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首页> 外文期刊>Molecular and Cellular Biology >Release Factor eRF3 Mediates Premature Translation Termination on Polylysine-Stalled Ribosomes in Saccharomyces cerevisiae
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Release Factor eRF3 Mediates Premature Translation Termination on Polylysine-Stalled Ribosomes in Saccharomyces cerevisiae

机译：释放因子eRF3介导酿酒酵母中多聚赖氨酸停滞的核糖体的过早翻译终止。

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Ribosome stalling is an important incident enabling the cellular quality control machinery to detect aberrant mRNA. Saccharomyces cerevisiae Hbs1-Dom34 and Ski7 are homologs of the canonical release factor eRF3-eRF1, which recognize stalled ribosomes, promote ribosome release, and induce the decay of aberrant mRNA. Polyadenylated nonstop mRNA encodes aberrant proteins containing C-terminal polylysine segments which cause ribosome stalling due to electrostatic interaction with the ribosomal exit tunnel. Here we describe a novel mechanism, termed premature translation termination, which releases C-terminally truncated translation products from ribosomes stalled on polylysine segments. Premature termination during polylysine synthesis was abolished when ribosome stalling was prevented due to the absence of the ribosomal protein Asc1. In contrast, premature termination was enhanced, when the general rate of translation elongation was lowered. The unconventional termination event was independent of Hbs1-Dom34 and Ski7, but it was dependent on eRF3. Moreover, premature termination during polylysine synthesis was strongly increased in the absence of the ribosome-bound chaperones ribosome-associated complex (RAC) and Ssb (Ssb1 and Ssb2). On the basis of the data, we suggest a model in which eRF3-eRF1 can catalyze the release of nascent polypeptides even though the ribosomal A-site contains a sense codon when the rate of translation is abnormally low.
机译：核糖体失速是一个重要事件，它使细胞质量控制机构能够检测异常的mRNA。酿酒酵母Hbs1-Dom34和Ski7是经典释放因子eRF3-eRF1的同源物，它们识别停滞的核糖体，促进核糖体释放，并诱导异常mRNA的衰变。聚腺苷酸化的不间断mRNA编码含有C端多聚赖氨酸片段的异常蛋白，这些蛋白会由于与核糖体出口通道的静电相互作用而导致核糖体停滞。在这里，我们描述了一种称为过早翻译终止的新型机制，该机制可从停在聚赖氨酸片段上的核糖体释放C端截短的翻译产物。当由于不存在核糖体蛋白Asc1而防止核糖体停转时，就消除了赖氨酸合成过程中的过早终止。相反，当总的翻译伸长率降低时，过早终止被增强。非常规终止事件独立于Hbs1-Dom34和Ski7，但它依赖于eRF3。此外，在缺乏核糖体结合的伴侣核糖体相关复合物（RAC）和Ssb（Ssb1和Ssb2）的情况下，聚赖氨酸合成过程中的过早终止会大大增加。根据这些数据，我们建议建立一个模型，其中当翻译速率异常低时，即使核糖体A位点包含有义密码子，eRF3-eRF1仍可以催化新生多肽的释放。

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