Analysis of the role of HP0208, a phase-variable open reading frame, and its homologues HP1416 and HP0159 in the biosynthesis of Helicobacter pylori lipopolysaccharide

Langdon, Rebecca R.; Craig, Jane E.; Goldrick, Marie; Houldsworth, Rebecca; High, Nicola J.

doi:10.1099/jmm.0.45842-0

Cited by 8 publications

(9 citation statements)

References 33 publications

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“…To investigate whether structures in the O‐antigen side‐chain of H. pylori LPS interact with galectin‐3, H. pylori 26695 and its isogenic galE mutant (Langdon et al ., 2005), which lacks O‐antigen, were labelled with fluorescein isothiocyanate (FITC) and their ability to adhere to recombinant human galectin‐3 compared using a solid‐phase binding assay. As a negative control, H. pylori adhesion to bovine serum albumin (BSA) which had been treated with sodium periodate (pBSA) to reduce glycosylation was also determined.…”

Section: Resultsmentioning

confidence: 99%

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Galectin-3 binds to Helicobacter pylori O-antigen: it is upregulated and rapidly secreted by gastric epithelial cells in response to H. pylori adhesion

et al. 2006

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Section: Resultsmentioning

confidence: 99%

“…Helicobacter pylori 26695 galE (Langdon et al ., 2005) was constructed by natural transformation of H. pylori 26695 with pNE1 that carries a copy of galE which has been disrupted by a kanamycin resistance gene cassette (Edwards et al ., 2000). H. pylori 84‐183 is a clinical isolate with an active TFSS.…”

Section: Methodsmentioning

confidence: 99%

Galectin-3 binds to Helicobacter pylori O-antigen: it is upregulated and rapidly secreted by gastric epithelial cells in response to H. pylori adhesion

et al. 2006

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“…In addition to point mutations, we noted repeat length differences (RLDs) in two different dinucleotide repeat sequences and one repeat consisting of multiple copies of an 8-bp motif. These RLDs were located in the outer membrane protein gene hopZ (HP0009) (16), an ORF encoding a putative glycosyl transferase, rfaJ2 (HP0208) (19), and one intergenic region (Table 3). hopZ contained a cytosine thymine (CT) × 6 repeat in the challenge strain H1 and a (CT) × 7 repeat in the reisolate 8A3, causing a frame shift and an early stop codon in hopZ of H1, whereas an intact hopZ gene is present in strain 8A3.…”

Section: Increased Frequency Of Imports In Genes Encoding Outer Membranementioning

confidence: 99%

Helicobacter pylori genome evolution during human infection

Kennemann

Didelot

Aebischer

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

243

284

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High genetic diversity is a hallmark of the gastric pathogen Helicobacter pylori. We used 454 sequencing technology to perform whole-genome comparisons for five sets of H. pylori strains that had been sequentially cultured from four chronically infected Colombians (isolation intervals = 3-16 y) and one human volunteer experimentally infected with H. pylori as part of a vaccine trial. The four sets of genomes from Colombian H. pylori differed by 27-232 isolated SNPs and 16-441 imported clusters of polymorphisms resulting from recombination. Imports (mean length = 394 bp) were distributed nonrandomly over the chromosome and frequently occurred in groups, suggesting that H. pylori first takes up long DNA fragments, which subsequently become partially integrated in multiple shorter pieces. Imports were present at significantly increased frequency in members of the hop family of outer membrane gene paralogues, some of which are involved in bacterial adhesion, suggesting diversifying selection. No evidence of recombination and few other differences were identified in the strain pair from an infected volunteer, indicating that the H. pylori genome is stable in the absence of mixed infection. Among these few differences was an OFF/ON switch in the phase-variable adhesin gene hopZ, suggesting strong in vivo selection for this putative adhesin during early colonization.comparative genomics | mutation M ore than one half of the human population is infected with Helicobacter pylori. Infection with this pathogen causes chronic gastritis, which can give rise to sequelae including peptic ulcers of stomach and duodenum, gastric atrophy, adenocarcinoma, and mucosa associated lymphoid tissue (MALT) lymphoma (1). Extensive allelic diversity and genetic variability are hallmarks of this species. They result from the combination of a high mutation rate (2) and frequent exchange of genetic material during mixed infections of one stomach with multiple H. pylori strains (3-7).We have previously analyzed the genetic relationships between strains of H. pylori that had been sequentially isolated from the same patient at time intervals ranging from 3 mo to 10 y (8) using multilocus sequence analysis of 10 (4) and 78 (8) loci, mostly from housekeeping genes. Bayesian inference was used to estimate recombination and mutation rates and the length of DNA fragments exchanged through recombination (imports). However, this multilocus approach did not allow conclusions about the chromosomal distribution of import events or about the relative frequencies of imports in different categories of genes.Here, we have used 454 pyrosequencing technology (9) to analyze the genomes of five sets of sequential isolates of H. pylori. In addition to four pairs of isolates from the earlier studies (with isolation intervals of 3 y), we also included recent follow-up isolates for two of the pairs that were obtained 16 y after the first isolates. Furthermore, we studied one pair of strains from a recent clinical trial where human volunteers were infected with H. pyl...

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“…Because of the analyzed H. pylori strains isolated from different continents, the 22 genes, even though they may not be present in all the clinic strains, should extensively exist in H. pylori strains and could have important contribution to adaptation. In addition to the functional confirmation of HP0208 [63], nine of the genes have also been demonstrated to be involved in the progress to chronic atrophic gastritis (orthologs: HPAG1_0785-HP0800; HPAG1_0783-HP0798; HPAG1_1035-HP0357; HPAG1_0985-HP0407; HPAG1_1536-HP1588; HPAG1_0212-HP0211; HPAG1_0452-HP0475; HPAG1_0455-HP0478; HPAG1_0838-HP0854) [28]. Most of these gene functions are not yet known in H. pylori and need to be clarified in the future research.…”

Section: Resultsmentioning

confidence: 99%

New Implications on Genomic Adaptation Derived from the Helicobacter pylori Genome Comparison

et al. 2011

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Background Helicobacter pylori has a reduced genome and lives in a tough environment for long-term persistence. It evolved with its particular characteristics for biological adaptation. Because several H. pylori genome sequences are available, comparative analysis could help to better understand genomic adaptation of this particular bacterium.Principal FindingsWe analyzed nine H. pylori genomes with emphasis on microevolution from a different perspective. Inversion was an important factor to shape the genome structure. Illegitimate recombination not only led to genomic inversion but also inverted fragment duplication, both of which contributed to the creation of new genes and gene family, and further, homological recombination contributed to events of inversion. Based on the information of genomic rearrangement, the first genome scaffold structure of H. pylori last common ancestor was produced. The core genome consists of 1186 genes, of which 22 genes could particularly adapt to human stomach niche. H. pylori contains high proportion of pseudogenes whose genesis was principally caused by homopolynucleotide (HPN) mutations. Such mutations are reversible and facilitate the control of gene expression through the change of DNA structure. The reversible mutations and a quasi-panmictic feature could allow such genes or gene fragments frequently transferred within or between populations. Hence, pseudogenes could be a reservoir of adaptation materials and the HPN mutations could be favorable to H. pylori adaptation, leading to HPN accumulation on the genomes, which corresponds to a special feature of Helicobacter species: extremely high HPN composition of genome.ConclusionOur research demonstrated that both genome content and structure of H. pylori have been highly adapted to its particular life style.

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Analysis of the role of HP0208, a phase-variable open reading frame, and its homologues HP1416 and HP0159 in the biosynthesis of Helicobacter pylori lipopolysaccharide

Cited by 8 publications

References 33 publications

Galectin-3 binds to Helicobacter pylori O-antigen: it is upregulated and rapidly secreted by gastric epithelial cells in response to H. pylori adhesion

Galectin-3 binds to Helicobacter pylori O-antigen: it is upregulated and rapidly secreted by gastric epithelial cells in response to H. pylori adhesion

Helicobacter pylori genome evolution during human infection

New Implications on Genomic Adaptation Derived from the Helicobacter pylori Genome Comparison

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