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群体感应和QsvR严格控制着编码一种活性核糖核酸酶II型蛋白的基因在……中的转录。 (注:原文中“encoding an active RNase II-type protein in.”表述不完整,推测可能是“encoding an active RNase II-type protein in [某个具体位置或生物体内]” ,以上译文根据推测进行了补充以使句子相对完整通顺,若有更准确原文可进一步完善。)

Quorum sensing and QsvR tightly control the transcription of encoding an active RNase II-type protein in .

作者信息

Zhang Yiquan, Xue Xingfan, Sun Fengjun, Li Xue, Zhang Miaomiao, Wu Qimin, Zhang Tingting, Luo Xi, Lu Renfei

机构信息

Department of Clinical Laboratory, Affiliated Nantong Hospital 3 of Nantong University, Nantong, Jiangsu, China.

School of Medicine, Jiangsu University, Zhenjiang, Jiangsu, China.

出版信息

Front Microbiol. 2023 Jan 19;14:1123524. doi: 10.3389/fmicb.2023.1123524. eCollection 2023.

Abstract

Vibrio parahaemolyticus, a Gram-negative, halophilic bacterium, is a leading cause of acute gastroenteritis in humans. AphA and OpaR are the master quorum sensing (QS) regulators operating at low cell density (LCD) and high cell density (HCD), respectively. QsvR is an AraC-type protein that integrates into the QS system to control gene expression by directly controlling the transcription of and . However, the regulation of QsvR itself remains unclear to date. In this study, we show that and are transcribed as an operon, -. AphA indirectly activates the transcription of at LCD, whereas OpaR and QsvR directly repress transcription at HCD, leading to the highest expression levels of occurs at LCD. Moreover, VPA0607 acts as an active RNase II-type protein in and feedback inhibits the expression of QsvR at the post-transcriptional level. Taken together, this work deepens our understanding of the regulation of QsvR and enriches the integration mechanisms of QsvR with the QS system in .

摘要

副溶血性弧菌是一种革兰氏阴性嗜盐菌,是人类急性肠胃炎的主要病因。AphA和OpaR分别是在低细胞密度(LCD)和高细胞密度(HCD)下发挥作用的主要群体感应(QS)调节因子。QsvR是一种AraC型蛋白,它整合到QS系统中,通过直接控制[具体基因1]和[具体基因2]的转录来控制基因表达。然而,迄今为止,QsvR自身的调控机制仍不清楚。在本研究中,我们发现[具体基因1]和[具体基因2]作为一个操纵子进行转录,即[操纵子名称]。在LCD条件下,AphA间接激活[具体基因1]的转录,而在HCD条件下,OpaR和QsvR直接抑制[具体基因1]的转录,导致[具体基因1]在LCD时表达水平最高。此外,VPA0607在[具体基因1]中作为一种活性核糖核酸酶II型蛋白发挥作用,并在转录后水平反馈抑制QsvR的表达。综上所述,这项工作加深了我们对QsvR调控的理解,并丰富了QsvR在[具体细菌名称]中与QS系统的整合机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b5a/9894610/c1287ace1868/fmicb-14-1123524-g001.jpg

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