Borrelia burgdorferi LuxS-mediated quorum sensing

超出所提供的空间。莱姆病的病原体伯氏疏螺旋体通过感染的硬蜱属的叮咬传播给人类和其他温血动物。滴答声。B.伯氏菌感染涉及细菌与多种脊椎动物宿主和节肢动物载体组织之间的许多相互作用。在这个感染周期的特定点上需要不同的细菌蛋白质，并且精确调节这些蛋白质的合成对于成功感染的发生至关重要。我们发现这些螺旋体利用一种调控机制来控制蛋白质表达模式，该机制涉及称为自诱导物-2（AI-2）的化学信号。这个分子是由B产生的。Burgdorferi LuxS蛋白，我们已经证明它是一种功能酶。我们的初步研究表明，B。burgdorferi可以调节LuxS的合成。向培养的B中加入AI-2。Burgdorferi显著改变了50多种不同蛋白质的表达，增加了一些蛋白质的表达水平，同时降低了其他蛋白质的表达。通过这种机制，莱姆病螺旋体的群体可以同步生产感染过程所需的蛋白质。我们假设B. burgdorferi使用AI-2作为重要的信号分子来控制莱姆病螺旋体自然感染周期中蛋白质的表达。拟议的研究将表征细菌感染期间LuxS的表达，B. burgdorferi控制AI-2的合成和AI-2调节蛋白的功能。这些研究的结果将增强我们对B之间复杂相互作用的理解。莱姆病及其宿主，以及确定潜在的细菌靶点，以改进预防和治疗莱姆病的疗法。性能现场=

EXCEED THE SPACE PROVIDED. The spirochete Borrelia burgdorferi, the causative agent of Lyme disease, is transmitted to humans and other warm blooded animals through the bite of infected Ixodes spp. ticks. The establishment of B. burgdorferi infection involves numerous interactions between the bacteria and a variety of vertebrate host and arthropod vector tissues. Different bacterial proteins are required at specific points of this infectious cycle, and precise regulation of the synthesis of such proteins is essential for successful infection to occur. We have discovered that these spirochetes utilize a regulatory mechanism to control protein expression patterns that involves a chemical signal known as autoinducer-2 (AI-2). This molecule is produced by the B. burgdorferi LuxS protein, which we have demonstrated to be a functional enzyme. Our preliminary studies suggest that B. burgdorferi can regulate LuxS synthesis. Addition of AI-2 to cultured B. burgdorferi dramatically alters the expression of more than 50 different proteins, increasing expression levels of some proteins, while decreasing expression of others. Through this mechanism, a population of Lyme disease spirochetes may synchronize production of proteins needed for infection processes. We hypothesize that B. burgdorferi uses AI-2 as an important signaling molecule to control expression of proteins during the natural infectious cycle of the Lyme disease spirochetes. The proposed studies will characterize the expression of LuxS during bacterial infection, the mechanisms by which B. burgdorferi controls synthesis of AI-2, and functions of AI-2-regulated proteins. Results from these studies will enhance our understanding of the complex interactions between B. burgdorferi and its hosts, as well as identifying potential bacterial targets for improved therapies to prevent and treat Lyme disease. PERFORMANCE SITE ========================================Section End===========================================