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A conserved role for cytoplasmic poly(A)-binding protein 1 (PABPC1) in nonsense-mediated mRNA decay.

机译:在无义介导的mRNA衰变中细胞质poly(A)结合蛋白1(PABPC1)的保守作用。

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摘要

The nonsense-mediated mRNA decay (NMD) pathway degrades mRNAs with premature translation termination codons (PTCs). The mechanisms by which PTCs and natural stop codons are discriminated remain unclear. We show that the position of stops relative to the poly(A) tail (and thus of PABPC1) is a critical determinant for PTC definition in Drosophila melanogaster. Indeed, tethering of PABPC1 downstream of a PTC abolishes NMD. Conversely, natural stops trigger NMD when the length of the 3' UTR is increased. However, many endogenous transcripts with exceptionally long 3' UTRs escape NMD, suggesting that the increase in 3' UTR length has co-evolved with the acquisition of features that suppress NMD. We provide evidence for the existence of 3' UTRs conferring immunity to NMD. We also show that PABPC1 binding is sufficient for PTC recognition, regardless of cleavage or polyadenylation. The role of PABPC1 in NMD must go beyond that of providing positional information for PTC definition, because its depletion suppresses NMD under conditions in which translation efficiency is not affected. These findings reveal a conserved role for PABPC1 in mRNA surveillance.
机译:无义介导的mRNA衰变(NMD)途径降解具有过早翻译终止密码子(PTC)的mRNA。区分PTC和自然终止密码子的机制仍不清楚。我们表明停止相对于poly(A)尾巴(因此PABPC1)的位置是果蝇PTC中PTC定义的关键决定因素。实际上,在PTC下游对PABPC1进行束缚将消除NMD。相反,当3'UTR的长度增加时,自然停止会触发NMD。但是,许多具有超长3'UTR的内源性转录本逃避了NMD,这表明3'UTR长度的增加与抑制NMD的特征的获得共同发展。我们提供了3'UTRs赋予对NMD免疫力的证据。我们还显示,无论裂解或聚腺苷酸化如何,PABPC1结合都足以实现PTC识别。 PABPC1在NMD中的作用必须超出为PTC定义提供位置信息的作用,因为它的耗竭会在不影响翻译效率的条件下抑制NMD。这些发现揭示了PABPC1在mRNA监测中的保守作用。

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