A new model for phenotypic suppression of frameshift mutations by mutant tRNAs.
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.
Qian
Q
Q
Department of Microbiology, Umeå University, Sweden.
Li
J N
JN
Zhao
H
H
Hagervall
T G
TG
Farabaugh
P J
PJ
Björk
G R
GR
D000926:Anticodon / Q000737:chemistry* / Q000235:genetics; D017931:DNA Primers; D016368:Frameshift Mutation / Q000235:genetics*; D015964:Gene Expression Regulation, Bacterial; D015966:Gene Expression Regulation, Fungal; D006151:Guanosine / Q000031:analogs & derivatives / Q000235:genetics; D009690:Nucleic Acid Conformation; D010641:Phenotype; D014176:Protein Biosynthesis / Q000235:genetics; D012333:RNA, Messenger / Q000737:chemistry; D012343:RNA, Transfer / Q000737:chemistry; D012441:Saccharomyces cerevisiae / Q000235:genetics*; D012486:Salmonella typhimurium / Q000235:genetics*
D000926:Anticodon; D017931:DNA Primers; D012333:RNA, Messenger; D006151:Guanosine; C020770:1-methylguanosine; D012343:RNA, Transfer