PMID:9660932
| Citation |
Qian, Q, Li, JN, Zhao, H, Hagervall, TG, Farabaugh, PJ and Björk, GR (1998) A new model for phenotypic suppression of frameshift mutations by mutant tRNAs. Mol. Cell 1:471-82 |
|---|---|
| Abstract |
According to the prevailing model, frameshift-suppressing tRNAs with an extra nucleotide in the anticodon loop suppress +1 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. |
| Links | |
| Keywords |
Anticodon/chemistry; Anticodon/genetics; DNA Primers; Frameshift Mutation/genetics; Gene Expression Regulation, Bacterial; Gene Expression Regulation, Fungal; Guanosine/analogs & derivatives; Guanosine/genetics; Nucleic Acid Conformation; Phenotype; Protein Biosynthesis/genetics; RNA, Messenger/chemistry; RNA, Transfer/chemistry; Saccharomyces cerevisiae/genetics; Salmonella typhimurium/genetics |
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