Small RNA Regulation of the Quorum Sensing Response in the Bacterial Pathogen Vibrio Cholerae

Abstract

Vibrio cholerae, the waterborne bacterium responsible for the deadly disease cholera, is both a transient human pathogen and a ubiquitous inhabitant of marine environments. The pathogenesis and ecology of this deadly microbe are the focus of research in the Hammer lab. V. cholerae has become a model organism to understand a process of microbial cell-cell communication called quorum sensing, which allows bacterial groups to act in unison by synchronizing gene expression in response to population density. V. cholerae, and many other Vibrio species, achieves quorum sensing by producing and then responding to chemical signal molecules, called autoinducers, which control the production of multiple regulatory small RNAs. In V. cholerae, these non-coding sRNAs are predicted to base-pair with, and alter the translation of, several mRNAs encoding protein regulators that alter the expression of >100 genes. Many of the quorum-sensing regulated genes (such as the cholera toxin and attachment factors) are critical for host colonization, while others (such as genes involved in horizontal gene transfer) are important in marine ecosystems. We are currently using genetic, biochemical, and computational methods to define the mechanism of sRNA control and the role of V. cholerae quorum sensing in clinical and environmental settings.