Frameshifting RNA pseudoknots: structure and mechanism.
Frameshifting RNA pseudoknots: structure and mechanism.
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DOI：
10.1016/j.virusres.2008.06.008
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发表时间：
2009-02
期刊：
影响因子：
5
通讯作者：
Cornish, Peter V.
中科院分区：
文献类型：
--
作者：
Giedroc, David P.;Cornish, Peter V.
关键词：
程序性核糖体移码（PRF）是一种多重翻译重编码过程，它通过延长核糖体从根本上改变信使RNA的三联体解码。核糖体在-1方向（-1 PRF）上改变翻译阅读框的能力被许多正链RNA病毒利用，包括经济上重要的植物病毒和许多人类病原体，如逆转录病毒，例如，HIV-1和冠状病毒，例如，严重急性呼吸道综合征（SARS）的病原体，以便正确表达它们的基因组。−1 PRF由嵌入mRNA中的二分信号编程，包括一个七核苷酸“滑动位点”，暂停的核糖体通过一个核苷酸“备份”，以及下游刺激元件，RNA假结或非常稳定的RNA茎环。这两个元件之间相隔6 ~ 8个核苷酸，下游刺激元件的5′端与30 S核糖体亚基的mRNA进入通道直接接触。下游RNA通过转运核糖体刺激-1 PRF的确切机制尚不清楚。这篇综述总结了最近的结构和生物物理研究的RNA pseudoknodes和地方这项工作的背景下，我们不断发展的翻译延伸的机制的理解。支持的假设，下游刺激元件提供了一个动力学屏障核糖体介导的展开进行了讨论。
Programmed ribosomal frameshifting (PRF) is one of the multiple translational recoding processes that fundamentally alters triplet decoding of the messenger RNA by the elongating ribosome. The ability of the ribosome to change translational reading frames in the −1 direction (−1 PRF) is employed by many positive strand RNA viruses, including economically important plant viruses and many human pathogens, such as retroviruses, e.g., HIV-1, and coronaviruses, e.g., the causative agent of severe acute respiratory syndrome (SARS), in order to properly express their genomes. −1 PRF is programmed by a bipartite signal embedded in the mRNA and includes a heptanucleotide “slip site” over which the paused ribosome “backs up” by one nucleotide, and a downstream stimulatory element, either an RNA pseudoknot or a very stable RNA stem–loop. These two elements are separated by six to eight nucleotides, a distance that places the 5′ edge of the downstream stimulatory element in direct contact with the mRNA entry channel of the 30S ribosomal subunit. The precise mechanism by which the downstream RNA stimulates −1 PRF by the translocating ribosome remains unclear. This review summarizes the recent structural and biophysical studies of RNA pseudoknots and places this work in the context of our evolving mechanistic understanding of translation elongation. Support for the hypothesis that the downstream stimulatory element provides a kinetic barrier to the ribosome-mediated unfolding is discussed.
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