Virulence of E. coli influenced by environmental signals

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Escherichia*coli pathogens often cycle between host dependent and host-independent*lifestyles. Thus, they must adapt to changing environments and respond to*different environmental cues. To endure the frequent changes in nutrient*availability, bacteria possess an arsenal of regulatory and metabolic genes*allowing rapid adaptation and high flexibility.  Using a*pathogenic E. coli model, we are exploring the potential cross-talk between*virulence and two types of bacterial metabolic responses:* ***a)*The animal gut environment contains a rich diversity of nutrients, coming in*part from the symbiotic relationships established by the microbiota. Using*functional genomics, we observed an important shift in the expression of*metabolic and virulence genes in pathogenic intestinal E. coli in the presence of metabolites from the gut*microbiota.  We are deciphering the*mechanistic details of the regulatory systems by which signals from the*intestinal microbiota environment influence E.*coli virulence.*** ***b) Bacterial pathogens, including those of humans, animals, and plants,*encounter phosphate (Pi)-limiting or Pi-rich environments. The*phosphate (Pi)-concentration modulates the expression of the Pho regulon, which*is controlled in part*by the PhoB/PhoR, a two component regulatory system (TCRS). This TCRS allows*bacteria to regulate phosphate assimilation pathways accordingly. Under Pi-limiting conditions, E. coli uses the*transcriptional-response regulator PhoB to translate the Pi starvation signal*sensed by the bacterium into gene activation or repression. We are exploring*how the Pi signal is not only emp