Abstract
The etiologic agent of bubonic plague, Yersinia pestis, senses self-produced, secreted chemical signals 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 observed at 30°C, indicating a potential role for quorum sensing regulation of metabolism at temperatures below the normal mammalian temperature. It is proposed that utilization of alternative carbon sources may enhance growth and/or survival during prolonged periods in natural habitats with limited nutrient sources, contributing to maintenance of plague in nature.
Highlights
Plague, or the Black Death, has killed over two hundred million people and remains the most devastating epidemic bacterial disease
We demonstrate that acyl-homoserine lactone (AHL)-based Quorum sensing (QS) is important for the regulation of metabolism in Y. pestis
This represents a significant departure from the functions QS regulates in related strains within the Yersinia genus
Summary
The Black Death, has killed over two hundred million people and remains the most devastating epidemic bacterial disease. Plague, caused by Yersinia pestis, is a zoonotic disease primarily spread between mammals by fleas. When a flea bites an infected rodent, Y. pestis is ingested with the blood meal. After a period of growth in the flea gut, transmission from the flea results from colonization of the proventricular valve, impairing valve function and allowing backflow of infectious blood into subsequently bit mammals. Yersinia pestis differentiated 2,600 to 28,000 years from Y. pseudotuberculosis [1], which causes mild enteritis in humans. With astonishingly few genetic changes, Y. pestis gained a dramatically enhanced ability to induce mortality in mammalian hosts, and it acquired the ability to colonize an additional host, the flea. As a parasite of both mammals and fleas, it has adapted to grow in two very different environments
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