MOLECULAR MECHANISMS OF THE MERCURY RESISTANCE SYSTEM

耐汞系统的分子机制

• 批准号: 8170037
• 负责人: ROBERT A SCOTT
• 金额: $ 0.92万
• 依托单位: STANFORD UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-05-01 至 2011-02-28
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8170037
• 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.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这不一定是调查员的机构。 我们建议使用X射线吸收光谱研究通过TN501 MER操纵子编码的细菌汞耐药系统的重金属排毒的分子机制。 MER系统采用金属转运蛋白，酶，用于转化和还原汞物种对元素挥发性Hg（0），以及范式的金属调节系统（基于MER），所有这些都证明了Hg的特异性。通常，我们有兴趣阐明所涉及的分子机制，并研究该系统处理其他重金属（CD，AU等）进行生物修复的潜力。该特定程序具有两个主要目标：（a）MERR，其与Mero/P和/或RNA聚合酶的相互作用，以及Merd的作用，似乎参与了缓解MERR激活的作用； （b）梅拉（汞还原酶）和现已证明的变体还可以催化Au（iii）为Au（i）的还原，最终形成Au（0）胶体的违约。