Evidence against a direct role for the Upf proteins in frameshifting or nonsense codon readthrough
Evidence against a direct role for the Upf proteins in frameshifting or nonsense codon readthrough
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DOI：
10.1261/rna.7120504
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发表时间：
2004-11-01
期刊：
影响因子：
4.5
通讯作者：
Dinman, JD
中科院分区：
文献类型：
--
作者：
Harger, JW;Dinman, JD
UPF蛋白在无意义介导的mRNA衰变(NMD)中起着至关重要的作用。它们还与病毒移码信号和提前终止密码子的翻译保真度的调节有关。这些因素如何在信使核糖核酸周转和翻译控制中发挥作用仍不清楚。在这项研究中，使用单顺反子和双顺反子报告系统在酵母中区分在mRNA周转水平和在翻译水平上的影响。我们证实，upfDelta突变不影响程序性移码，并表明这也适用于eIF1/Sui1p的突变形式。此外，双顺反子记者没有检测到由于UPF基因缺失而导致的翻译通读缺陷，这表明它们在终止过程中的功能并不像之前认为的那样普遍。证明UPF sui1双突变体是合成致死的，这表明NMD和翻译起始途径之间存在重要的功能相互作用。
The Upf proteins are essential for nonsense-mediated mRNA decay (NMD). They have also been implicated in the modulation of translational fidelity at viral frameshift signals and premature termination codons. How these factors function in both mRNA turnover and translational control remains unclear. In this study, mono- and bicistronic reporter systems were used in the yeast Saccharomyces cerevisae to differentiate between effects at the levels of mRNA turnover and those at the level of translation. We confirm that upfDelta mutants do not affect programmed frameshifting, and show that this is also true for mutant forms of eIF1/Sui1p. Further, bicistronic reporters did not detect defects in translational readthrough due to deletion of the UPF genes, suggesting that their function in termination is not as general a phenomenon as was previously believed. The demonstration that upf sui1 double mutants are synthetically lethal demonstrates an important functional interaction between the NMD and translation initiation pathway.