期刊
JOURNAL OF BACTERIOLOGY
卷 189, 期 17, 页码 6109-6117出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JB.00246-07
关键词
-
类别
资金
- NIDDK NIH HHS [R56 DK075667-01, R56 DK075667] Funding Source: Medline
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 sigma(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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据