Hfq binding at RhlB-recognition region of RNase E is crucial for the rapid degradation of target mRNAs mediated by sRNAs in Escherichia coli
Hfq binding at RhlB-recognition region of RNase E is crucial for the rapid degradation of target mRNAs mediated by sRNAs in Escherichia coli
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DOI：
10.1111/j.1365-2958.2010.07454.x
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发表时间：
2011-01-01
影响因子：
3.6
通讯作者：
Aiba, Hiroji
中科院分区：
文献类型：
--
作者：
Ikeda, Yoshiki;Yagi, Mieko;Aiba, Hiroji
在大肠杆菌中，一个RNA伴侣分子Hfq沿着与Hfq结合的sRNA稳定地结合RNase E。Hfq-RNase E相互作用的作用是募集RNase E靶向sRNA的mRNA，导致mRNA-sRNA杂合体的快速降解。RNase E的C-末端支架区负责与Hfq的相互作用。在这里，我们证明了支架区域可以被删除到残基750，而不会失去导致由Hfq/sRNAs介导的靶mRNA快速降解的能力。截短的RNase E750仍然可以与Hfq结合，尽管截短显著降低了Hfq结合能力。我们得出结论，711和750之间的子区域是足够的功能相互作用与Hfq支持ptsG mRNA的快速降解，虽然支架内的其他子区域也参与Hfq结合。702-750区域的缺失极大地削弱了RNase E引起ptsG mRNA降解的能力。此外，对应于支架区域的多肽在没有RNA的帮助下结合Hfq。最后，我们证明了RhlB的过表达部分抑制了Hfq与RNase E的结合和ptsG mRNA的快速降解。
P>An RNA chaperon Hfq along with Hfq-binding sRNAs stably binds to RNase E in Escherichia coli. The role of the Hfq-RNase E interaction is to recruit RNase E to target mRNAs of sRNAs resulting in the rapid degradation of the mRNA-sRNA hybrid. The C-terminal scaffold region of RNase E is responsible for the interaction with Hfq. Here, we demonstrate that the scaffold region can be deleted up to residue 750 without losing the ability to cause the rapid degradation of target mRNAs mediated by Hfq/sRNAs. The truncated RNase E750 can still bind to Hfq although the truncation significantly reduces the Hfq-binding ability. We conclude that the subregion between 711 and 750 is sufficient for the functional interaction with Hfq to support the rapid degradation of ptsG mRNA although additional subregions within the scaffold are also involved in Hfq binding. Deletion of the 702-750 region greatly impairs the ability of RNase E to cause the degradation of ptsG mRNA. In addition, a polypeptide corresponding to the scaffold region binds to Hfq without the help of RNA. Finally, we demonstrate that overexpression of RhlB partially inhibits the Hfq binding to RNase E and the rapid degradation of ptsG mRNA.