Please note that we have stopped the regular imports of Gene Expression Omnibus (GEO) data into ArrayExpress. This may not be the latest version of this experiment.
E-GEOD-14752 - H. pylori G27 HP0518 mutant showed greater motility
Released on 22 December 2010, last updated on 1 May 2014
Helicobacter pylori is a human gastric pathogen associated with gastric and duodenal ulcers as well as specific gastric cancers. It is well-evidenced that motility is essential for this pathogen to colonize human gastric tissues. We found that the H. pylori G27 HP0518 mutant showed greater motility than the parental strain, leading to increased cell adhesion and subsequent CagA translocation and NF-κB activation in AGS cells. This mutant expressed a higher molecular mass flagellin A (FlaA) than the parental wild-type strain and the complemented HP0518 mutant, which correlated with differences in motility. Deglycosylation assays indicated that the increased molecular mass of the FlaA protein expressed by the mutant was due to O-linked glycoside modifications. Electron micrographs demonstrated that expression of bundle-formed flagellin filaments in the HP0518 mutant was enhanced in comparison to the wild-type strain. Different degrees of FlaA glycosylation between H. pylori strains suggested that glycosylation could affect both virulence and persistence in vivo. In conclusion, HP0518 inactivation resulted in FlaA hyper-glycosylation leading to increased virulence and motility. Microarray experiments were carried out as two-color hybridizations with a color-swap dye-reversal setting to compensate Cy-dye specific effects and to ensure statistically relevant data.
transcription profiling by array
Hans-Joachim Mollenkopf <email@example.com>, Hans Molenkopf, Hiroshi Asakura, Thomas F Meyer
Helicobacter pylori HP0518 affects flagellin glycosylation to alter bacterial motility. Asakura H, Churin Y, Bauer B, Boettcher JP, Bartfeld S, Hashii N, Kawasaki N, Mollenkopf HJ, Jungblut PR, Brinkmann V, Meyer TF. , PMID:21091500