Department of Chemistry, The University of Michigan, 930 N University Ave, Ann Arbor, MI 48109, USA.
Metallomics. 2013 Apr;5(4):372-83. doi: 10.1039/c3mt20217h.
Intracellular zinc homeostasis is regulated by an extensive network of transporters, ligands and transcription factors. The zinc detoxification functions of three transporters and a periplasmic protein regulated by the BaeSR two-component system were explored in this work by evaluating the effect of single gene knockouts in the BaeSR regulon on the cell growth rate, free zinc, total zinc and total copper after zinc shock. Two exporters, MdtABC and MdtD, and the periplasmic protein, Spy, are involved in zinc detoxification based on the growth defects at high cell density and increases in free (>1000-fold) and total zinc/copper (>2-fold) that were observed in the single knockout strains upon exposure to zinc. These proteins complement the ATP-driven zinc export mediated by ZntA in E. coli to limit zinc toxicity. These results highlight the functions of the BaeSR regulon in metal homeostasis.
细胞内锌稳态由广泛的转运蛋白、配体和转录因子网络调节。本研究通过评估 BaeSR 调控子中单个基因敲除对锌冲击后细胞生长速率、游离锌、总锌和总铜的影响，研究了三种转运蛋白和一种由 BaeSR 双组分系统调节的周质蛋白的锌解毒功能。基于高细胞密度下的生长缺陷以及在锌暴露时观察到的游离（>1000 倍）和总锌/铜（>2 倍）的增加，MdtABC 和 MdtD 两种外排泵以及周质蛋白 Spy 被认为参与了锌解毒。这些蛋白在大肠杆菌中与 ATP 驱动的 ZntA 介导的锌外排作用互补，以限制锌毒性。这些结果突出了 BaeSR 调控子在金属稳态中的作用。
