The Quorum-Sensing Molecule Autoinducer 2 Regulates Motility and Flagellar Morphogenesis in Helicobacter pylori

Abstract

The genome of the gastric pathogen Helicobacter pylori contains a homologue of the gene luxS, which has been shown to be responsible for production of the quorum-sensing signal autoinducer 2 (AI-2). We report here that deletion of the luxS gene in strain G27 resulted in decreased motility on soft agar plates, a defect that was complemented by a wild-type copy of the luxS gene and by the addition of cell-free supernatant containing AI-2. Many bacterial species regulate aspects of their behavior through an intercellular signaling system called quorum sensing (4). Bacteria produce small molecules, termed autoinducers (AIs), that travel across the bacterial membrane and accumulate in the environment. Increases in cell density result in corresponding increases in AI concentration in the extracellular environment and cell cytoplasm. At threshold AI concentrations, the interaction between the AI and its transduction machinery results in the coordinated transcription of target genes required for specific group behaviors (52).

Escherichia coli transcription factor YncC (McbR) regulates colanic acid and biofilm formation by repressing expression of periplasmic protein YbiM (McbA)

“…This result is consistent with the recent finding that in the oral bacterium Aggregatibacter actinomycetemcomitans, AI-2 regulates its biofilm formation most likely through its QseBC system (Shao et al, 2007). Also, in the human gastric pathogen Helicobacter pylori, AI-2 controls motility by controlling genes upstream of the motility and flagellar regulator FlhA (Rader et al, 2007). Further proof that AI-2 controls motility in different genera is that AI-2 regulates transcription of the flagellin gene, flaA, in the human pathogen Campylobacter jejuni (Jeon et al, 2003).…”

Quorum sensing dependent phenotypes and their molecular mechanisms inCampylobacterales

“…This confirms that the loss of AI-2 rather than the loss of metabolic or regulatory LuxS functions were responsible for these effects [47]. Rader et al [46] determined that AI-2 functions as signalling molecule up-stream of the flagellar regulator flhA in H. pylori. These data suggest that bacterial motility or flagella formation and function in C. jejuni is dependent on a functional luxS but not AI-2 at 37 °C while in H. pylori it is partially under control of AI-2.…”

“…Only Holmes et al [43] complemented the luxS mutant by the addition of exogenously produced AI-2 but observed no restoration in gene expression or motility, and concluded that these effects were due to deletion of luxS and not of AI-2 depletion. The luxS mutants of the H. pylori strains X47-2AL and Alston did not show any obvious defects compared to corresponding wild type strains [39,44], while motility of other H. pylori luxS mutants of the strains TK1402, G27, SS1 and J99 was reduced as observed in soft agar motility assays and by microscopy [44][45][46][47]. In contrast, no differences in flagella formation were detected using scanning electron microscopy [45,46].…”

“…The luxS mutants of the H. pylori strains X47-2AL and Alston did not show any obvious defects compared to corresponding wild type strains [39,44], while motility of other H. pylori luxS mutants of the strains TK1402, G27, SS1 and J99 was reduced as observed in soft agar motility assays and by microscopy [44][45][46][47]. In contrast, no differences in flagella formation were detected using scanning electron microscopy [45,46]. However, the number and the length of individual flagella were reduced in H. pylori J99 luxS mutants and these mutants showed reduced transcription of flaA, flgE, motA, motB, flhA and fliI but not flaB genes [47].…”

Can bacteria actively search to join groups?

“…In the case of E. coli, this could be the gastrointestinal tract of vertebrates and/or the external environment. Finally, as AI-2 has been reported to regulate the motility of other bacteria such as Campylobacter jejuni and Helicobacter pylori as well (Elvers and Park, 2002;Rader et al, 2007), this active grouping behavior might not be restricted to E. coli and might add yet another dimension to microbial ecology.…”