Evidence map›Paper›PMID 16217547›Full record

ArticlePLoS genetics2005

Gain and loss of multiple genes during the evolution of Helicobacter pylori.

Helga Gressmann, Bodo Linz, Rohit Ghai, Klaus-Peter Pleissner, Ralph Schlapbach, Yoshio Yamaoka, Christian Kraft, Sebastian Suerbaum, Thomas F Meyer, Mark Achtman

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
130citing papers in PubMed, 3 pooled it
15.2field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

130 citing papers in PubMed, 3 syntheses or guidelines pooled it, 231 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Host andGut microbes · 2026
    Article
  6. Microbiology and molecular biology reviews : MMBR · 2026
    Review
  7. Review
  8. Article
  9. Global diversity of integrating conjugative elements (ICEs) inbioRxiv : the preprint server for biology · 2025
    Article
  10. Article
  11. Article
  12. Helicobacter pylori infection.Nature reviews. Disease primers · 2023
    Review
  13. Review
  14. Article
  15. Pathogenomics of Helicobacter pylori.Current topics in microbiology and immunology · 2023
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Whole-Genome Sequencing and Comparative Genomics of ThreePathogens (Basel, Switzerland) · 2021
    Article

70 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 5 institutions in 3 countries.

Helga GressmannDepartment of Molecular Biology, Max-Planck-Institut für Infektionsbiologie, Berlin, Germany.
Bodo Linz
Rohit Ghai
Klaus-Peter Pleissner
Ralph Schlapbach
Yoshio Yamaoka
Christian Kraft
Sebastian Suerbaum
Thomas F Meyer
Mark Achtman
Max Planck Institute for Infection Biology · DEMax Planck Society · DEMedizinische Hochschule Hannover · DEBaylor College of Medicine · USUniversity of Giessen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sequence diversity and gene content distinguish most isolates of Helicobacter pylori. Even greater sequence differences differentiate distinct populations of H. pylori from different continents, but it was not clear whether these populations also differ in gene content. To address this question, we tested 56 globally representative strains of H. pylori and four strains of Helicobacter acinonychis with whole genome microarrays. Of the weighted average of 1,531 genes present in the two sequenced genomes, 25% are absent in at least one strain of H. pylori and 21% were absent or variable in H. acinonychis. We extrapolate that the core genome present in all isolates of H. pylori contains 1,111 genes. Variable genes tend to be small and possess unusual GC content; many of them have probably been imported by horizontal gene transfer. Phylogenetic trees based on the microarray data differ from those based on sequences of seven genes from the core genome. These discrepancies are due to homoplasies resulting from independent gene loss by deletion or recombination in multiple strains, which distort phylogenetic patterns. The patterns of these discrepancies versus population structure allow a reconstruction of the timing of the acquisition of variable genes within this species. Variable genes that are located within the cag pathogenicity island were apparently first acquired en bloc after speciation. In contrast, most other variable genes are of unknown function or encode restriction/modification enzymes, transposases, or outer membrane proteins. These seem to have been acquired prior to speciation of H. pylori and were subsequently lost by convergent evolution within individual strains. Thus, the use of microarrays can reveal patterns of gene gain or loss when examined within a phylogenetic context that is based on sequences of core genes.

Indexed as

Evolution, MolecularGene Expression RegulationGene Transfer, HorizontalGenomeGenome, BacterialHelicobacterHelicobacter pyloriModels, GeneticOligonucleotide Array Sequence AnalysisPhylogenyRecombination, GeneticSpecies Specificity

Identifiers

PMID16217547
PMCPMC1245399
OpenAlexW2023510054

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.