AUTOGENOUS SUPPRESSION OF AN OPAL MUTATION IN THE GENE ENCODING PEPTIDE-CHAIN RELEASE FACTOR-II

被引:45
作者
KAWAKAMI, K
NAKAMURA, Y
机构
[1] Department of Tumor Biology, Institute of Medical Science, University of Tokyo, Tokyo 108, P.O. Takanawa
关键词
Peptide chain release factor; prfB/; SupK; Transition termination; UGA suppression;
D O I
10.1073/pnas.87.21.8432
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
The peptide chain release factor 2 (RF2) gene, prfB, was cloned from Salmonella typhimurium by DNA hybridization using the Escherichia coli prfB probe. The nucleotide and amino acid sequences of prfB are 87.0% and 95.6% homologous between E. coli and S. typhimurium, respectively, including an in-frame premature UGA stop codon at position 26, the site of +1 frameshift for mature RF2 synthesis. The supK584 mutation, which had been isolated as a recessive UGA suppressor in S. typhimurium, caused an opal (UGA) substitution at amino acid position 144 in the prfB gene. Complementation, reversion, and gene fusion analyses led to the conclusion that supK is a S. typhimurium RF2 mutation and this opal RF2 mutation generates a UGA suppressor activity, presumably because of inefficient translation termination due to the reduced cellular level of RF2. In fact, suppression of the supK opal mutation results from a form of autogenous control of RF2 synthesis.
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页码:8432 / 8436
页数:5
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