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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Inhibition of glutamate receptor 2 translation by a polymorphic repeat sequence in the 5'-untranslated leaders.
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Inhibition of glutamate receptor 2 translation by a polymorphic repeat sequence in the 5'-untranslated leaders.

机译：通过5'-非翻译前导序列中的多态性重复序列抑制谷氨酸受体2的翻译。

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摘要

Previous studies have identified multiple transcription initiation sites for the glutamate receptor 2 (GluR2) gene, resulting in a heterogeneous population of GluR2 transcripts in vivo that differ in the length of their 5'-untranslated leaders (5'-UTR). We designed a series of monocistronic and dicistronic GluR2 cDNA constructs that model the natural in vivo transcripts and investigated their translation efficiencies in rabbit reticulocyte lysates, Xenopus oocytes, and primary cultured neurons. Transcripts containing long 5' leaders (429 and 481 bases) were translated poorly compared with those with shorter leaders (341 or fewer bases). None of the five initiation codons in the 5'-UTR or the leader length per se were responsible for translation regulation. Rather, control of translation was mediated by a sequence containing a 34-42 nucleotide imperfect GU repeat predicted to form secondary structure in vivo. This translation suppression domain is included in some but not all rat and human GluR2 transcripts in vivo, depending on the site of transcription initiation. Rat cortex GluR2 transcripts that lack the translation suppression sequence were preferentially associated with polyribosomes. Furthermore, the GU-repeat cluster was found to be polymorphic in humans, raising the possibility that expansion or contraction of the GU-repeat cluster in certain populations might modify the level of GluR2 protein expression in neurons.
机译：先前的研究已经确定了谷氨酸受体2（GluR2）基因的多个转录起始位点，从而导致体内的GluR2转录本异质群体的5'-非翻译前导序列（5'-UTR）的长度不同。我们设计了一系列单顺反子和双顺反子GluR2 cDNA构建体，它们对天然的体内转录本进行建模，并研究了它们在兔网织红细胞裂解液，爪蟾卵母细胞和原代培养神经元中的翻译效率。与具有较短的前导者（341个或更少的碱基）的转录本相比，包含长5'导子（429和481个碱基）的转录本的翻译质量较差。 5'-UTR的五个起始密码子或前导长度本身都不负责翻译调控。相反，翻译的控制是通过包含34-42个核苷酸的不完美GU重复的序列介导的，该GU重复被预测在体内形成二级结构。取决于转录起始位点，该翻译抑制域包含在体内的某些但不是全部大鼠和人GluR2转录物中，但并非全部。缺少翻译抑制序列的大鼠皮质GluR2转录物优先与多核糖体相关。此外，发现GU-重复簇在人类中是多态的，从而增加了某些人群中GU-重复簇的扩增或收缩可能会改变神经元中GluR2蛋白表达的水平。

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