大肠杆菌16S rRNA解码区1409 - 1491碱基对处的无义抑制突变和反抑制突变。
Nonsense suppressor and antisuppressor mutations at the 1409-1491 base pair in the decoding region of Escherichia coli 16S rRNA.
作者信息
Gregory S T, Dahlberg A E
机构信息
Section of Biochemistry, Brown University, Providence, RI 02912, USA.
出版信息
Nucleic Acids Res. 1995 Nov 11;23(21):4234-8. doi: 10.1093/nar/23.21.4234.
Abstract
Using a genetic selection for suppressors of a UGA nonsense mutation in trpA, we have isolated a G to A transition mutation at position 1491 in the decoding region of 16S rRNA. This suppressor displayed no codon specificity, suppressing UGA, UAG and UAA nonsense mutations and +1 and -1 frameshift mutations in lacZ. Subsequent examination of a series of mutations at G1491 and its base-pairing partner C1409 revealed various effects on nonsense suppression and frameshifting. Mutations that prevented Watson-Crick base pairing between these residues were observed to increase misreading and frameshifting. However, double mutations that retained pairing potential produced an antisuppressor or hyperaccurate phenotype. Previous studies of antibiotic resistance mutations and antibiotic and tRNA footprints have placed G1491 and C1409 near the site of codon-anticodon pairing. The results of this study demonstrate that the nature of the interaction of these two residues influences the fidelity of tRNA selection.
摘要
利用对trpA基因中UGA无义突变抑制子的遗传筛选，我们在16S rRNA解码区的1491位分离出一个由G到A的转换突变。该抑制子没有密码子特异性，可抑制UGA、UAG和UAA无义突变以及lacZ基因中的+1和-1移码突变。随后对G1491及其碱基配对伙伴C1409处的一系列突变进行检测，发现它们对无义抑制和移码有不同影响。观察到阻止这些残基间沃森-克里克碱基配对的突变会增加错读和移码。然而，保留配对潜能的双突变产生了反抑制或超精确表型。先前关于抗生素抗性突变以及抗生素和tRNA足迹的研究已将G1491和C1409定位在密码子-反密码子配对位点附近。本研究结果表明这两个残基相互作用的性质会影响tRNA选择的保真度。
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