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在大肠杆菌16S rRNA中含有C1054缺失突变的核糖体在所有三个无义密码子处都起抑制作用。

Ribosomes containing the C1054-deletion mutation in E. coli 16S rRNA act as suppressors at all three nonsense codons.

作者信息

Prescott C, Krabben L, Nierhaus K

机构信息

Max Planck Institut für Molekulare Genetik, Berlin, FRG.

出版信息

Nucleic Acids Res. 1991 Oct 11;19(19):5281-3. doi: 10.1093/nar/19.19.5281.

DOI:10.1093/nar/19.19.5281
PMID:1923812
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC328888/
Abstract

It was established some time ago that the deletion of base C1054 in E. coli 16S rRNA specifically affects UGA-dependent termination of translation. Based on this observation, a model for the termination event was proposed in which the UGA nonsense codon on the mRNA base-pairs with a complementary motif in 'helix 34' of the 16S rRNA, thus potentially providing a recognition signal for the binding of the release factor. This model has been re-examined here and evidence is presented which demonstrates that ribosomes containing the C1054 delta mutation enhance the activity of suppressors of both UAG and UAA termination codons introduced into the host. The results do not support the nonsense codon-16S rRNA base pairing model, and rather imply a more general involvement of 'helix 34' in the translation termination reactions.

摘要

前段时间确定，大肠杆菌16S rRNA中C1054碱基的缺失会特异性影响依赖UGA的翻译终止。基于这一观察结果，提出了一种终止事件模型，其中mRNA上的UGA无义密码子与16S rRNA“螺旋34”中的互补基序形成碱基对，从而可能为释放因子的结合提供识别信号。本文对该模型进行了重新研究，并给出了证据，证明含有C1054缺失突变的核糖体增强了引入宿主的UAG和UAA终止密码子的抑制子的活性。结果不支持无义密码子与16S rRNA碱基配对模型，而是暗示“螺旋34”在翻译终止反应中更广泛的参与。

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