MOLECULAR MECHANISMS OF THE MERCURY RESISTANCE SYSTEM

耐汞系统的分子机制

• 批准号: 8362122
• 负责人: ROBERT A SCOTT
• 金额: $ 0.27万
• 依托单位: STANFORD UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-03-01 至 2012-02-29
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8362122
• 关键词: Bioremediations; Carrier Proteins; Colloids; DNA-Directed RNA Polymerase; Drug Metabolic Detoxication; Engineering; Enzymes; Funding; Grant; Heavy Metals; Mercury; Mercury (II) reductase; Metals; Molecular; National Center for Research Resources; Operon; Principal Investigator; Radiation; Research; Research Infrastructure; Resistance; Resources; Roentgen Rays; Role; Source; Specificity; Spectrum Analysis; System; United States National Institutes of Health; Variant; absorption; base; cost; interest; programs; structural biology

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. 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.

该子项目是利用资源的众多研究子项目之一 由 NIH/NCRR 资助的中心拨款提供。子项目的主要支持 并且子项目的主要研究者可能是由其他来源提供的， 包括其他 NIH 来源。 子项目可能列出的总成本 代表子项目使用的中心基础设施的估计数量， NCRR 赠款不直接向子项目或子项目工作人员提供资金。 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）和变体现已证明也能催化 Au(III) 还原为 Au(I)，并最终歧化形成 Au(0) 胶体。