Post-transcriptional processing of the LEE4 operon in enterohaemorrhagic Escherichia coli.
Post-transcriptional processing of the LEE4 operon in enterohaemorrhagic Escherichia coli.
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Lee4操纵子在Enterohaemorrhagic Escherichia Coli中的转录后处理。
DOI：
10.1111/j.1365-2958.2008.06530.x
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发表时间：
2009-01
影响因子：
3.6
通讯作者：
Kaper JB
中科院分区：
文献类型：
--
作者：
Lodato PB;Kaper JB
肠出血性大肠杆菌（EHEC）采用III型分泌系统（T3 SS）输出粘膜定植所需的转运蛋白和效应蛋白。T3 SS编码在一个称为肠上皮细胞消失位点（LEE）的致病岛中，该致病岛由五个主要操纵子（LEE 1至LEE 5）组成。LEE 4编码分泌调节因子（SepL）、转位因子（EspA、D和B）、两个分子伴侣（CesD 2和L0017）、T3 SS组分（EscF）和效应蛋白（EspF）。最初提出esp转录本是从位于sepL末端的启动子转录的，但其他作者认为该转录本是转录后加工事件的结果。在这项研究中，我们建立了espADB mRNA是通过转录后加工产生的sepL编码序列的末端。RNase E是参与切割的核酸内切酶，但这种酶通过其C-末端的一半与其他蛋白质的相互作用是不稳定的。cesD 2编码区中的推定转录终止事件将产生转录物的3'端。类似于已经描述的其他加工转录物，LEE 4的切割似乎是差异调节SepL和Esp蛋白质产生的机制。
Enterohemorrhagic 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.
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影响因子：
3.6
作者：
Daniell, SJ;Kocsis, E;Frankel, G
通讯作者：
Frankel, G
影响因子：
16
作者：
Celesnik, Helena;Deana, Atilio;Belasco, Joel G.
通讯作者：
Belasco, Joel G.
影响因子：
3.1
作者：
DONNENBERG, MS;KAPER, JB
通讯作者：
KAPER, JB
影响因子：
14.9
作者：
Chenna, R;Sugawara, H;Thompson, JD
通讯作者：
Thompson, JD
影响因子：
64.8
作者：
Callaghan, AJ;Marcaida, MJ;Luisi, BF
通讯作者：
Luisi, BF