Affordable Access

deepdyve-link deepdyve-link
Publisher Website

Regulation of Helicobacter pylori adherence by gene conversion.

Authors
  • Talarico, Sarah1
  • Whitefield, Shawn E
  • Fero, Jutta
  • Haas, Rainer
  • Salama, Nina R
  • 1 Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA.
Type
Published Article
Journal
Molecular Microbiology
Publisher
Wiley (Blackwell Publishing)
Publication Date
Jun 01, 2012
Volume
84
Issue
6
Pages
1050–1061
Identifiers
DOI: 10.1111/j.1365-2958.2012.08073.x
PMID: 22519812
Source
Medline
License
Unknown

Abstract

Genetic diversification of Helicobacter pylori adhesin genes may allow adaptation of adherence properties to facilitate persistence despite host defences. The sabA gene encodes an adhesin that binds sialyl-Lewis antigens on inflamed gastric tissue. We found variability in the copy number and locus of the sabA gene and the closely related sabB and omp27 genes due to gene conversion among 51 North American paediatric H. pylori strains. We determined that sabB to sabA gene conversion is predominantly the result of intra-genomic recombination and RecA, RecG and AddA influence the rate at which it occurs. Although all clinical strains had at least one sabA gene copy, sabA and sabB were lost due to gene conversion at similar rates in vitro, suggesting host selection to maintain the sabA gene. sabA gene duplication resulted in increased SabA protein production and increased adherence to sialyl-Lewis antigens and mouse gastric tissue. In conclusion, gene conversion is a mechanism for H. pylori to regulate sabA expression level and adherence.

Report this publication

Statistics

Seen <100 times