内部核糖体进入序列介导的翻译起始引发无义介导的衰变。
Internal ribosome entry sequence-mediated translation initiation triggers nonsense-mediated decay.
作者信息
Holbrook Jill A, Neu-Yilik Gabriele, Gehring Niels H, Kulozik Andreas E, Hentze Matthias W
机构信息
European Molecular Biology Laboratory, University Hospital Heidelberg, Molecular Medicine Partnership Unit, University of Heidelberg, Im Neuenheimer Feld 150, Heidelberg 69120, Germany.
出版信息
EMBO Rep. 2006 Jul;7(7):722-6. doi: 10.1038/sj.embor.7400721. Epub 2006 Jun 16.
Abstract
In eukaryotes, a surveillance pathway known as nonsense-mediated decay (NMD) regulates the abundance of messenger RNAs containing premature termination codons (PTCs). In mammalian cells, it has been asserted that the NMD-relevant first round of translation is special and involves initiation by a specific protein heterodimer, the nuclear cap-binding complex (CBC). Arguing against a requirement for CBC-mediated translation initiation, we show that ribosomal recruitment by the internal ribosomal entry sequence of the encephalomyocarditis virus triggers NMD of a PTC-containing transcript under conditions in which ribosome entry from the cap is prohibited. These data generalize the previous model and suggest that translation per se, irrespective of how it is initiated, can mediate NMD.
摘要
在真核生物中，一种称为无义介导衰变（NMD）的监测途径可调节含有提前终止密码子（PTC）的信使核糖核酸（mRNA）的丰度。在哺乳动物细胞中，有人断言与NMD相关的第一轮翻译很特殊，涉及由一种特定的蛋白质异二聚体——核帽结合复合体（CBC）起始。与CBC介导的翻译起始的必要性观点相反，我们发现，在帽依赖性核糖体进入被阻断的条件下，脑心肌炎病毒的内部核糖体进入序列介导的核糖体募集可触发含PTC转录本的NMD。这些数据拓展了先前的模型，并表明翻译本身，无论其起始方式如何，均可介导NMD。
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