Mechanismus und Kontrolle der Zink-Aufnahme im Modellorganismus Cupriavidus metallidurans CH34

复杂的细胞生物化学需要金属作为辅助因子。大约40%的酶具有金属辅因子。如何将正确的金属分配给正确的蛋白质是一个有趣的问题，这对于具有相似离子直径和体积电荷比的二价金属阳离子尤其复杂，并且相互竞争酶中的金属结合位点。β-蛋白杆菌Cupriavidus metallidurans菌株CH 34能够在各种不利条件下保持其金属稳态，并成为研究这一过程的原核模式生物。其大多数的流出系统，需要从细胞中去除多余的金属，是已知的。在提案的第一部分，确定了许多锌的吸收系统。我们希望继续追求以下目标：（i）应完成菌株CH 34中锌输入者的库存，（ii）应将来自金属抗性菌株CH 34的输入者的金属转运能力与来自E.大肠杆菌，和（iii）运输系统的基因表达的调节剂进行鉴定。第四个目标源于一个意想不到的观察结果，即锌饥饿会导致外排蛋白复合物CzcCBA的主要成分CzcA消失。我们想确定这一进程背后的机制。

Sophisticated cellular biochemistry needs metals as cofactors. About 40% of all enzymes have metal cofactors. It is an interesting question how the correct metal is allocated to the right protein, which is especially complicated for divalent metal cations that have a similar ionic diameter and volume-tocharge ratios, and compete with each other for the metal binding sites in enzymes. The β−proteobacterium Cupriavidus metallidurans strain CH34 is able to keep its metal homeostasis under a variety of adverse conditions and became a prokaryotic model organism to study such a process. Most of its’ efflux systems, required to remove surplus metals from the cells, are known. In the first part of the proposal, many uptake systems for zinc were identified. We would like to continue by pursuing the following goals: (i) the inventory of zinc importers in strain CH34 shall be completed, (ii) the metal transport capacities of the importers from the metal-resistant strain CH34 shall be compared to those from E. coli, and (iii) the regulators of gene expression of the transport systems are to be identified. Goal number four stems from the unexpected observation that zinc starvation leads to disappearance of CzcA, the major component of the efflux protein complex CzcCBA. We would like to identify the mechanism behind this process.