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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Mutational analysis of a viral RNA element that counteracts rapid RNA decay by interaction with the polyadenylate tail
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Mutational analysis of a viral RNA element that counteracts rapid RNA decay by interaction with the polyadenylate tail

机译：病毒RNA元件的突变分析，可通过与聚腺苷酸尾巴相互作用来抵消快速RNA衰变

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摘要

We previously demonstrated that the Kaposi's sarcoma-associated herpesvirus polyadenylated nuclear RNA contains a 79-nt cis-acting element, the ENE, which allows intronless polyadenylated transcripts to accumulate to high nuclear levels by protecting them from rapid degradation. We proposed a model based on the predicted structure of the ENE in which a U-rich internal loop hybridizes with the 3-polyadenylate (polyA) tail to sequester it from exonucleolytic attack. We have tested this model by mutational analysis of the ENE. Point mutations in the predicted U-rich internal loop and in the flanking stems abolish the ENE's ability to (ⅰ) interact with the polyA tail, (ⅱ) inhibit deadenylation in vitro, and (ⅲ) stabilize transcripts in vivo. In all but one case, compensatory mutations in the flanking stems restore ENE activities, demonstrating the importance of these stems and uncovering a unique role for the loop-proximal G-C base pair in the lower stem. Increasing the U content of the U-rich internal loop surprisingly decreases stability in vivo but does not affect deadenylation in vitro, comparable to the effects of deleting certain "unstructured" regions of the ENE. Taken together, our data support the formation of the proposed ENE secondary structure in vivo and argue that the specific ENE structure inhibits rapid RNA decay in cis by engaging in a limited set of base-pairing interactions with the polyA tail.
机译：我们先前证明，卡波济氏肉瘤相关的疱疹病毒多腺苷酸化核RNA包含一个79 nt顺式作用元件ENE，它通过保护无内含子的多腺苷酸转录物免于迅速降解而积累到高核水平。我们提出了一个基于ENE预测结构的模型，其中一个富含U的内部环与3-聚腺苷酸（polyA）尾部杂交，以使其免受外切核酸攻击的影响。我们已经通过ENE的突变分析测试了该模型。预测的富含U的内环和侧翼茎中的点突变消除了ENE（ⅰ）与polyA尾相互作用，（，）体外抑制腺苷酸化和（ⅲ）体内稳定转录本的能力。在除一种情况外的所有情况下，侧翼茎中的代偿性突变均可恢复ENE活性，这说明了这些茎的重要性，并揭示了下部茎中最接近环的G-C碱基对的独特作用。与删除ENE的某些“非结构化”区域的效果相比，增加富含U的内环的U含量出人意料地降低了体内稳定性，但不影响体外的腺苷酸化。两者合计，我们的数据支持体内拟议的ENE二级结构的形成，并认为特定的ENE结构通过与polyA尾巴进行有限的碱基配对相互作用来抑制顺式快速RNA降解。

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