Project description:Yersinia pestis, the etiological agent of plague, is able to sense cell density by quorum sensing. The function of quorum sensing in Y. pestis is not clear. Here, the process of quorum sensing was investigated by comparing transcript profiles when three quorum-sensing signals are added in. The strain ∆pgm (pigmentation-negative) mutant R88 was used as wild type. The three signals are AI-2, AHLs (N-(3-Oxooctanoyl)-L-homoserine lactone and N-Hexanoyl-DL-homoserine lactone).The control consisted of cells grown and treated under the same conditions without added signals.
Project description:Yersinia pestis, the etiological agent of plague, is able to sense cell density by quorum sensing. The function of quorum sensing in Y. pestis is not clear. Here, the process of AHL quorum sensing was investigated by comparing transcript profiles when two AHL quorum-sensing signals are added in. The strain ∆pgm (pigmentation-negative) mutant R88 was called wild type. The two AHLs signals are N-(3-Oxooctanoyl)-L-homoserine lactone and N-Hexanoyl-DL-homoserine lactone.The control consisted of cells grown and treated under the same conditions without added signals.
Project description:Yersinia pestis, the etiological agent of plague, is able to sense cell density by quorum sensing. The function of quorum sensing in Y. pestis is not clear. Here, the process of AHL quorum sensing was investigated by comparing transcript profiles when two AHL quorum-sensing signals are added in. The strain Δpgm (pigmentation-negative) mutant was called wild type. The two AHLs signals are N-(3-Oxooctanoyl)-L-homoserine lactone and N-Hexanoyl-DL-homoserine lactone.The control consisted of cells grown and treated under the same conditions without added signals.
Project description:Yersinia pestis, the etiological agent of plague, is able to sense cell density by quorum sensing. The function of quorum sensing in Y. pestis is not clear. Here, the process of quorum sensing was investigated by comparing transcript profiles when three quorum-sensing signals are added in. The strain M-bM-^HM-^Fpgm (pigmentation-negative) mutant R88 was used as wild type. The three signals are AI-2, AHLs (N-(3-Oxooctanoyl)-L-homoserine lactone and N-Hexanoyl-DL-homoserine lactone).The control consisted of cells grown and treated under the same conditions without added signals. Six independent RNA samples from Y. pestis CO92 M-bM-^HM-^Fpgm cultures were paired with six independent RNA samples from 3 signals added cultures for hybridization to six two-color microarrays. A dye-swap design was used to remove the Cy5 and Cy3 dye bias.
Project description:The etiologic agent of bubonic plague, Yersinia pestis, senses cell density-dependent chemical signals to synchronize transcription between cells of the population in a process named quorum sensing. Though the closely related enteric pathogen Y. pseudotuberculosis uses quorum sensing system to regulate motility, the role of quorum sensing in Y. pestis has been unclear. In this study we performed transcriptional profiling experiments to identify Y. pestis quorum sensing regulated functions. Our analysis revealed that acyl-homoserine lactone based quorum sensing controls the expression of several metabolic functions. Maltose fermentation and the glyoxylate bypass are induced by acyl-homoserine lactone signaling. This effect was seen to be temperature conditional. Metabolism is unresponsive to quorum sensing regulation at mammalian body temperature, indicating a potential role for quorum sensing regulation of metabolism specifically during colonization of the flea vector. It is proposed that utilization of alternative carbon sources may enhance growth and/or survival during prolonged flea colonization, contributing to maintenance of plague in nature.
Project description:Yersinia pestis, the etiological agent of plague, is able to sense cell density by quorum sensing. The function of quorum sensing in Y. pestis is not clear. Here, the process of AHL quorum sensing was investigated by comparing transcript profiles when two AHL quorum-sensing signals are added in. The strain âpgm (pigmentation-negative) mutant R88 was called wild type. The two AHLs signals are N-(3-Oxooctanoyl)-L-homoserine lactone and N-Hexanoyl-DL-homoserine lactone.The control consisted of cells grown and treated under the same conditions without added signals. Six independent RNA samples from R88 cultures were paired with six independent RNA samples from two AHLs added cultures for hybridization to six two-color microarrays. A dye-swap design was used to remove the Cy5 and Cy3 dye bias.
Project description:Yersinia pestis, the etiological agent of plague, is able to sense cell density by quorum sensing. The function of quorum sensing in Y. pestis is not clear. Here, the process of AHL quorum sensing was investigated by comparing transcript profiles when two AHL quorum-sensing signals are added in. The strain Îpgm (pigmentation-negative) mutant was called wild type. The two AHLs signals are N-(3-Oxooctanoyl)-L-homoserine lactone and N-Hexanoyl-DL-homoserine lactone.The control consisted of cells grown and treated under the same conditions without added signals. Six independent RNA samples from Y. pestis CO92 Îpgm cultures were paired with six independent RNA samples from two AHLs added cultures for hybridization to six two-color microarrays. A dye-swap design was used to remove the Cy5 and Cy3 dye bias.
Project description:Quorum sensing controls the expression of multiple virulence factors. PA14 genes lasR and rhlR are necessary for quorum sensing via homoserine lactones. A PA14 lasR rhlR deficient mutant exhibits a reduced oxidative stress response. Here we conducted a microarray to determine oxidative stress response gene regulation mediated by the homoserine lactone quorum sensing circuits.
Project description:The quorum-sensing system has been linked to diverse phenotypes and regulatory changes in pathogenic bacteria. In strain CO92, the AI-2 signal is produced in a luxS-dependent manner, reaching maximal levels of 2.5 μM in late logarithmic growth, and both wild type and pigmentation mutant strains made equivalent levels of AI-2. Yersinia pestis CO92 possesses a chromosomal lsr locus encoding factors involved in the binding and import of AI-2, and confirming this assignment, an lsr deletion increased extracellular pools of AI-2. To assess the functional role of 3 quorum sensing singlas in Y. pestis, microarray study was conducted comparing the 3 quorum sensing signals added in to control at 30°C to mimic the flea gut. Here, the ΔPgm (pigmentation-negative) R88 strain was used. The three signals are one AI-2 and two AHLs (N-(3-Oxooctanoyl)-L-homoserine lactone and N-Hexanoyl-DL-homoserine lactone).The control consisted of cells grown and treated under the same conditions without added signals.
Project description:Acyl-homoserine lactone (acyl-HSL) quorum sensing was first discovered in Vibrio fischeri where it serves as a key control element of the seven-gene luminescence (lux) operon. Since this initial discovery, other bacteria have been shown to control hundreds of genes by acyl-HSL quorum sensing. Until recently, it has been difficult to examine the global nature of quorum sensing in V. fischeri. However, the complete genome sequence of V. fischeri is now available and this has enabled us to use transcriptomics to identify quorum-sensing regulated genes and to study the quorum-controlled regulon of this bacterium. In this study, we used DNA microarray technology to identify over two-dozen V. fischeri genes regulated by the quorum sensing signal N-3-oxohexanoyl-L-homoserine lactone (3OC6-HSL). Keywords: Comparison of transcriptome profiles