SIGNAL TRANSDUCTION IN CAULOBACTER CELL CYCLE REGULATION

茎杆菌细胞周期调节中的信号转导

• 批准号: 6490266
• 负责人: AUSTIN NEWTON
• 金额: $ 34.8万
• 依托单位: PRINCETON UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 1999
• 资助国家: 美国
• 起止时间: 1999-01-01 至 2004-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6490266
• 关键词: Caulobacter; bacterial genetics; biological signal transduction; cell cycle; cell cycle proteins; cell motility; cellular polarity; enzyme activity; immunoprecipitation; phosphorylation; protein tyrosine kinase; site directed mutagenesis; yeast two hybrid system

Unequal cell division is a central mechanism in the generation of new cell types. In Caulobacter crescentus differentiation is the direct result of repeated, asymmetric cell division and this aquatic bacterium provides an ideal model for elucidating the mechanisms underlying developmental control. The patterns of differentiation and cell cycle progression in these cells are closely coordinated by two- component signal transduction systems. Possibly unique aspects of these two-component proteins is the fact that they respond to internal cell cycle cues instead of environmental conditions and some of them are essential for division and cell viability. The organization of the signal transduction pathways is not fully defined, however, and how these pathways coordinate the precise temporal and spatial patterns of developmental events during the cell cycle is far from clear. Experiments described in the proposal are designed to address the following goals: I. Identify and characterize components in the essential signal transduction pathway, DivJ => DivK => X => CtrA, which regulates cell cycle progression and differentiation; 2. Determine how the essential response regulator DivK functions in a signal transduction pathway(s) to control both cell division and motility; 3. Characterize mechanism of action and function of tyrosine kinase DivL in signal transduction; 4. Analyze the roles of histidine kinase DivJ and response regulator PleD in establishing cellular polarity; and 5. Examine the regulation of cell division genes in vivo by the essential signal transduction pathway responsible for phosphorylation and activation of CtrA.

不平等的细胞分裂是产生新细胞类型的核心机制。 在新月柄杆菌分化是重复的，不对称的细胞分裂的直接结果，这种水生细菌提供了一个理想的模型，阐明发展控制的机制。 这些细胞的分化模式和细胞周期进程由双组分信号转导系统密切协调。这些双组分蛋白质可能独特的方面是它们响应内部细胞周期信号而不是环境条件，其中一些对于分裂和细胞活力至关重要。然而，信号转导通路的组织结构尚未完全确定，这些通路如何协调细胞周期中发育事件的精确时间和空间模式也远不清楚。该提案中描述的实验旨在解决以下目标：I。鉴定和表征调控细胞周期进程和分化的基本信号转导途径DivJ => DivK => X => CtrA中的组分; 2.确定基本反应调节因子DivK如何在信号转导通路中起作用以控制细胞分裂和运动; 3.研究酪氨酸激酶DivL在信号转导中的作用机制和功能; 4.分析组氨酸激酶DivJ和反应调节剂PleD在建立细胞极性中的作用;和5.通过负责CtrA磷酸化和激活的基本信号转导途径，检查体内细胞分裂基因的调节。