Schendel P F, Fogliano M, Strausbaugh L D
J Bacteriol. 1982 May;150(2):676-85. doi: 10.1128/jb.150.2.676-685.1982.
The UV light inducibility of the uvrB operon of Escherichia coli K-12 was previously demonstrated by exploiting a strain in which the gene for the enzyme beta-galactosidase was inserted into the uvrB operon. This insert is now shown to be located within the structural gene for the uvrB enzyme, leaving the regulatory sequences of the operon intact. Analyses to quantitate the induction of this system show that derepression of the operon is first detectable 5 min after UV exposure, with the rate of synthesis increasing to four to six times the uninduced rate during the subsequent 30 min. Induction is unaffected by mutations in other components of nucleotide excision repair. The control of uvrB was found to result from direct repression by the lexA gene product, with the recA gene product playing an indirect role. Nucleotide excision repair thus seems to be part of the SOS response.
以前通过利用一种将β-半乳糖苷酶基因插入uvrB操纵子的菌株，证明了大肠杆菌K-12的uvrB操纵子的紫外线诱导性。现在表明该插入片段位于uvrB酶的结构基因内，而操纵子的调控序列保持完整。定量分析该系统的诱导情况表明，操纵子的去阻遏在紫外线照射后5分钟首次可检测到，随后30分钟内合成速率增加到未诱导速率的四到六倍。诱导不受核苷酸切除修复其他组分突变的影响。发现uvrB的调控是由lexA基因产物直接抑制导致的，recA基因产物起间接作用。因此，核苷酸切除修复似乎是SOS反应的一部分。
