SPOOK EFFECT ON FLAGELLIN SYNTHESIS IN B SUBTILIS

描述：在几个鞭毛结构的存在或不存在， 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 非致病性的土壤有机体已被证明是调节子的一部分， 在交替西格玛因子控制下的基因。 同源调节子 已在几种致病和非致病生物中鉴定出 包括大肠杆菌和鼠伤寒沙门氏菌，空肠弯曲杆菌， 结肠弯曲杆菌，新月柄杆菌，铜绿假单胞菌， 苜蓿根瘤菌和霍乱弧菌。 的总体目标 拟议的研究是为了更好地确定调节 鞭毛基因在B中的表达。枯草杆菌。 重点在于遗传 和SpoOK信号转导级联的分子表征， 它在控制鞭毛蛋白基因表达中的重要性。 spoOK基因产物形成一个膜转运系统， 寡肽的内化。 该系统已被提议为 细胞外信号转导的最上游成分 环境和孢子形成和其他指数后的启动 B中的现象。枯草杆菌。 这些研究不仅提供 一个重要的信号转导级联的额外信息，但将 进一步明确了鞭毛蛋白基因在B中的表达调控。枯草杆菌。 这些信息将有助于更好地理解这一点， 致病菌的过程。 我们建议通过1）研究SpoOK信号转导级联 研究spoOK基因产物在调节 鞭毛蛋白基因的转录; 2）描绘环境 影响鞭毛蛋白表达的信号; 3）确定鞭毛蛋白的作用。 由SpoOK信号激活的KinA激酶在鞭毛蛋白调节中的作用 表达;和4）鉴定和表征顺式作用元件 Spook-dependent的鞭毛蛋白基因表达调控所需的 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.