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Antimicrob Agents Chemother. 2020 May 21;64(6). doi: 10.1128/AAC.02252-19.
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Mutations in MetG (methionyl-tRNA synthetase) and TrmD [tRNA (guanine-N1)-methyltransferase] conferring meropenem tolerance in Burkholderia thailandensis.在鲍曼不动杆菌中，MetG（甲硫氨酰-tRNA 合成酶）和 TrmD [tRNA（鸟嘌呤-N1）-甲基转移酶]的突变赋予了美罗培南耐药性。
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Mechanisms of bacterial persistence during stress and antibiotic exposure.细菌在应激和抗生素暴露期间的持续存在机制。
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Comparative Protein Structure Modeling Using MODELLER.使用MODELLER进行比较蛋白质结构建模。
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Distinguishing between resistance, tolerance and persistence to antibiotic treatment.区分抗生素治疗的耐药性、耐受性和持久性。
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Recent functional insights into the role of (p)ppGpp in bacterial physiology.近期对（p）ppGpp在细菌生理学中作用的功能见解。
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ArgS 精氨酸-tRNA 合成酶的突变赋予产生超广谱β-内酰胺酶的鲍曼不动杆菌额外的抗生素耐受保护。

Mutations in ArgS Arginine-tRNA Synthetase Confer Additional Antibiotic Tolerance Protection to Extended-Spectrum-β-Lactamase-Producing Burkholderia thailandensis.

机构信息

Division of Biosystems & Biomedical Sciences, College of Health Sciences, Korea University, Seoul, South Korea.

School of Systems Biomedical Science and Research Center for Integrative Basic Science, Soongsil University, Seoul, South Korea.

出版信息

Antimicrob Agents Chemother. 2020 May 21;64(6). doi: 10.1128/AAC.02252-19.

DOI:10.1128/AAC.02252-19
PMID:32205346
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7269490/
Abstract

Highly conserved PenI-type class A β-lactamase in pathogenic members of species can evolve to extended-spectrum β-lactamase (ESBL), which exhibits hydrolytic activity toward third-generation cephalosporins, while losing its activity toward the original penicillin substrates. We describe three single-amino-acid-substitution mutations in the ArgS arginine-tRNA synthetase that confer extra antibiotic tolerance protection to ESBL-producing This pathway can be exploited to evade antibiotic tolerance induction in developing therapeutic measures against species, targeting their essential aminoacyl-tRNA synthetases.

摘要

在种的致病性成员中高度保守的 PenI 型 A 类β-内酰胺酶可以进化为扩展谱β-内酰胺酶（ESBL），它对第三代头孢菌素具有水解活性，而对原始青霉素底物失去活性。我们描述了 ArgS 精氨酸-tRNA 合成酶中的三个单氨基酸取代突变，赋予产生 ESBL 的 额外的抗生素耐受保护。这条途径可以被利用来逃避针对种的治疗措施中抗生素耐受诱导，针对它们的必需氨酰-tRNA 合成酶。