A new model for phenotypic suppression of frameshift mutations by mutant tRNAs
A new model for phenotypic suppression of frameshift mutations by mutant tRNAs
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DOI：
10.1016/s1097-2765(00)80048-9
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发表时间：
1998-03-01
期刊：
影响因子：
16
通讯作者：
Bjork, GR
中科院分区：
文献类型：
--
作者：
Qian, Q;Li, JN;Bjork, GR
根据流行的模型，在反密码子环中具有额外核苷酸的移码抑制性tRNA通过识别四碱基密码子并促进四联体易位来抑制tl移码突变。我们提出了三组实验，提出了一个通用的替代这个模型。首先，碱基修饰实际上应该通过两个经典的移码抑制子来阻止这种四碱基相互作用。第二，对于一种沙门氏菌抑制tRNA，它不是突变的tRNA，而是结构正常的近同源物，导致+1框内移位。最后，移码发生在与下一个框内密码子的正常解码的竞争中，这与易位步骤后在核糖体P位点发生的事件一致。这些结果表明了一种替代模型，涉及肽基-tRNA在经典CCC-N和GGG-N移码抑制位点的滑动。
According to the prevailing model, frameshift-suppressing tRNAs with an extra nucleotide in the anticodon loop suppress tl frameshift mutations by recognizing a four-base codon and promoting quadruplet translocation. We present three sets of experiments that suggest a general alternative to this model. First, base modification should actually block such a four-base interaction by two classical frameshift suppressors. Second, for one Salmonella suppressor tRNA, it is not mutant tRNA but a structurally normal near cognate that causes the +1 shift in-frame. Finally, frameshifting occurs in competition with normal decoding of the next in-frame codon, consistent with an event that occurs in the ribosomal P site after the translocation step. These results suggest an alternative model involving peptidyl-tRNA slippage at the classical CCC-N and GGG-N frameshift suppression sites.