Adaptation to zinc restriction in Streptococcus agalactiae: role of the ribosomal protein and zinc-importers regulated by AdcR.

IF 3.7 2区 生物学 Q2 MICROBIOLOGY
mSphere Pub Date : 2024-10-31 DOI:10.1128/msphere.00614-24
M Melet, S Blanchet, P Barbarin, E A Maunders, S L Neville, V Rong, L Mereghetti, C A McDevitt, A Hiron
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Abstract

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 Streptococcus agalactiae, 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 in silico 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 S. agalactiae adaptation to Zn deficiency.

Importance: Streptococcus agalactiae is a bacterial human pathobiont causing invasive diseases in neonates. Upon infection, S. agalactiae 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 S. agalactiae 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 S. agalactiae adaptation under conditions of metal deprivation.

无乳链球菌对锌限制的适应:受 AdcR 调节的核糖体蛋白和锌输入器的作用。
锌(Zn)是许多细菌蛋白质的重要辅助因子,改变锌的供应是宿主先天免疫的重要组成部分。在感染过程中,对锌缺乏和过剩的适应对病原菌的发展至关重要。为了了解引起新生儿侵袭性感染的病原体--无乳链球菌对锌供应的适应性反应,我们进行了全局转录谱分析。结果表明,为了应对锌限制,属于链球菌锌平衡主调节器 AdcR 调节子的基因被过度表达。通过硅学分析和实验验证,我们发现了新的 AdcR 调控靶标。其中,我们发现了一个重复的核糖体蛋白 RpsNb 和一个 ABC 转运体,并研究了这些基因在锌限制条件下细菌生长中的作用。我们的研究结果表明,在锌限制条件下,RpsNb 蛋白和一个潜在的次级锌转运体对于无乳链球菌适应锌缺乏非常重要:重要意义:无乳链球菌是一种人类致病细菌,可导致新生儿侵袭性疾病。感染后,S. agalactiae 会出现锌限制和过量,但使细菌适应这些条件的遗传系统在很大程度上仍未确定。对 S. agalactiae 对锌可用性的全局转录反应的全面分析表明,这种病原体主要通过 AdcR 调节子的上调来管理锌限制。我们证明,在锌缺乏期间,包括在人体生物液体中,几个由 AdcR 调节的基因对细菌的生长非常重要。总之,这些发现揭示了 S. agalactiae 在金属匮乏条件下的新适应机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
mSphere
mSphere Immunology and Microbiology-Microbiology
CiteScore
8.50
自引率
2.10%
发文量
192
审稿时长
11 weeks
期刊介绍: mSphere™ is a multi-disciplinary open-access journal that will focus on rapid publication of fundamental contributions to our understanding of microbiology. Its scope will reflect the immense range of fields within the microbial sciences, creating new opportunities for researchers to share findings that are transforming our understanding of human health and disease, ecosystems, neuroscience, agriculture, energy production, climate change, evolution, biogeochemical cycling, and food and drug production. Submissions will be encouraged of all high-quality work that makes fundamental contributions to our understanding of microbiology. mSphere™ will provide streamlined decisions, while carrying on ASM''s tradition for rigorous peer review.
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