Horsburgh B C, Kollmus H, Hauser H, Coen D M
Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115, USA.
Cell. 1996 Sep 20;86(6):949-59. doi: 10.1016/s0092-8674(00)80170-1.
We investigated a herpesvirus mutant that contains a single base insertion in its thymidine kinase (tk) gene yet expresses low levels of TK via a net +1 translational recoding event. Within this mutant gene, we defined a G-rich signal that is sufficient to induce recoding. Unlike other translational recoding events, downstream RNA structures or termination codons did not stimulate recoding, and paused ribosomes were not detected. Mutational analysis indicated that specific tRNAs or codon-anticodon slippage were unlikely to account for recoding. Rather, recoding efficiency correlated with the G-richness of the signal and its ability to form unusual structures. These findings identify a mechanism of translational recoding with unique features and potential implications for clinical drug resistance and other biological systems.
我们研究了一种疱疹病毒突变体，该突变体在其胸苷激酶（tk）基因中存在单个碱基插入，但通过净 +1 翻译重编码事件表达低水平的 TK。在这个突变基因中，我们定义了一个富含 G 的信号，该信号足以诱导重编码。与其他翻译重编码事件不同，下游 RNA 结构或终止密码子不会刺激重编码，并且未检测到停顿的核糖体。突变分析表明，特定的 tRNA 或密码子 - 反密码子滑动不太可能解释重编码现象。相反，重编码效率与信号的富含 G 程度及其形成异常结构的能力相关。这些发现确定了一种具有独特特征的翻译重编码机制，对临床耐药性和其他生物系统具有潜在影响。
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