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Virulence role and regulation of Shigella suf genes

志贺氏菌 suf 基因的毒力作用和调控

基本信息

批准号：
6806174
负责人：
Laura Jane Runyen-Janecky
金额：
$ 18.06万
依托单位：
UNIVERSITY OF RICHMOND
依托单位国家：
美国
项目类别：
财政年份：
2004
资助国家：
美国
起止时间：
2004-09-01 至 2007-08-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/6806174
关键词：
Shigella bacillary dysentery bacteria infection mechanism bacterial genetics biological signal transduction cytoplasm environmental adaptation eukaryote gene expression genetic regulation host organism interaction microorganism culture microorganism growth operon oxidative stress polymerase chain reaction tissue /cell culture virulence

项目摘要

DESCRIPTION (provided by applicant): Shigella species are the causative agents of shigellosis, which results in approximately 600,000 deaths per year. Transmission usually occurs via contaminated food or water, or through person-to-person contact. Basic research aimed at characterizing the genes that Shigella uses to adapt to the human host will be useful in designing effective therapies and vaccines. Furthermore, since Shigella virulence depends largely on its ability to live inside human colon cells, a complete understanding of the mechanisms that Shigella uses to survive and multiply in the intracellular environment will provide better insight into the lifestyles of intracellular pathogens. The long-term research goal is to elucidate the metabolic and physiological processes that Shigella employs to survive and multiply the eukaryotic cell. An approach to accomplishing this goal was to characterize Shigella genes that are induced when Shigella is in the eukaryotic cytoplasm. One particular locus (suf) that is induced in response to the eukaryotic intracellular environment is homologous to a locus that enhances virulence and oxidative stress survival in the plant pathogen Erwinia chrysanthemi. Three of the six suf genes are predicted to mediate iron-sulfur cluster synthesis. This led to the hypothesis that the Shigella suf genes mediate adaptation to the eukaryotic cytoplasm, possibly through enhanced iron-sulfur cluster metabolism and/or oxidative stress survival. The goal of this project is to characterize the S. flexneri suf locus, specifically the regulation of the suf genes and the contribution of the Suf system to Shigella adaptation to the eukaryotic cytoplasm. Specific aim 1 is to identify the elements that regulate suf expression in vitro and in vivo. Because the sufA gene is induced when Shigella is in the eukaryotic cytoplasm, specific aim 2 is to assess whether the Shigella Suf proteins are required for survival and/or multiplication in the eukaryotic intracellular environment. Characterization of the Shigella suf genes will provide information about the importance of the suf genes when Shigella is in the intracellular environment and will provide a better understanding of how Shigella senses and adapts to the eukaryotic intracellular environment.

描述（由申请人提供）：志贺氏菌属是志贺氏菌病的病原体，每年导致约600，000人死亡。传播通常通过受污染的食物或水，或通过人与人之间的接触发生。旨在表征志贺氏菌用于适应人类宿主的基因的基础研究将有助于设计有效的疗法和疫苗。此外，由于志贺氏菌的毒力在很大程度上取决于其在人类结肠细胞内生存的能力，因此完全了解志贺氏菌在细胞内环境中生存和繁殖的机制将更好地了解细胞内病原体的生活方式。长期的研究目标是阐明志贺菌在真核细胞中生存和繁殖的代谢和生理过程。实现这一目标的一种方法是表征志贺菌在真核细胞质中时诱导的志贺菌基因。响应于真核细胞内环境而诱导的一个特定基因座（suf）与增强植物病原体欧文氏菌（Erwiniachilli）中的毒力和氧化应激存活的基因座同源。预测六个suf基因中的三个介导铁硫簇的合成。这导致了这样的假设，即志贺氏菌suf基因介导适应真核细胞质，可能通过增强铁硫簇代谢和/或氧化应激生存。本项目的目标是表征S。本研究对福氏痢疾杆菌suf基因座的功能进行了综述，特别是对suf基因的调控以及Suf系统在志贺菌适应真核细胞质中的作用进行了研究。具体目标1是确定在体外和体内调控suf表达的元件。因为当志贺氏菌在真核细胞质中时sufA基因被诱导，所以具体目标2是评估志贺氏菌Suf蛋白是否是真核细胞内环境中存活和/或增殖所需的。志贺氏菌suf基因的表征将提供有关志贺氏菌在细胞内环境中时suf基因的重要性的信息，并将更好地理解志贺氏菌如何感知和适应真核细胞内环境。