Transition metals from manganese to zinc function as catalytic and structural cofactors for an amazing diversity of proteins and enzymes, and thus are essential for all forms of life. During infection, inflammatory host proteins limit the accessibility of multiple transition metals to invading pathogens in a process termed nutritional immunity. In order to respond to host-mediated metal starvation, bacteria employ both protein and RNA-based mechanisms to sense prevailing transition metal concentrations that collectively regulate systems-level strategies to maintain cellular metallostasis. In this review, we discuss a number of recent advances in our understanding of how bacteria orchestrate the adaptive response to host-mediated multi-metal restriction, highlighting crosstalk among these regulatory systems.

中文翻译：

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微生物病原体中金属稳态系统中的多金属养分限制和串扰。

从锰到锌的过渡金属可作为催化和结构辅助因子，使蛋白质和酶具有惊人的多样性，因此对于所有形式的生命都是必不可少的。在感染过程中，炎症性宿主蛋白在称为营养免疫的过程中限制了多种过渡金属入侵病原体的能力。为了对宿主介导的金属饥饿做出反应，细菌利用蛋白质和基于RNA的机制来检测主要的过渡金属浓度，这些浓度共同调节系统水平的策略来维持细胞的金属稳态。在这篇综述中，我们讨论了细菌在如何协调对宿主介导的多金属限制的适应性反应方面的最新进展，突出了这些调节系统之间的串扰。