DNA聚合酶III的ε亚基过量产生可抵消大肠杆菌的SOS诱变反应。
Overproduction of the epsilon subunit of DNA polymerase III counteracts the SOS mutagenic response of Escherichia coli.
作者信息
Jonczyk P, Fijalkowska I, Ciesla Z
机构信息
Institute of Biochemistry and Biophysics, Polish Academy of Sciences, Warsaw.
出版信息
Proc Natl Acad Sci U S A. 1988 Dec;85(23):9124-7. doi: 10.1073/pnas.85.23.9124.
Abstract
It has been found that the mutator phenotype of the recA441 and recA730 strains that express the SOS response constitutively is suppressed by pIP1, a high-copy plasmid carrying the dnaQ gene encoding the 3'----5' exonuclease subunit (epsilon) of DNA polymerase III. We have constructed plasmid pIP11, in which the dnaQ gene is fused to the strong tac (trp-lac) promoter. Enhanced synthesis of the epsilon subunit stimulated by isopropyl beta-D-thiogalactopyranoside, the inducer of tac, prevents expression of the mutator phenotype of recA441 and markedly decreases the frequency of UV-induced mutations. These results strongly suggest that a loss of editing capacity by the epsilon subunit of DNA polymerase III holoenzyme plays a crucial role in generation of mutations during the SOS response.
摘要
已发现持续表达SOS应答的recA441和recA730菌株的突变体表型被pIP1抑制，pIP1是一种携带编码DNA聚合酶III 3'→5'核酸外切酶亚基（ε）的dnaQ基因的高拷贝质粒。我们构建了质粒pIP11，其中dnaQ基因与强tac（trp-lac）启动子融合。由tac的诱导剂异丙基β-D-硫代半乳糖苷刺激的ε亚基的增强合成可阻止recA441突变体表型的表达，并显著降低紫外线诱导突变的频率。这些结果有力地表明，DNA聚合酶III全酶的ε亚基编辑能力的丧失在SOS应答期间的突变产生中起关键作用。
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