Project description:Temperature is a key environmental factor for facultative pathogens during the host adaptation response. To assess the functional role of temperature in Yersinia pestis, a microarray study was conducted comparing the Δpgm (pigmentation-negative) R88 strain grown at 37°C or 30°C.
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: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 YpeIR quorum sensing in Y. pestis has been unclear. YpeIR is one of the AHL quorum sensing system in Y. pestis. In this study we performed transcriptional profiling experiments to identify Y. pestis YpeIR quorum sensing regulated functions at 37°C.
Project description:A microarray was developed to screen rodent samples for pathogens of zoonotic importance In the work described here, a homologue to Yersinia pestis was found in rodent samples after screening with the microarray
Project description:A microarray was developed to screen rodent samples for pathogens of zoonotic importance In the work described here, a homologue to Yersinia pestis was found in rodent samples after screening with the microarray A number of rodent samples from the UK and Canada were identified as carrying a homologue to a Yersinia pestis gene
Project description:Temperature is a key environmental factor for facultative pathogens during the host adaptation response. To assess the functional role of temperature in Yersinia pestis, a microarray study was conducted comparing the Îpgm (pigmentation-negative) R88 strain grown at 37°C or 30°C. Six independent RNA samples from 37°C cultures were paired with six independent RNA samples from 30°C 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 agent of plague, is transmitted to mammals by infected fleas. Y. pestis exhibits a distinct life stage in the flea, where it grows in the form of a cohesive biofilm that promotes transmission. After transmission, the temperature shift to 37°C induces many known virulence factors of Y. pestis that confer resistance to innate immunity. These factors are not produced in the low-temperature environment of the flea, however, suggesting that Y. pestis is vulnerable to the initial encounter with innate immune cells at the flea bite site. In this study, we used whole-genome microarrays to compare the Y. pestis in vivo transcriptome in infective fleas to in vitro transcriptomes in temperature-matched biofilm and planktonic cultures, and to the previously characterized in vivo gene expression profile in the rat bubo. In addition to genes involved in metabolic adaptation to the flea gut and biofilm formation, several genes with known or predicted roles in resistance to innate immunity and pathogenicity in the mammal were upregulated in the flea. Y. pestis from infected fleas were more resistant to phagocytosis than in vitro-grown bacteria, which was largely attributable to a cluster of insecticidal-like toxin genes that were highly expressed only in the flea. Our results indicate that cycling through the flea vector preadapts Y. pestis to face the mammalian innate immune response that it encounters immediately after transmission.