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本文引用的文献

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Gene l0017 encodes a second chaperone for EspA of enterohaemorrhagic Escherichia coli O157 : H7.基因l0017编码肠出血性大肠杆菌O157 : H7的EspA的第二种伴侣蛋白。
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The enteropathogenic E. coli effector EspB facilitates microvillus effacing and antiphagocytosis by inhibiting myosin function.肠道致病性大肠杆菌效应蛋白EspB通过抑制肌球蛋白功能促进微绒毛消失和抗吞噬作用。
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肠出血性大肠杆菌中LEE4操纵子的转录后加工

Post-transcriptional processing of the LEE4 operon in enterohaemorrhagic Escherichia coli.

作者信息

Lodato Patricia B, Kaper James B

机构信息

Center for Vaccine Development and Department of Microbiology and Immunology, University of Maryland School of Medicine, 685 W. Baltimore St, Baltimore, MD 21201, USA.

出版信息

Mol Microbiol. 2009 Jan;71(2):273-90. doi: 10.1111/j.1365-2958.2008.06530.x. Epub 2008 Nov 4.

DOI:10.1111/j.1365-2958.2008.06530.x
PMID:19019141
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2782684/
Abstract

Enterohaemorrhagic Escherichia coli (EHEC) employs a type III secretion system (T3SS) to export translocator and effector proteins required for mucosal colonization. The T3SS is encoded in a pathogenicity island called the locus of enterocyte effacement (LEE) that is organized in five major operons, LEE1 to LEE5. LEE4 encodes a regulator of secretion (SepL), translocators (EspA, D and B), two chaperones (CesD2 and L0017), a T3SS component (EscF) and an effector protein (EspF). It was originally proposed that the esp transcript is transcribed from a promoter located at the end of sepL but other authors suggested that this transcript is the result of a post-transcriptional processing event. In this study, we established that the espADB mRNA is generated by post-transcriptional processing at the end of the sepL coding sequence. RNase E is the endonuclease involved in the cleavage, but the interaction of this enzyme with other proteins through its C-terminal half is dispensable. A putative transcription termination event in the cesD2 coding region would generate the 3' end of the transcript. Similar to what has been described for other processed transcripts, the cleavage of LEE4 seems a mechanism to differentially regulate SepL and Esp protein production.

摘要

肠出血性大肠杆菌(EHEC)利用III型分泌系统(T3SS)输出黏膜定植所需的转运蛋白和效应蛋白。T3SS由一个称为肠上皮细胞损伤位点(LEE)的致病岛编码,该致病岛由五个主要操纵子LEE1至LEE5组成。LEE4编码一种分泌调节因子(SepL)、转运蛋白(EspA、D和B)、两个分子伴侣(CesD2和L0017)、一个T3SS组分(EscF)和一个效应蛋白(EspF)。最初有人提出esp转录本是从位于sepL末端的一个启动子转录而来,但其他作者认为该转录本是转录后加工事件的结果。在本研究中,我们确定espADB mRNA是由sepL编码序列末端的转录后加工产生的。核糖核酸酶E是参与切割的内切核酸酶,但该酶通过其C末端一半与其他蛋白质的相互作用是可有可无的。cesD2编码区域中一个假定的转录终止事件将产生转录本的3'末端。与其他加工转录本的情况类似,LEE4的切割似乎是一种差异调节SepL和Esp蛋白产生的机制。