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本文引用的文献

1
Flagellin phase-dependent swimming on epithelial cell surfaces contributes to productive Salmonella gut colonisation.鞭毛蛋白在上皮细胞表面的相依赖游动有助于沙门氏菌在肠道的有效定殖。
Cell Microbiol. 2017 Aug;19(8). doi: 10.1111/cmi.12739. Epub 2017 Apr 18.
2
tRNA -mediated downregulation of elongation factor P is required for mgtCBR expression during Salmonella infection.在沙门氏菌感染期间,mgtCBR表达需要tRNA介导的延伸因子P的下调。
Mol Microbiol. 2016 Oct;102(2):221-232. doi: 10.1111/mmi.13454. Epub 2016 Aug 2.
3
Small RNAs in Bacterial Virulence and Communication.细菌毒力和通讯中的小 RNA 。
Microbiol Spectr. 2016 Jun;4(3). doi: 10.1128/microbiolspec.VMBF-0028-2015.
4
An RNA motif advances transcription by preventing Rho-dependent termination.一种RNA基序通过阻止Rho依赖性终止来促进转录。
Proc Natl Acad Sci U S A. 2015 Dec 15;112(50):E6835-43. doi: 10.1073/pnas.1515383112. Epub 2015 Nov 16.
5
Regulation and function of the Salmonella MgtC virulence protein.鼠伤寒沙门氏菌毒力蛋白MgtC的调控与功能
J Microbiol. 2015 Oct;53(10):667-72. doi: 10.1007/s12275-015-5283-1. Epub 2015 Aug 1.
6
Salmonella promotes virulence by repressing cellulose production.沙门氏菌通过抑制纤维素的产生来促进毒力。
Proc Natl Acad Sci U S A. 2015 Apr 21;112(16):5183-8. doi: 10.1073/pnas.1500989112. Epub 2015 Apr 6.
7
Bacterial flagella: twist and stick, or dodge across the kingdoms.细菌鞭毛:扭转并附着,还是在不同界间穿梭躲避。
PLoS Pathog. 2015 Jan 15;11(1):e1004483. doi: 10.1371/journal.ppat.1004483. eCollection 2015 Jan.
8
Trimmomatic: a flexible trimmer for Illumina sequence data.Trimmomatic:一款适用于 Illumina 测序数据的灵活修剪工具。
Bioinformatics. 2014 Aug 1;30(15):2114-20. doi: 10.1093/bioinformatics/btu170. Epub 2014 Apr 1.
9
Control of a Salmonella virulence operon by proline-charged tRNA(Pro).脯氨酸荷电 tRNA(Pro)对沙门氏菌毒力操纵子的控制。
Proc Natl Acad Sci U S A. 2014 Feb 25;111(8):3140-5. doi: 10.1073/pnas.1316209111. Epub 2014 Feb 10.
10
featureCounts: an efficient general purpose program for assigning sequence reads to genomic features.featureCounts:一个用于将序列读取分配给基因组特征的高效通用程序。
Bioinformatics. 2014 Apr 1;30(7):923-30. doi: 10.1093/bioinformatics/btt656. Epub 2013 Nov 13.

来自毒力基因的 A 类作用先导 RNA。

A -acting leader RNA from a virulence gene.

机构信息

Department of Genetic Engineering, Graduate School of Biotechnology, College of Life Sciences, Kyung Hee University, Yongin 17104, South Korea.

Unit of Antarctic K-Route Expedition, Korea Polar Research Institute, Incheon 21990, South Korea.

出版信息

Proc Natl Acad Sci U S A. 2017 Sep 19;114(38):10232-10237. doi: 10.1073/pnas.1705437114. Epub 2017 Sep 5.

DOI:10.1073/pnas.1705437114
PMID:28874555
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5617274/
Abstract

Bacteria use flagella to move toward nutrients, find its host, or retract from toxic substances. Because bacterial flagellum is one of the ligands that activate the host innate immune system, its synthesis should be tightly regulated during host infection, which is largely unknown. Here, we report that a bacterial leader mRNA from the virulence operon in the intracellular pathogen serovar Typhimurium binds to the coding region of mRNAs in the operon encoding the FljB phase 2 flagellin, a main component of bacterial flagella and the FljA repressor for the FliC phase 1 flagellin, and degrades mRNAs in an RNase E-dependent fashion during infection. A nucleotide substitution of the flagellin gene that prevents the leader RNA-mediated down-regulation increases the -encoded flagellin synthesis, leading to a hypermotile phenotype inside macrophages. Moreover, the nucleotide substitution renders hypervirulent, indicating that FljB-based motility must be compromised in the phagosomal compartment where resides. This suggests that this pathogen promotes pathogenicity by producing a virulence protein and limits locomotion by a -acting leader RNA from the same virulence gene during infection.

摘要

细菌利用鞭毛向营养物质移动,寻找宿主,或从有毒物质中缩回。由于细菌鞭毛是激活宿主先天免疫系统的配体之一,因此在宿主感染期间,其合成应该受到严格调控,但这在很大程度上是未知的。在这里,我们报告了一种来自细胞内病原体血清型鼠伤寒沙门氏菌毒力操纵子的细菌前导 mRNA,它与编码 FljB 相 2 鞭毛蛋白的 操纵子中的 mRNAs 的 编码区结合,FljB 相 2 鞭毛蛋白是细菌鞭毛的主要成分,也是 FljA 对 FliC 相 1 鞭毛蛋白的抑制剂,并且在感染过程中以依赖于 RNase E 的方式降解 mRNAs。一种阻止 前导 RNA 介导下调的鞭毛基因核苷酸取代增加了编码的鞭毛蛋白合成,导致巨噬细胞内的超动力表型。此外,该核苷酸取代使 毒力增强,表明在 存在的吞噬体隔间中必须损害 FljB 为基础的运动能力。这表明该病原体通过产生一种毒力蛋白来促进致病性,并在感染期间通过来自同一毒力基因的 前导 RNA 来限制运动。