Dimpfl J, Echols H
Department of Molecular Biology, University of California, Berkeley 94720.
Genetics. 1989 Oct;123(2):255-60. doi: 10.1093/genetics/123.2.255.
The SOS response in Escherichia coli involves the induction of a multioperon regulatory system, which copes with the presence of DNA lesions that interfere with DNA replication. Induction depends on activation of the RecA protein to cleave the LexA repressor of SOS operons. In addition to inducible DNA repair, the SOS system produces a large increase in the frequency of point mutations. To examine the possibility that other types of mutations are induced as part of the SOS response, we have studied the production of tandem duplications. To avoid the complications of indirect effects of the DNA lesions, we have activated the SOS response by a constitutive mutation in the recA gene, recA730. The introduction of the recA730 mutation results in an increase in duplications in the range of tenfold or greater, as judged by two different criteria. Based on its genetic requirements, the pathway for induced duplication formation is distinct from the point mutation pathway and also differs from the major normal recombination pathway. The induction of pathways for both duplications and point mutations shows that the SOS system produces a broad mutagenic response. We have suggested previously that many types of mutations might be induced by severe environmental stress, thereby enhancing genetic variation in an endangered population.
大肠杆菌中的SOS反应涉及一个多操纵子调节系统的诱导,该系统应对干扰DNA复制的DNA损伤的存在。诱导依赖于RecA蛋白的激活以切割SOS操纵子的LexA阻遏物。除了可诱导的DNA修复外,SOS系统还使点突变频率大幅增加。为了研究作为SOS反应一部分是否会诱导其他类型的突变,我们研究了串联重复的产生。为了避免DNA损伤间接影响的复杂性,我们通过recA基因中的组成型突变recA730激活了SOS反应。根据两种不同的标准判断,recA730突变的引入导致重复增加了十倍或更多。根据其遗传需求,诱导重复形成的途径不同于点突变途径,也不同于主要的正常重组途径。重复和点突变途径的诱导表明SOS系统产生广泛的诱变反应。我们之前曾提出,许多类型的突变可能由严重的环境压力诱导,从而增加濒危种群的遗传变异。