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大肠杆菌埃希氏菌中肠上皮细胞消失区的转录和转录后调控。

Transcriptional and posttranscriptional regulation of the locus of enterocyte effacement in Escherichia albertii.

机构信息

Department of Biology, Saint Joseph's University, 5600 City Avenue, Philadelphia, 19131, PA, USA; Department of Microbiology, University of Pennsylvania, 3610 Hamilton Walk, Philadelphia, 19104, PA, USA.

Department of Biology, Saint Joseph's University, 5600 City Avenue, Philadelphia, 19131, PA, USA.

出版信息

Microb Pathog. 2019 Oct;135:103643. doi: 10.1016/j.micpath.2019.103643. Epub 2019 Jul 20.

Abstract

The diarrheic bacterium Escherichia albertii is a recent addition to the attaching and effacing (A/E) morphotype of pathogens. A/E pathogens cause disease by tightly attaching to intestinal cells, destroying their actin-rich microvilli, and triggering re-localization and repolymerization of actin at the bacterial-host interface to form actin-filled membranous protrusions, termed A/E lesions, beneath the adherent bacterium. The locus of enterocyte effacement (LEE) is required for the biogenesis of these lesions. Whereas regulation of the LEE has been intensively investigated in EPEC and EHEC, it remains cryptic in E. albertii. In this study we characterized the very first transcriptional and posttranscriptional regulators of the LEE in this emerging pathogen. Our results suggest that Ler and GrlA globally activate transcription from the LEE, whereas GrlR negatively regulates the LEE. Additionally, we demonstrate that the RNA chaperone Hfq posttranscriptionally represses the LEE by specifically targeting the 5' UTR of grlR. In summary, our findings provide the very first glimpse of the regulatory landscape of the LEE in E. albertii - a bacterium that has been implicated in multiple diarrheal outbreaks worldwide.

摘要

产黏附侵袭性大肠杆菌是新近归入黏附侵袭(AE)病原体形态的一种致腹泻细菌。AE 病原体通过紧密黏附于肠细胞,破坏富含肌动蛋白的微绒毛,并引发肌动蛋白在细菌-宿主界面处的重新定位和重新聚合,在黏附细菌下方形成填充有肌动蛋白的膜状突起,称为 AE 病变。肠上皮细胞消失(LEE)基因座是这些病变形成所必需的。尽管 EPEC 和 EHEC 中 LEE 的调控已得到深入研究,但在 E. albertii 中仍不清楚。在这项研究中,我们对这种新兴病原体中 LEE 的第一批转录和转录后调控因子进行了表征。我们的结果表明,Ler 和 GrlA 全局激活 LEE 的转录,而 GrlR 则负调控 LEE。此外,我们证明 RNA 伴侣 Hfq 通过特异性靶向 grlR 的 5'UTR 来转录后抑制 LEE。总之,我们的研究结果提供了 E. albertii 中 LEE 调控景观的最初全貌 - 这种细菌已被牵连到全球多次腹泻性暴发中。

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