In:
Applied and Environmental Microbiology, American Society for Microbiology, Vol. 72, No. 10 ( 2006-10), p. 6615-6622
Kurzfassung:
Furanone
metabolites called AI-2 (autoinducer 2), used by some bacterial species for signaling and cell density-regulated changes in gene expression,
are made while regenerating S -adenosyl methionine (SAM) after
its use as a methyl donor. The luxS -encoded enzyme, in
particular, participates in this activated methyl cycle by generating both a pentanedione, which is transformed chemically into these AI-2
compounds, and homocysteine, a precursor of methionine and SAM. Helicobacter pylori seems to contain the genes for this
activated methyl cycle, including luxS , but not genes for AI-2
uptake and transcriptional regulation. Here we report that deletion of luxS in H. pylori reference strain SS1 diminished its
competitive ability in mice and motility in soft agar, whereas no such effect was seen with an equivalent ΔluxS derivative of
the unrelated strain X47. These different outcomes are consistent with H. pylori 's considerable genetic diversity and are reminiscent
of phenotypes seen after deletion of another nonessential metabolic gene, that encoding polyphosphate kinase 1. We suggest that synthesis
of AI-2 by H. pylori may be an inadvertent consequence of
metabolite flux in its activated methyl cycle and that impairment of this cycle and/or pathways affected by it, rather than loss of quorum
sensing, is deleterious for some H. pylori strains. Also
tenable is a model in which AI-2 affects other microbes in H.
pylori 's gastric ecosystem and thereby modulates the gastric
environment in ways to which certain H. pylori strains are
particularly sensitive.
Materialart:
Online-Ressource
ISSN:
0099-2240
,
1098-5336
DOI:
10.1128/AEM.01291-06
Sprache:
Englisch
Verlag:
American Society for Microbiology
Publikationsdatum:
2006
ZDB Id:
223011-2
ZDB Id:
1478346-0
SSG:
12
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