Ruiz-Rubio M, Bridges B A
MRC Cell Mutation Unit, University of Sussex, Falmer, Brighton, UK.
Mol Gen Genet. 1987 Jul;208(3):542-8. doi: 10.1007/BF00328153.
We introduced the dnaE486 and polC74 mutations (which are associated with decreased DNA polymerase III replication fidelity) into excision defective Escherichia coli strains with varying SOS responses. These mutations increased the UV-induced frequency of base pair substitution mutations in all strains tested, except recA430 and umuC122 derivatives. This UV mutator effect therefore requires expression of the SOS error-prone repair system. In recA441 lexA51 strains where the SOS system is constitutively expressed, the UV mutator effect of the dnaE alleles was similar in relative terms (though greater in absolute terms). Since these dnaE alleles decrease rather than increase survival after UV it is argued that they promote a burst of untargeted mutations close to UV photoproducts ("hitch-hiking" mutations) rather than increase the number of translesion synthesis events. The fact that there was no UV mutagenesis in dnaE486 umuC122 or polC74 umuC122 strains indicates that infidelity associated with these dnaE alleles did not of itself enable translesion synthesis to occur. The spontaneous mutator effect conferred by dnaE486 and polC74 was not affected by umuC122 or recA430 indicating that it is not dependent upon error-prone repair ability. In recA441 lexA51 bacteria, where SOS error-prone repair is constitutively induced, the mutator effect of dnaE486 was greater and was largely blocked by umuC122. It is suggested that spontaneously occurring cryptic lesions that are themselves unable to induce the SOS system are subject to translesion synthesis under these conditions and trigger a burst of hitch-hiking mutations that are therefore effectively umuC dependent.
我们将dnaE486和polC74突变(这两个突变与DNA聚合酶III复制保真度降低相关)引入具有不同SOS反应的切除缺陷型大肠杆菌菌株中。这些突变增加了紫外线诱导所有测试菌株中的碱基对替换突变频率,但recA430和umuC122衍生物除外。因此,这种紫外线诱变效应需要易错SOS修复系统的表达。在SOS系统组成型表达的recA441 lexA51菌株中,dnaE等位基因的紫外线诱变效应相对相似(尽管绝对值更大)。由于这些dnaE等位基因降低而非增加紫外线照射后的存活率,有人认为它们促进了靠近紫外线光产物处的大量非靶向突变(“搭便车”突变),而非增加跨损伤合成事件的数量。dnaE486 umuC122或polC74 umuC122菌株中不存在紫外线诱变这一事实表明,与这些dnaE等位基因相关的保真度下降本身并不能使跨损伤合成发生。dnaE486和polC74赋予的自发诱变效应不受umuC122或recA430的影响,表明它不依赖于易错修复能力。在组成型诱导SOS易错修复的recA441 lexA51细菌中,dnaE486的诱变效应更大,并且在很大程度上被umuC122阻断。有人提出,在这些条件下,自身无法诱导SOS系统的自发隐匿性损伤会经历跨损伤合成,并引发大量搭便车突变,因此这些突变实际上依赖于umuC。