Pathogenomics of Helicobacter

Josenhans, Christine; Beier, Dagmar; Linz, Bodo; Meyer, Thomas F.; Suerbaum, Sebastian

doi:10.1016/j.ijmm.2007.02.006

Cited by 14 publications

(11 citation statements)

References 97 publications

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“…In other eubacteria, RNA polymerase sigma (σ) factors and transcriptional regulators control gene expression at the mRNA level. These likely play a diminished role in H. pylori , as only three σ-factors (σ 80 , σ 54 and σ 28 ) and few classical trans-acting regulators are present [21]–[23]. Thus, fine-tuning of mRNA levels in H. pylori likely involve alternative processes.…”

Section: Introductionmentioning

confidence: 99%

A Repetitive DNA Element Regulates Expression of the Helicobacter pylori Sialic Acid Binding Adhesin by a Rheostat-like Mechanism

et al. 2014

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During persistent infection, optimal expression of bacterial factors is required to match the ever-changing host environment. The gastric pathogen Helicobacter pylori has a large set of simple sequence repeats (SSR), which constitute contingency loci. Through a slipped strand mispairing mechanism, the SSRs generate heterogeneous populations that facilitate adaptation. Here, we present a model that explains, in molecular terms, how an intergenically located T-tract, via slipped strand mispairing, operates with a rheostat-like function, to fine-tune activity of the promoter that drives expression of the sialic acid binding adhesin, SabA. Using T-tract variants, in an isogenic strain background, we show that the length of the T-tract generates multiphasic output from the sabA promoter. Consequently, this alters the H. pylori binding to sialyl-Lewis x receptors on gastric mucosa. Fragment length analysis of post-infection isolated clones shows that the T-tract length is a highly variable feature in H. pylori. This mirrors the host-pathogen interplay, where the bacterium generates a set of clones from which the best-fit phenotypes are selected in the host. In silico and functional in vitro analyzes revealed that the length of the T-tract affects the local DNA structure and thereby binding of the RNA polymerase, through shifting of the axial alignment between the core promoter and UP-like elements. We identified additional genes in H. pylori, with T- or A-tracts positioned similar to that of sabA, and show that variations in the tract length likewise acted as rheostats to modulate cognate promoter output. Thus, we propose that this generally applicable mechanism, mediated by promoter-proximal SSRs, provides an alternative mechanism for transcriptional regulation in bacteria, such as H. pylori, which possesses a limited repertoire of classical trans-acting regulatory factors.

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Section: Introductionmentioning

confidence: 99%

A Repetitive DNA Element Regulates Expression of the Helicobacter pylori Sialic Acid Binding Adhesin by a Rheostat-like Mechanism

et al. 2014

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“…In conclusion, the construction of such a system for recombinant CagA antigen expression may be a pilot study for the development of our own ELISA tests in Turkey, and also will help the clinicians for the prediction of disease outcome and decision of the appropriate antimicrobial treatment by the help of anti-CagA antibody detection. 3,4 . Ülkemizde yapılan çalışmalarda H.pylori seroprevalansı, yaş gruplarına göre değişmek üzere ortalama %20-85 oranları arasında bildirilmekte olup, enfeksiyonun genellikle 10 yaşına kadar kazanıldığı ve yaş ilerledikçe seropozitifliğin arttığı vurgulanmaktadır [5][6][7][8] .…”

Section: Introductionunclassified

Production of a Recombinant CagA Protein for the Detection of Helicobacter pylori CagA Antibodies

Akgüç

Karataylı²,

Çelik³

et al. 2014

Mikrobiyol Bul

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“…Despite a limited genome-wide mutagenesis approach [50], relatively little about the genomic basis for H. mustelae persistence and pathogenesis in the ferret is known, since this organism has not benefitted from the pathogenomics approach that was applied to other Helicobacter species [51]. We report here the genome sequence of H. mustelae type strain 12198, which is the first whole genome of a non- H. pylori - H. acinonychis gastric Helicobacter species.…”

Section: Introductionmentioning

confidence: 99%

Comparative genomics and proteomics of Helicobacter mustelae, an ulcerogenic and carcinogenic gastric pathogen

et al. 2010

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BackgroundHelicobacter mustelae causes gastritis, ulcers and gastric cancer in ferrets and other mustelids. H. mustelae remains the only helicobacter other than H. pylori that causes gastric ulceration and cancer in its natural host. To improve understanding of H. mustelae pathogenesis, and the ulcerogenic and carcinogenic potential of helicobacters in general, we sequenced the H. mustelae genome, and identified 425 expressed proteins in the envelope and cytosolic proteome.ResultsThe H. mustelae genome lacks orthologs of major H. pylori virulence factors including CagA, VacA, BabA, SabA and OipA. However, it encodes ten autotransporter surface proteins, seven of which were detected in the expressed proteome, and which, except for the Hsr protein, are of unknown function. There are 26 putative outer membrane proteins in H. mustelae, some of which are most similar to the Hof proteins of H. pylori. Although homologs of putative virulence determinants of H. pylori (NapA, plasminogen adhesin, collagenase) and Campylobacter jejuni (CiaB, Peb4a) are present in the H. mustelae genome, it also includes a distinct complement of virulence-related genes including a haemagglutinin/haemolysin protein, and a glycosyl transferase for producing blood group A/B on its lipopolysaccharide. The most highly expressed 264 proteins in the cytosolic proteome included many corresponding proteins from H. pylori, but the rank profile in H. mustelae was distinctive. Of 27 genes shown to be essential for H. pylori colonization of the gerbil, all but three had orthologs in H. mustelae, identifying a shared set of core proteins for gastric persistence.ConclusionsThe determination of the genome sequence and expressed proteome of the ulcerogenic species H mustelae provides a comparative model for H. pylori to investigate bacterial gastric carcinogenesis in mammals, and to suggest ways whereby cag minus H. pylori strains might cause ulceration and cancer.The genome sequence was deposited in EMBL/GenBank/DDBJ under accession number FN555004.

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Pathogenomics of Helicobacter

Cited by 14 publications

References 97 publications

A Repetitive DNA Element Regulates Expression of the Helicobacter pylori Sialic Acid Binding Adhesin by a Rheostat-like Mechanism

A Repetitive DNA Element Regulates Expression of the Helicobacter pylori Sialic Acid Binding Adhesin by a Rheostat-like Mechanism

Production of a Recombinant CagA Protein for the Detection of Helicobacter pylori CagA Antibodies

Comparative genomics and proteomics of Helicobacter mustelae, an ulcerogenic and carcinogenic gastric pathogen

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