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Rsp 以 - 非依赖的方式促进 在 中的毒力因子的转录。

Rsp promotes the transcription of virulence factors in an -independent manner in .

机构信息

Department of Oncology, The First Affiliated Hospital, University of Science and Technology of China, Hefei, People's Republic of China.

出版信息

Emerg Microbes Infect. 2020 Dec;9(1):796-812. doi: 10.1080/22221751.2020.1752116.

DOI:10.1080/22221751.2020.1752116
PMID:32248753
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7241556/
Abstract

is a major human pathogen that causes a great diversity of community- and hospital-acquired infections. Rsp, a member of AraC/XylS family of transcriptional regulators (AFTRs), has been reported to play an important role in the regulation of virulence determinants in via an -dependent pathway. Here we demonstrated that Rsp could bind to the promoter to positively regulate its own expression. We then constructed an isogenic deletion strain and compared the haemolysis in the wild-type and mutant strains. Our results indicated that the mutant strain displayed decreased haemolytic activity, which was correlated with a dramatic decrease in the expression of and . Furthermore, we analysed the regulatory effects of Rsp in the mutant strain and found that they are -independent. Electrophoretic mobility shift assay indicated that Rsp can directly bind to the promoter regions of and . The mouse model of subcutaneous abscess showed that the mutant strain displayed a significant defect in virulence compared to the wild-type strain. These findings reveal that Rsp positively regulates the virulence of by promoting the expression of and through direct binding to their promoter regions.

摘要

是一种主要的人类病原体,可引起多种社区获得性和医院获得性感染。Rsp 是 AraC/XylS 家族转录调节因子(AFTRs)的成员,据报道,它通过依赖途径在调节毒力决定因素方面发挥重要作用。在这里,我们证明 Rsp 可以结合到 启动子上,从而正向调节自身表达。然后,我们构建了一个同源缺失菌株,并比较了野生型和 突变菌株的溶血情况。我们的结果表明,突变菌株表现出降低的溶血活性,这与 和 的表达显著下降相关。此外,我们分析了 Rsp 在 突变菌株中的调节作用,发现它们是依赖的。电泳迁移率变动分析表明,Rsp 可以直接结合到 和 的启动子区域。皮下脓肿的小鼠模型表明,与野生型菌株相比,突变菌株的毒力显著降低。这些发现表明,Rsp 通过直接结合到它们的启动子区域,促进 和 的表达,从而正向调节 的毒力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d250/7241556/e9a927532da7/TEMI_A_1752116_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d250/7241556/8926fe3c036c/TEMI_A_1752116_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d250/7241556/ef95c8037150/TEMI_A_1752116_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d250/7241556/fadfdfa193fd/TEMI_A_1752116_F0003_OB.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d250/7241556/924a3a152e27/TEMI_A_1752116_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d250/7241556/0158844f9afc/TEMI_A_1752116_F0005_OB.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d250/7241556/c1b021f315d2/TEMI_A_1752116_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d250/7241556/e9a927532da7/TEMI_A_1752116_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d250/7241556/8926fe3c036c/TEMI_A_1752116_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d250/7241556/ef95c8037150/TEMI_A_1752116_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d250/7241556/fadfdfa193fd/TEMI_A_1752116_F0003_OB.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d250/7241556/924a3a152e27/TEMI_A_1752116_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d250/7241556/0158844f9afc/TEMI_A_1752116_F0005_OB.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d250/7241556/c1b021f315d2/TEMI_A_1752116_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d250/7241556/e9a927532da7/TEMI_A_1752116_F0007_OC.jpg

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