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SmpB 下调气单胞菌质子动力势以产生耐氨基糖苷类药物的持续生存能力。

SmpB down-regulates proton-motive force for the persister tolerance to aminoglycosides in Aeromonas veronii.

机构信息

Hainan Key Laboratory for Sustainable Utilization of Tropical Bioresources, Institute of Tropical Agriculture and Forestry, Hainan University, 570228, Haikou, China.

出版信息

Biochem Biophys Res Commun. 2018 Dec 9;507(1-4):407-413. doi: 10.1016/j.bbrc.2018.11.052. Epub 2018 Nov 16.

Abstract

Bacterial persisters comprise a small fraction of phenotypically heterogeneous variants with transient capability for survival when exposed to high concentrations of antibiotic. In aquatic pathogenic bacteria Aeromonas veronii, Small Protein B (SmpB), the core factor of trans-translation system, was identified as a new persistence-related gene. The SmpB deletion exhibited a higher susceptibility and lower persister cell formation under aminoglycosides antibiotics pressure compared with wild type. The transcriptional and translational activities of smpB gene were significantly enhanced by the gentamicin challenge in exponential phase, but not changed in stationary phase. The transcriptomic analysis revealed that the smpB deletion stimulated the production of proton-motive force (PMF). The cell survival induced by carbonyl cyanide m-chlorophenyl hydrazone (CCCP) further verified that SmpB variation affected the quantities of PMF. Taken together, these results uncovered a novel mechanism of persister formation mediated by SmpB under aminoglycosides treatments.

摘要

细菌持久体是表型异质的一小部分,当暴露于高浓度抗生素时,具有短暂的生存能力。在水生病原菌嗜水气单胞菌中,Small Protein B(SmpB)作为转译系统的核心因子,被鉴定为一个新的与持续生存相关的基因。与野生型相比,SmpB 缺失在氨基糖苷类抗生素压力下表现出更高的敏感性和更低的持久细胞形成。在指数生长期,庆大霉素的挑战显著增强了 smpB 基因的转录和翻译活性,但在静止期没有变化。转录组分析显示,smpB 缺失刺激质子动力势(PMF)的产生。细胞的生存能力诱导由羰基氰化物 m-氯代苯腙(CCCP)进一步验证了 SmpB 变异影响 PMF 的数量。总的来说,这些结果揭示了一种新的由 SmpB 介导的氨基糖苷类药物处理下持久体形成的机制。

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