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应激反应和发病过程中细菌锰稳态的调节及其利用

Regulation of Bacterial Manganese Homeostasis and Usage During Stress Responses and Pathogenesis.

作者信息

Martin Julia E, Waters Lauren S

机构信息

Department of Biological Sciences, Idaho State University, Pocatello, ID, United States.

Department of Chemistry, University of Wisconsin Oshkosh, Oshkosh, WI, United States.

出版信息

Front Mol Biosci. 2022 Jul 15;9:945724. doi: 10.3389/fmolb.2022.945724. eCollection 2022.

DOI:10.3389/fmolb.2022.945724
PMID:35911964
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9334652/
Abstract

Manganese (Mn) plays a multifaceted role in the survival of pathogenic and symbiotic bacteria in eukaryotic hosts, and it is also important for free-living bacteria to grow in stressful environments. Previous research has uncovered components of the bacterial Mn homeostasis systems that control intracellular Mn levels, many of which are important for virulence. Multiple studies have also identified proteins that use Mn once it is inside the cell, including Mn-specific enzymes and enzymes transiently loaded with Mn for protection during oxidative stress. Emerging evidence continues to reveal proteins involved in maintaining Mn homeostasis, as well as enzymes that can bind Mn. For some of these enzymes, Mn serves as an essential cofactor. For other enzymes, mismetallation with Mn can lead to inactivation or poor activity. Some enzymes may even potentially be regulated by differential metallation with Mn or zinc (Zn). This review focuses on new developments in regulatory mechanisms that affect Mn homeostasis and usage, additional players in Mn import that increase bacterial survival during pathogenesis, and the interplay between Mn and other metals during Mn-responsive physiological processes. Lastly, we highlight lessons learned from fundamental research that are now being applied to bacterial interactions within larger microbial communities or eukaryotic hosts.

摘要

锰(Mn)在真核宿主中致病细菌和共生细菌的存活中发挥着多方面作用,对于自由生活的细菌在应激环境中生长也很重要。先前的研究揭示了控制细胞内锰水平的细菌锰稳态系统的组成部分,其中许多对毒力很重要。多项研究还鉴定了细胞内利用锰的蛋白质,包括锰特异性酶和在氧化应激期间短暂装载锰以进行保护的酶。新出现的证据不断揭示参与维持锰稳态的蛋白质以及能够结合锰的酶。对于其中一些酶,锰作为必需的辅因子。对于其他酶,与锰的错配金属化可导致失活或活性不佳。一些酶甚至可能受锰或锌(Zn)的差异金属化调节。本综述重点关注影响锰稳态和利用的调节机制的新进展、在发病过程中增加细菌存活的锰导入的其他参与者,以及锰响应生理过程中锰与其他金属之间的相互作用。最后,我们强调从基础研究中学到的经验教训,这些经验教训现在正应用于更大的微生物群落或真核宿主内的细菌相互作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/370e/9334652/2c7769cd303d/fmolb-09-945724-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/370e/9334652/130125b249ba/fmolb-09-945724-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/370e/9334652/2c7769cd303d/fmolb-09-945724-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/370e/9334652/130125b249ba/fmolb-09-945724-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/370e/9334652/2c7769cd303d/fmolb-09-945724-g002.jpg

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