Phage transcription activator RinA regulates Staphylococcus aureus virulence by governing sarA expression.

Phage transcription activator RinA regulates Staphylococcus aureus virulence by governing sarA expression.
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噬菌体转录激活剂 RinA 通过控制 sarA 表达来调节金黄色葡萄球菌毒力

DOI:
10.1007/s13258-022-01352-8
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发表时间:
2023-02
期刊:
影响因子:
2.1
通讯作者:
Li, Yujie
Li, Yujie
中科院分区:
生物学4区
文献类型:
--
作者:
Jiang, Ming;Li, Yilin;Sun, Baolin;Xu, Shiwen;Pan, Ting;Li, Yujie

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金黄色葡萄球菌是一种主要的人类病原体,可导致各种社区和医院获得性感染。RinA是S.金黄色葡萄球菌噬菌体φ 11参与噬菌体包装和毒力基因转移。然而,关于RinA在毒力调控中的分子机制知之甚少。本研究旨在探索RinA基因在调节沙门氏菌毒力方面的新作用,为沙门氏菌的治疗提供新的药物靶点。金黄色葡萄球菌感染。RinA在S.采用生长曲线、实时荧光定量PCR(RT-qPCR)、亚细胞定位、电泳迁移率变动分析(EMSA)、大蜡螟幼虫感染模型和小鼠皮下脓肿模型等方法,对金黄色葡萄球菌的生长情况进行分析。在这项研究中,我们证明了RinA是一种均匀分布在细胞质中的蛋白。aureus,其缺失可导致生长缺陷。RT-qPCR和EMSA证实rinA通过直接与sarA启动子结合来负调控sarA的表达,反之亦然。大蜡螟幼虫感染模型和小鼠皮下脓肿模型显示rinA突变株具有明显的毒力缺陷。当sarA基因被敲除后,金黄色葡萄球菌的毒力与rinA基因被敲除与否无明显差异。我们的发现表明噬菌体转录激活因子RinA调节S.金黄色葡萄球菌的毒力通过控制sarA的表达。
Staphylococcus aureus is a major human pathogen, that can lead to various community- and hospital-acquired infections. RinA is a transcription activator of S. aureus phage φ 11 involved in phage packaging and virulence gene transfer. However, little is known about the molecular mechanism of RinA in the regulation of virulence. We aimed to explore a novel contribution of RinA in the regulation of virulence and provide a new drug target in the treatment of S. aureus infections. The specific functions of RinA in S. aureus were analyzed by the methods of growth curve, real-time quantitative PCR (RT-qPCR), subcellular localization, electrophoretic mobility shift assay (EMSA), infection model of Galleria mellonella larvae and the mouse subcutaneous abscess model. In this study, we demonstrated that RinA is a protein evenly distributed in the cytoplasm of S. aureus, and its deletion could cause the growth defects. RT-qPCR and EMSA determined that rinA could negatively regulate the expression of sarA by directly binding to its promoter, and vice versa. The Galleria mellonella larvae infection and mouse subcutaneous abscess models revealed that the rinA mutant strain exhibited obvious virulence defects. When sarA is knocked out, the virulence of S.aureus had no significantly changes whether rinA is knocked out or not. Our fndings demonstrated that phage transcription activator RinA regulates S. aureus virulence by governing sarA expression.
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