MOLECULAR MECHANISMS OF THE MERCURY RESISTANCE SYSTEM

耐汞系统的分子机制

• 批准号: 7722015
• 负责人: ROBERT A SCOTT
• 金额: $ 0.19万
• 依托单位: STANFORD UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2008
• 资助国家: 美国
• 起止时间: 2008-03-01 至 2009-02-28
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7722015
• 关键词: Bioremediations; Carrier Proteins; Colloids; Computer Retrieval of Information on Scientific Projects Database; DNA-Directed RNA Polymerase; Drug Metabolic Detoxication; Engineering; Enzymes; Funding; Grant; Heavy Metals; Institution; Mercury; Mercury (II) reductase; Metals; Molecular; Operon; Research; Research Personnel; Resistance; Resources; Roentgen Rays; Role; Source; Specificity; Spectrum Analysis; System; United States National Institutes of Health; Variant; absorption; base; interest; programs

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. We propose to use X-ray absorption spectroscopy to study the molecular mechanisms of heavy metal detoxification by the bacterial mercury resistance system, encoded by the Tn501 mer operon. The mer system employs metal transport proteins, enzymes for transformation and reduction of mercury species to elemental volatile Hg(0), and a paradigmatic metalloregulatory system (based on MerR), all of which demonstrate specificity for Hg. In general, we are interested in elucidating the molecular mechanisms involved and in investigating the potential for engineering this system to handle other heavy metals (Cd, Au, etc.) for bioremediation. This particular program has two major targets: (a) MerR, its interactions with merO/P and/or RNA polymerase, and the role of MerD which appears to be involved in relieving MerR activation; (b) MerA (mercuric reductase) and variants that have now been shown to also catalyze the reduction of Au(III) to Au(I), with eventual disproportionation to form Au(0) colloids.

这个子项目是许多利用 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 我们建议使用X射线吸收光谱研究重金属解毒的分子机制的细菌耐汞系统，编码的Tn 501 mer操纵子。mer系统采用金属转运蛋白、将汞物质转化和还原为元素挥发性Hg（0）的酶以及一个典型的金属调节系统（基于MerR），所有这些都表现出对Hg的特异性。在一般情况下，我们有兴趣在阐明所涉及的分子机制，并在调查工程这一系统处理其他重金属（镉，Au等）的潜力。用于生物修复。该特定程序有两个主要目标：（a）MerR，其与merO/P和/或RNA聚合酶的相互作用，以及MerD的作用，其似乎参与缓解MerR活化;（B）MerA（汞还原酶）和变体，其现在已显示也催化Au（III）还原为Au（I），最终沉淀形成Au（0）胶体。