Virulence of E. coli influenced by environmental signals

大肠杆菌病原体经常在依赖宿主和不依赖宿主之间循环。因此，它们必须适应不断变化的环境，对不同的环境线索做出反应。为了忍受养分供应的频繁变化，细菌拥有大量的调节和代谢基因，允许快速适应和高度灵活性。使用致病性大肠杆菌模型，我们正在探索毒性与两种细菌代谢反应之间的潜在交互作用：* ***a)*动物肠道环境包含丰富多样的营养物质，部分来自微生物群建立的共生关系。利用功能基因组学，我们观察到在肠道微生物群代谢物存在的情况下，致病性肠道大肠杆菌中代谢和毒力基因的表达发生了重要变化。我们正在破译来自肠道菌群环境的信号影响大肠杆菌毒力的调控系统的机制细节。*** *b)细菌性病原体，包括人类、动物和植物的病原体，*会遇到限制磷酸盐（Pi）或富含Pi的环境。磷酸(Pi)-浓度调节Pho调控子的表达，而Pho调控子部分受PhoB/PhoR双组分调控系统（TCRS）的控制。这种TCRS允许细菌相应地调节磷酸盐同化途径。在Pi限制条件下，大肠杆菌利用转录反应调节因子PhoB将细菌感知到的Pi饥饿信号转化为基因激活或抑制。我们正在探索π信号是如何不仅仅是空的

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