (R-M) systems. Around 4 % of the genome codes for components of R-M systems. hpyAVIBM, which codes for a putative phase-variable C5 - cytosine methyltransferase (MTase) from H. pylori lacks a cognate restriction enzyme.
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Project description:Helicobacter pylori colonizes the stomach of half of the world's population, causing a wide spectrum of disease ranging from asymptomatic gastritis to ulcers to gastric cancer. Although the basis for these diverse clinical outcomes is not understood, more severe disease is associated with strains harboring a pathogenicity island. To characterize the genetic diversity of more and less virulent strains, we examined the genomic content of 15 H. pylori clinical isolates by using a whole genome H. pylori DNA microarray. We found that a full 22% of H. pylori genes are dispensable in one or more strains, thus defining a minimal functional core of 1281 H. pylori genes. While the core genes encode most metabolic and cellular processes, the strain-specific genes include genes unique to H. pylori, restriction modification genes, transposases, and genes encoding cell surface proteins, which may aid the bacteria under specific circumstances during their long-term infection of genetically diverse hosts. We observed distinct patterns of the strain-specific gene distribution along the chromosome, which may result from different mechanisms of gene acquisition and loss. Among the strain-specific genes, we have found a class of candidate virulence genes identified by their coinheritance with the pathogenicity island. Keywords: other
2001-07-25 | GSE6 | GEO
Project description:Helicobacter pylori (H. pylori) is a human pathogen that infects almost half of the world’s population. Infection with H. pylori is frequently associated with chronic gastritis and can even lead to gastric and duodenal ulcers and gastric cancer. Although the persistent colonization of H. pylori and the development of H. pylori-associated gastritis remain poorly understood, it is believed that, in gastric mucosa, the modulated gastric epithelial cells (GECs) by H. pylori are key contributors. We used microarrays to detail the global programme of gene expression in Helicobacter pylori infected-gastric epithelial cell line AGS cells and identified up-regulated genes induced by Helicobacter pylori infection.
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Project description:Bone marrow-derived macrophages from Dhps fl/fl mice and mice with specific deletion of Dhps in myeloid cells were infected with Helicobacter pylori PMSS1 for 24 hours. Cells were washed and lysed. Proteins were analyzed by isobaric tags for relative and absolute quantitation (iTRAQ).
2021-09-09 | PXD018187 | Pride
Project description:Helicobacter pylori, a gastroenteric pathogen believed to have co-evolved with humans for 100.000 years, has a high genetic variability that motivates the study of different H. pylori populations and the diseases caused by them in order to find determinants for disease evolution. In this study we utilized both genomic and proteomic tools to compare a H. pylori strain (Nic25_A) from Nicaragua isolated from a patient with intestinal metaplasia with the P12 strain from Europe isolated from a patient with duodenal ulcer. Differences in the protein expression levels between the two strains were determined by both label-free quantification (MaxQuant) and labelling methods (tandem mass tags, TMT), utilizing a lipid-based protein immobilization (LPI™) technique to target surface protein peptides. Using the MaxQuant software, we found 52 proteins significantly differing between the two strains (up-or-down regulated by a factor of 1.5) and with TMT we were able to find 18 proteins with different expression levels between the strains. The P12 (duodenal ulcer) strain had higher expression of genes belonging to the cagPAI operon, while Nic25_A (intestinal metaplasia) had higher expression of the acid response regulator ArsR, as well as proteins regulated by ArsR; KatA, AmiE, and proteins involved in urease production. The results show that differences in protein expression can be detected by proteomic approaches in H. pylori strains of different pathogenicity, which might have implications for studies of disease progression.
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Project description:Helicobacter pylori colonizes the stomach of half of the world's population, causing a wide spectrum of disease ranging from asymptomatic gastritis to ulcers to gastric cancer. Although the basis for these diverse clinical outcomes is not understood, more severe disease is associated with strains harboring a pathogenicity island. To characterize the genetic diversity of more and less virulent strains, we examined the genomic content of 15 H. pylori clinical isolates by using a whole genome H. pylori DNA microarray. We found that a full 22% of H. pylori genes are dispensable in one or more strains, thus defining a minimal functional core of 1281 H. pylori genes. While the core genes encode most metabolic and cellular processes, the strain-specific genes include genes unique to H. pylori, restriction modification genes, transposases, and genes encoding cell surface proteins, which may aid the bacteria under specific circumstances during their long-term infection of genetically diverse hosts. We observed distinct patterns of the strain-specific gene distribution along the chromosome, which may result from different mechanisms of gene acquisition and loss. Among the strain-specific genes, we have found a class of candidate virulence genes identified by their coinheritance with the pathogenicity island.
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