Suppression of amber codons in vivo as evidence that mutants derived from Escherichia coli initiator tRNA can act at the step of elongation in protein synthesis.

作者: B L Seong , C P Lee , U L RajBhandary

DOI: 10.1016/S0021-9258(18)83376-2

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摘要: Abstract The absence of a Watson-Crick base pair at the end amino acid acceptor stem is one features which distinguishes prokaryotic initiator tRNAs as class from all other tRNAs. We show that this structural feature prevents Escherichia coli tRNA acting an elongator in protein synthesis vivo. generated mutant E. anticodon sequence changed CAU to CUA (the T35A36 mutant). This has potential read amber termination codon UAG. then coupled mutation others change C1.A72 mismatch either U1:A72 (T1 mutant) or C1:G72 (G72 Transformation CA274 (HfrC Su- lacZ125am trpEam) with multicopy plasmids carrying genes changes both and suppress codons vivo, whereas alone does not. Mutant above are aminoacylated glutamine vitro. Measurement kinetic parameters for aminoacylation by glutaminyl-tRNA synthetase nature presence position can affect kinetics. discuss implications result on recognition synthetase.

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