Institute for Cell and Molecular Biosciences, Newcastle University, Newcastle upon Tyne, NE24HH, UK.
Metallomics. 2019 Jan 23;11(1):50-63. doi: 10.1039/c8mt00218e.
In bacteria, copper (Cu) is often recognised for its potential toxicity and its antibacterial activity is now considered a key component of the mammalian innate immune system. Cu ions bound in weak sites can catalyse harmful redox reactions while Cu ions in strong but adventitious sites can disrupt protein or enzyme function. For these reasons, the outward transport of Cu from bacteria has received significant attention. Yet, Cu is also a bacterial nutrient, required as a cofactor by enzymes that catalyse electron transfer processes, for instance in aerobic and anaerobic respiration. To date, the inward flow of this metal ion as a nutrient and its insertion into target cuproenzymes remain poorly defined. Here we revisit the available evidence related to bacterial nutrient Cu trafficking and identify gaps in knowledge. Particularly intriguing is the evidence that bacterial cuproenzymes do not always require auxiliary metallochaperones to insert nutrient Cu into their active sites. This review outlines our effort to consolidate the available experimental data using an established energy-driven model for metalation.
在细菌中，铜（Cu）通常因其潜在毒性而受到关注，其抗菌活性现在被认为是哺乳动物先天免疫系统的关键组成部分。结合在弱配位位置的 Cu 离子可以催化有害的氧化还原反应，而结合在强配位但偶然位置的 Cu 离子可以破坏蛋白质或酶的功能。出于这些原因，细菌中 Cu 的外向转运受到了广泛关注。然而，Cu 也是一种细菌营养素，作为催化电子转移过程的酶的辅助因子，例如在需氧和厌氧呼吸中。迄今为止，这种金属离子作为营养素的内流及其插入靶标铜酶的过程仍未得到很好的定义。在这里，我们重新审视了与细菌营养 Cu 转运相关的现有证据，并确定了知识空白。特别有趣的是，有证据表明，细菌铜酶并不总是需要辅助金属伴侣蛋白将营养 Cu 插入其活性部位。本综述概述了我们使用已建立的能量驱动的金属化模型来整合现有实验数据的努力。
