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编码于基因组岛OI-29中的转录激活因子GmrA控制肠出血性O157:H7的运动性。

Transcriptional Activator GmrA, Encoded in Genomic Island OI-29, Controls the Motility of Enterohemorrhagic O157:H7.

作者信息

Yang Bin, Wang Shaomeng, Huang Jianxiao, Yin Zhiqiu, Jiang Lingyan, Hou Wenqi, Li Xiaomin, Feng Lu

机构信息

TEDA Institute of Biological Sciences and Biotechnology, Nankai University, Tianjin, China.

Key Laboratory of Molecular Microbiology and Technology, Ministry of Education, Tianjin, China.

出版信息

Front Microbiol. 2018 Feb 22;9:338. doi: 10.3389/fmicb.2018.00338. eCollection 2018.

Abstract

Enterohemorrhagic O157:H7 is a major human enteric pathogen capable of causing large outbreaks of severe infections that induce bloody diarrhea, hemorrhagic colitis, and hemolytic uremic syndrome. Its genome contains 177 unique O islands (OIs) including those carrying the main virulence elements, Shiga toxin-converting phages (OI-45 and OI-93) and locus for enterocyte effacement (OI-148). However, many of these islands harbor only genes of unknown function. Here, we demonstrate that OI-29 encodes a newly discovered transcriptional activator, Z0639 (named GmrA), that is required for motility and flagellar synthesis in O157:H7. GmrA directly binds to the promoter of , an RNA polymerase sigma factor, and thereby regulates flagellar genes controlled by FliA. Expression of is maximal under host conditions (37°C, neutral pH, and physiological osmolarity), and in the presence of host epithelial cells, indicative of a role of this gene in infection by promoting motility. Finally, GmrA was found to be a widespread regulator of bacterial motility and flagellar synthesis in different pathotypes of . Our work largely enriches our understanding of bacterial motility control, and provides another example of regulators acquired laterally that mediate flagellar synthesis.

摘要

肠出血性O157:H7是一种主要的人类肠道病原体,能够引发严重感染的大规模暴发,导致血性腹泻、出血性结肠炎和溶血尿毒综合征。其基因组包含177个独特的O岛(OIs),包括那些携带主要毒力元件的O岛,如志贺毒素转换噬菌体(OI-45和OI-93)和肠细胞脱落位点(OI-148)。然而,这些岛屿中的许多仅含有功能未知的基因。在这里,我们证明OI-29编码一种新发现的转录激活因子Z0639(命名为GmrA),它是O157:H7运动性和鞭毛合成所必需的。GmrA直接结合到一种RNA聚合酶σ因子的启动子上,从而调节由FliA控制的鞭毛基因。在宿主条件下(37°C、中性pH和生理渗透压)以及存在宿主上皮细胞时,该因子的表达最高,这表明该基因通过促进运动性在感染中发挥作用。最后,发现GmrA是不同致病型细菌运动性和鞭毛合成的广泛调节因子。我们的工作极大地丰富了我们对细菌运动性控制的理解,并提供了另一个横向获得的介导鞭毛合成的调节因子的例子。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35ae/5826968/5aea10a17559/fmicb-09-00338-g001.jpg

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