Laboratory of Molecular Microbiology, School of Biological Sciences, and Institute of Microbiology, Seoul National University, Seoul 151-742, Korea.
Department of Chemistry and Nano Science, Ewha Womans University, Seoul 03760, Republic of Korea.
Nat Commun. 2017 Jun 9;8:15812. doi: 10.1038/ncomms15812.
In most bacteria, zinc depletion is sensed by Zur, whereas the surplus is sensed by different regulators to achieve zinc homeostasis. Here we present evidence that zinc-bound Zur not only represses genes for zinc acquisition but also induces the zitB gene encoding a zinc exporter in Streptomyces coelicolor, a model actinobacteria. Zinc-dependent gene regulation by Zur occurs in two phases. At sub-femtomolar zinc concentrations (phase I), dimeric Zur binds to the Zur-box motif immediately upstream of the zitB promoter, resulting in low zitB expression. At the same time, Zur represses genes for zinc uptake. At micromolar zinc concentrations (phase II), oligomeric Zur binding with footprint expansion upward from the Zur box results in high zitB induction. Our findings reveal a mode of zinc-dependent gene activation that uses a single metalloregulator to control genes for both uptake and export over a wide range of zinc concentrations.
在大多数细菌中，锌耗竭由 Zur 感知，而锌过剩则由不同的调节剂感知，以实现锌稳态。在这里，我们提供的证据表明，锌结合的 Zur 不仅抑制锌摄取基因，还诱导链霉菌中编码锌外排蛋白的 zitB 基因，链霉菌是一种模式放线菌。 Zur 对锌的依赖型基因调控发生在两个阶段。在亚皮摩尔浓度的锌（第一阶段），二聚 Zur 结合到 zitB 启动子上游的 Zur 盒基序，导致 zitB 表达水平低。同时， Zur 抑制锌摄取基因。在微摩尔浓度的锌（第二阶段），寡聚 Zur 结合伴随着足迹扩展到 Zur 盒上方，导致 zitB 高诱导。我们的研究结果揭示了一种锌依赖型基因激活模式，该模式使用单个金属调节剂来控制摄取和外排基因，以应对广泛的锌浓度范围。
