SPOOK EFFECT ON FLAGELLIN SYNTHESIS IN B SUBTILIS

描述：有或没有鞭毛结构的几个 病原菌已被证明是疾病的病原体 这些有机体。鞭毛蛋白基因在枯草芽孢杆菌中的表达 非致病的土壤有机体已被证明是 另一种西格玛因子控制下的基因。一种同源调控子 已在几种致病和非致病生物中发现 包括大肠杆菌、鼠伤寒沙门氏菌、空肠弯曲杆菌、 结肠弯曲杆菌、新月弯杆菌、金黄色假单胞菌、 紫花苜蓿根瘤菌和霍乱弧菌。《公约》的总体目标 提出的研究是为了更好地定义调控的分子机制 鞭毛基因在枯草杆菌中的表达。重点放在基因上 以及SPOCK信号转导级联的分子特征和 它在控制鞭毛基因表达中的重要性。 斯波克基因产物形成一种膜运输系统，允许 寡肽的内在化。这一系统已被提议成为 外部设备之间信号转导的最上游组件 环境与产孢量和其他指数后的启动 枯草杆菌中的现象。拟议的研究不仅将提供 关于一个重要的信号转导级联的更多信息，但将 进一步明确鞭毛蛋白基因在枯草杆菌中的表达调控。 这些信息将有助于更好地理解这一点 在病原菌中的过程。 我们建议通过1)来研究SPOCK信号转导级联 探讨SPOCK基因产物在调控中的作用 鞭毛基因的转录；2)描述环境 影响鞭毛蛋白表达的信号；3)确定鞭毛蛋白的作用 在鞭毛蛋白调节中被信号转导信号激活的一种激酶 表达；以及4)识别和表征顺式作用元件 SPOCK依赖调控鞭毛基因表达所必需的 信号转导。

DESCRIPTION: The presence or absence of flagellar structures in several pathogenic bacteria has been shown to be the etiologic agent for disease in these organisms. Flagellin gene expression in Bacillus subtilis, a non-pathogenic, soil-organism has been shown to be part of a regulon of genes under the control of an alternate sigma factor. A homologous regulon has been identified in several pathogenic and non-pathogenic organisms including Escherichia coli and Salmonella typhimurium, Campylobacter jejuni, Campylobacter coli, Caulobacter crescentus, Pseudomonas aeuriginosa, Rhizobium meliloti, and Vibrio cholerae. The overall objective of the proposed research is to better define the molecular mechanisms regulating flagellar gene expression in B. subtilis. The emphasis is on the genetic and molecular characterization of the SpoOK signal transduction cascade and its importance in controlling flagellin gene expression. The spoOK gene products form a membrane transport system that allows for the internalization of oligopeptides. This system has been proposed to be the most upstream component of signal transduction between the external environment and the initiation of sporulation and other post-exponential phenomena in B. subtilis. The proposed studies will not only provide additional information on an important signal transduction cascade, but will further define the regulation of flagellin gene expression in B. subtilis. This information will then facilitate a greater understanding of this process in pathogenic bacteria. We propose to study the SpoOK signal transduction cascade by 1) investigating the role of the spoOK gene products in regulating transcription of the flagellin gene; 2) delineating the environmental signals that affect flagellin expression; 3) determining the role of the KinA kinase, activated by the SpoOK signal, in regulating flagellin expression; and 4) identifying and characterizing cis acting elements required for regulation of flagellin gene expression by SpoOK-dependent signal transduction.