Abstract

When a ribosome encounters the stop codon of an mRNA, it terminates translation, releases the newly made protein, and is recycled to initiate translation on a new mRNA. Termination is a highly dynamic process in which release factors (RF1 and RF2 in bacteria; eRF1•eRF3•GTP in eukaryotes) coordinate peptide release with large-scale molecular rearrangements of the ribosome. Ribosomes stalled on aberrant mRNAs are rescued and recycled by diverse bacterial, mitochondrial, or cytoplasmic quality control mechanisms. These are catalyzed by rescue factors with peptidyl-tRNA hydrolase activity (bacterial ArfA•RF2 and ArfB, mitochondrial ICT1 and mtRF-R, and cytoplasmic Vms1), that are distinct from each other and from release factors. Nevertheless, recent structural studies demonstrate a remarkable similarity between translation termination and ribosome rescue mechanisms. This review describes how these pathways rely on inherent ribosome dynamics, emphasizing the active role of the ribosome in all translation steps.

中文翻译：

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细菌、线粒体和细胞质翻译中终止和核糖体拯救的多样性和相似性

摘要

当核糖体遇到 mRNA 的终止密码子时，它会终止翻译，释放新生成的蛋白质，然后再循环以启动新 mRNA 的翻译。终止是一个高度动态的过程，其中释放因子（细菌中的 RF1 和 RF2；真核生物中的 eRF1•eRF3•GTP）协调肽释放与核糖体的大规模分子重排。停滞在异常 mRNA 上的核糖体通过不同的细菌、线粒体或细胞质质量控制机制得到拯救和回收。这些由具有肽基-tRNA 水解酶活性的拯救因子（细菌 ArfA•RF2 和 ArfB、线粒体 ICT1 和 mtRF-R 以及细胞质 Vms1）催化，这些因子彼此不同并且与释放因子不同。尽管如此，最近的结构研究表明翻译终止和核糖体拯救机制之间存在显着的相似性。这篇综述描述了这些途径如何依赖于固有的核糖体动力学，强调核糖体在所有翻译步骤中的积极作用。