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Expression of the eRF1 translation termination factor is controlled by an autoregulatory circuit involving readthrough and nonsense-mediated decay in plants

机译:eRF1翻译终止因子的表达受自动调节电路控制该电路涉及植物的通读和无义介导的衰变

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摘要

When a ribosome reaches a stop codon, the eukaryotic Release Factor 1 (eRF1) binds to the A site of the ribosome and terminates translation. In yeasts and plants, both over- and underexpression of eRF1 lead to altered phenotype indicating that eRF1 expression should be strictly controlled. However, regulation of eRF1 level is still poorly understood. Here we show that expression of plant eRF1 is controlled by a complex negative autoregulatory circuit, which is based on the unique features of the 3΄untranslated region (3΄UTR) of the eRF1-1 transcript. The stop codon of the eRF1-1 mRNA is in a translational readthrough promoting context, while its 3΄UTR induces nonsense-mediated decay (NMD), a translation termination coupled mRNA degradation mechanism. We demonstrate that readthrough partially protects the eRF1-1 mRNA from its 3΄UTR induced NMD, and that elevated eRF1 levels inhibit readthrough and stimulate NMD. Thus, high eRF1 level leads to reduced eRF1-1 expression, as weakened readthrough fails to protect the eRF1-1 mRNA from the more intense NMD. This eRF1 autoregulatory circuit might serve to finely balance general translation termination efficiency.
机译:当核糖体到达终止密码子时,真核生物释放因子1(eRF1)结合到核糖体的A位点并终止翻译。在酵母和植物中,eRF1的过度表达和表达不足都会导致表型改变,这表明应严格控制eRF1的表达。但是,对eRF1水平的调节仍知之甚少。在这里,我们显示植物eRF1的表达受复杂的负自动调节电路控制,该电路基于eRF1-1转录物的3′非翻译区(3′UTR)的独特特征。 eRF1-1 mRNA的终止密码子处于翻译通读促进环境中,而其3΄UTR则诱导了无义介导的衰变(NMD),即翻译终止偶联的mRNA降解机制。我们证明,通读部分地保护eRF1-1 mRNA不受其3΄UTR诱导的NMD的影响,而升高的eRF1水平抑制通读并刺激NMD。因此,高的eRF1水平会导致eRF1-1的表达降低,因为减弱的通读无法保护eRF1-1 mRNA免受更强烈的NMD的侵害。此eRF1自动调节电路可能会很好地平衡一般的翻译终止效率。

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