Affiliation:
1. Institute of Molecular Biology, University of Oregon, Eugene, Oregon 97403
2. Department of Chemistry
3. Howard Hughes Medical Institute and Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544
Abstract
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. The flagella of the
luxS
mutant appeared normal; however, in genetic backgrounds lacking any of three flagellar regulators—the two-component sensor kinase
flgS
, the sigma factor σ
28
(also called
fliA
), and the anti-sigma factor
flgM
—loss of
luxS
altered flagellar morphology. In all cases, the double mutant phenotypes were restored to the
luxS
+
phenotype by the addition of synthetic 4,5-dihydroxy-2,3-pentanedione (DPD), which cyclizes to form AI-2. Furthermore, in all mutant backgrounds loss of
luxS
caused a decrease in transcript levels of the flagellar regulator
flhA
. Addition of DPD to
luxS
cells induced
flhA
transcription in a dose-dependent manner. Deletion of
flhA
in a wild-type or
luxS
mutant background resulted in identical loss of motility, flagella, and flagellar gene expression. These data demonstrate that AI-2 functions as a secreted signaling molecule upstream of FlhA and plays a critical role in global regulation of flagellar gene transcription in
H. pylori
.
Publisher
American Society for Microbiology
Subject
Molecular Biology,Microbiology
Cited by
82 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献