MOLECULAR MECHANISMS OF THE MERCURY RESISTANCE SYSTEM

耐汞系统的分子机制

• 批准号: 7954354
• 负责人: ROBERT A SCOTT
• 金额: $ 0.33万
• 依托单位: STANFORD UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-03-01 至 2010-02-28
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7954354
• 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; structural biology; synchrotron radiation

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.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目及 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 我们建议使用 X 射线吸收光谱来研究由 Tn501 mer 操纵子编码的细菌耐汞系统重金属解毒的分子机制。 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，以及典型的金属调节系统（基于 MerR），所有这些都证明了对 Hg 的特异性。总的来说，我们感兴趣的是阐明所涉及的分子机制，并研究设计该系统以处理其他重金属（Cd、Au 等）进行生物修复的潜力。这个特定的程序有两个主要目标：(a) MerR，它与 merO/P 和/或 RNA 聚合酶的相互作用，以及 MerD 的作用，它似乎参与缓解 MerR 的激活； (b) MerA（汞还原酶）和变体现已被证明也能催化 Au(III) 还原为 Au(I)，并最终歧化形成 Au(0) 胶体。