O'Mahony D J, Mims B H, Thompson S, Murgola E J, Atkins J F
Department of Biochemistry, University College, Cork, Ireland.
Proc Natl Acad Sci U S A. 1989 Oct;86(20):7979-83. doi: 10.1073/pnas.86.20.7979.
Mutations in the acceptor stem, the 5-methyluridine-pseudouridine-cytidine (TFC) arm, and the anticodon of Salmonella tRNA2Gly can cause -1 frameshifting. The potential for standard base pairing between acceptor stem positions 1 and 72 is disrupted in the mutant sufS627. This disruption may interfere with the interaction of the tRNA with elongation factor-Tu.GTP or an as-yet-unspecified domain of the ribosome. The potential for standard base pairing in part of the TFC stem is disrupted in mutant sufS625. The nearly universal C-61 base of the TFC stem is altered in mutant sufS617, and the TFC loop is extended in mutant sufS605. These changes are expected to interfere with the stability of the TFC loop and its interaction with the D arm. The mutation in mutant sufS605, and possibly other mutants, alters nucleoside modification in the D arm. Three mutants, sufS601, sufS607, and sufS609, have a cytidine substituted for the modified uridine at position 34, the first anticodon position. None of the alterations grossly disrupts in-frame triplet decoding by the mutant tRNAs. The results show that -1 frameshifting in vivo can be caused by tRNAs with normal anticodon loop size and suggest that alternative conformational states of the mutant tRNAs may allow them to read a codon in frame or to shift reading frame.
沙门氏菌tRNA2Gly的受体茎、5-甲基尿苷-假尿苷-胞苷（TFC）臂和反密码子中的突变可导致-1移码。在突变体sufS627中，受体茎位置1和72之间的标准碱基配对潜力被破坏。这种破坏可能会干扰tRNA与延伸因子-Tu.GTP或核糖体尚未明确的结构域之间的相互作用。在突变体sufS625中，TFC茎部分的标准碱基配对潜力被破坏。在突变体sufS617中，TFC茎几乎通用的C-61碱基发生改变，在突变体sufS605中，TFC环延长。这些变化预计会干扰TFC环的稳定性及其与D臂的相互作用。突变体sufS605以及可能的其他突变体中的突变改变了D臂中的核苷修饰。三个突变体sufS601、sufS607和sufS609在反密码子的第一个位置34处，用胞苷取代了修饰的尿苷。这些改变均未严重破坏突变tRNA的框内三联体解码。结果表明，体内-1移码可由具有正常反密码子环大小的tRNA引起，并表明突变tRNA的替代构象状态可能使它们能够框内读取密码子或改变阅读框。
