Molecular Cell：反义RNA新机制核糖体竞争mRNA起始位点

生物谷

生物谷援引华文生技网报道：Uppsala大学研究人员最近发现了一种全新RNA抑制途径，即反义RNA与核糖体竞争mRNA的起始位点，从而达到抑制或影响RNA转录的作用。文章发表于近日出版的Molecular Cell上。

以往人们一直认为反义RNA通过与mRNA结合，从而抑制核糖体阅读目标基因，抑制了mRNA转录。研究人员已经在细菌中证实，反义RNA与核糖体阅读起始位点的特定mRNA而形成碱基对，抑制了mRNA转录。

然而，Uppsala大学原核生物微生物学教授Gerhart Wagner发现一种调节蛋白合成的全新机制，不能用反义RNA阻碍核糖体在 mRNA上的起始位点解释，相反的，反义RNA与远离阅读起始位点的mRNA外成碱基对，但仍然能够阻断阅读。意外的是，核糖体到达一个封闭的起始位点时，它会选择远离此位点的开放性位点，而等待正确位点恢复。研究人员认为反义RNA与核糖体竞争结合这个后备位点。如果反义RNA先到，便中止蛋白合成。

(资料来源 : Bio.com)

英文原文链接：

http://www.bio.com/newsfeatures/newsfeatures_research.jhtml;jsessionid=VFT2QMKJFCG0RR3FQLMCFEWHUWBNSIV0?cid=29000078

原始出处:

Molecular Cell，Volume 26, Issue 3, 11 May 2007, Pages 381-392

Article

An Antisense RNA Inhibits Translation by Competing with Standby Ribosomes

Fabien Darfeuille1, 3, 4, Cecilia Unoson1, 3, Jörg Vogel2 and E. Gerhart H. Wagner1, Corresponding Author Contact Information , E-mail The Corresponding Author
1Department of Cell and Molecular Biology, Biomedical Center, Uppsala University, Box 596, S-75124 Uppsala, Sweden
2RNA Biology Group, Max Planck Institute for Infection Biology, Charitéplatz 1, D-10117 Berlin, Germany
Received 21 February 2007; revised 25 March 2007; accepted 5 April 2007. Published: May 10, 2007. Available online 10 May 2007.

Summary

Most antisense RNAs in bacteria inhibit translation by competing with ribosomes for translation initiation regions (TIRs) on nascent mRNA. We propose a mechanism by which an antisense RNA inhibits translation without binding directly to a TIR. The tisAB locus encodes an SOS-induced toxin, and IstR-1 is the antisense RNA that counteracts toxicity. We show that full-length tisAB mRNA (+1) is translationally inactive and endonucleolytic processing produces an active mRNA (+42). IstR-1 binding inhibits translation of this mRNA, and subsequent RNase III cleavage generates a truncated, inactive mRNA (+106). In vitro translation, toeprinting, and structure mapping suggest that active, but not inactive, tisAB mRNAs contain an upstream ribosome loading or “standby” site. Standby binding is required for initiation at the highly structured tisB TIR. This may involve ribosome sliding to a transiently open tisB TIR. IstR-1 competes with ribosomes by base pairing to the standby site located not, vert, similar 100 nucleotides upstream.