Aulin M R, Hughes D
Department of Molecular Biology, Biomedical Center, Uppsala, Sweden.
J Bacteriol. 1990 Dec;172(12):6721-6. doi: 10.1128/jb.172.12.6721-6726.1990.
Mutant forms of elongation factor Tu encoded by tufA8 and tufB103 in Salmonella typhimurium cause suppression of some but not all frameshift mutations. All of the suppressed mutations in S. typhimurium have frameshift windows ending in the termination codon UGA. Because both tufA8 and tufB103 are moderately efficient UGA suppressors, we asked whether the efficiency of frameshifting is influenced by the level of misreading at UGA. We introduced plasmids synthesizing either one of the release factors into strains in which the tuf mutations suppress a test frameshift mutation. We found that overproduction of release factor 2 (which catalyzes release at UGA and UAA) reduced frameshifting promoted by the tuf mutations at all sites tested. However, at one of these sites, trpE91, overproduction of release factor 1 also reduced suppression. The spontaneous level of frameshift "leakiness" at three sites in trpE, each terminating in UGA, was reduced in strains carrying the release factor 2 plasmid. We conclude that both spontaneous and suppressor-enhanced reading-frame shifts are influenced by the activity of peptide chain release factors. However, the data suggest that the effect of release factor on frameshifting does not necessarily depend on the presence of the normal triplet termination signal.
鼠伤寒沙门氏菌中由tufA8和tufB103编码的延伸因子Tu的突变形式可抑制部分而非全部移码突变。鼠伤寒沙门氏菌中所有被抑制的突变其移码窗口均以终止密码子UGA结尾。由于tufA8和tufB103都是中等效率的UGA抑制子，我们探究移码效率是否受UGA处错读水平的影响。我们将合成任一释放因子的质粒导入tuf突变抑制测试移码突变的菌株中。我们发现，释放因子2（催化UGA和UAA处的释放）的过量表达在所有测试位点均降低了由tuf突变促进的移码。然而，在其中一个位点trpE91，释放因子1的过量表达也降低了抑制作用。携带释放因子2质粒的菌株中，trpE三个均以UGA结尾位点的移码“渗漏”自发水平降低。我们得出结论，自发的和抑制子增强的读码框移位均受肽链释放因子活性的影响。然而，数据表明释放因子对移码的影响不一定取决于正常三联体终止信号的存在。
