ISP, Université de Tours, Tours, France.
Department of Microbiology and Immunology, The Peter Doherty Institute for Infection and Immunity, University of Melbourne, Melbourne, Australia.
mSphere. 2024 Nov 21;9(11):e0061424. doi: 10.1128/msphere.00614-24. Epub 2024 Oct 31.
Zinc (Zn) is an essential cofactor for numerous bacterial proteins and altering Zn availability is an important component of host innate immunity. During infection, adaptation to both Zn deprivation and excess is critical for pathogenic bacteria development. To understand the adaptive responses to Zn availability of , a pathogen causing invasive infections of neonates, global transcriptional profiling was conducted. Results highlight that in response to Zn limitation, genes belonging to the AdcR regulon, the master regulator of Zn homeostasis in streptococci, were overexpressed. Through a combination of analysis and experimental validation, new AdcR-regulated targets were identified. Among them, we identified a duplicated ribosomal protein, RpsNb, and an ABC transporter, and examined the role of these genes in bacterial growth under Zn-restricted conditions. Our results indicated that, during Zn restriction, both the RpsNb protein and a potential secondary Zn transporter are important for adaptation to Zn deficiency.
is a bacterial human pathobiont causing invasive diseases in neonates. Upon infection, is presented with Zn limitation and excess but the genetic systems that allow bacterial adaptation to these conditions remain largely undefined. A comprehensive analysis of global transcriptional response to Zn availability shows that this pathogen manages Zn limitation mainly through upregulation of the AdcR regulon. We demonstrate that several AdcR-regulated genes are important for bacterial growth during Zn deficiency, including human biological fluids. Taken together, these findings reveal new mechanisms of adaptation under conditions of metal deprivation.
锌（Zn）是许多细菌蛋白的必需辅因子，改变锌的可用性是宿主先天免疫的重要组成部分。在感染过程中，适应锌缺乏和过量是致病菌发展的关键。为了了解导致新生儿侵袭性感染的病原体 对锌可用性的适应性反应，对其进行了全基因组转录谱分析。结果表明，在锌限制下，属于 AdcR 调控子的基因（该调控子是链球菌中锌稳态的主要调节剂）过度表达。通过 分析和实验验证的结合，鉴定了新的 AdcR 调控靶标。其中，我们鉴定了一个重复的核糖体蛋白 RpsNb 和一个 ABC 转运蛋白，并研究了这些基因在锌限制条件下细菌生长中的作用。我们的结果表明，在锌限制下，RpsNb 蛋白和潜在的二级锌转运蛋白对于 适应锌缺乏都很重要。
是一种细菌人共生菌，可引起新生儿侵袭性疾病。感染后， 面临锌限制和过量，但允许细菌适应这些条件的遗传系统在很大程度上仍未确定。对 全球对锌可用性的转录响应的全面分析表明，这种病原体主要通过上调 AdcR 调控子来管理锌限制。我们证明，在锌缺乏时，几个 AdcR 调节的基因对于细菌生长很重要，包括人类生物体液。总之，这些发现揭示了在金属剥夺条件下适应的新机制。
