| Summary: | 碩士 === 慈濟大學 === 微免暨分子醫學研究所 === 95 === Helicobacter pylori possesses a homologue of luxS gene, luxS gene exists in numerous gram-positive and gram-negative bacteria. It regulates virulence genes expression, biofilm formation, and bacteriocin production through quorum sensing system with a growth phase-dependent manner. Previous studies have revealed that the flaA expression and biofilm formation were regulated by luxS gene. During the cultivation, H. pylori changed its morphology from rod to coccoid form. Studies have shown that H. pylori cells underwent spontaneous autolysis during cultivation. In our study, we constructed a luxS mutant to characterize its function and elucidate what important role it may play in H. pylori. In this report, the luxS mutant was grown slower than wild type. The LuxS expression was growth phase dependent. Live and dead staining revealed that in the luxS mutant the dead cells appeared after 60h cultivation (death phase), but the coccoid forms appeared at lag phase. The autolysis assay demonstrated that luxS mutation would induce autolysis. The disc diffusion assay have shown that when incubated with high concentrations of transition elements which was toxic to cells, the luxS mutant presented significantly better tolerance than wild type. We suggested that luxS was associated with growth and autolysis regulation and may participate in the transportation of transition elements. We constructed a luxS complementary strain in which the luxS gene was under the control of flaA promoter, but the LuxS protein was not expressed. We considered it resulted from the luxS mutation would repress the the flaA expression.
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