Kenyon C J, Walker G C
Proc Natl Acad Sci U S A. 1980 May;77(5):2819-23. doi: 10.1073/pnas.77.5.2819.
Operon fusions in Escherichia coli were obtained that showed increased beta-galactosidase expression in response to treatment with the DNA-damaging agent mitomycin C. These fusions were generated by using the Mud(ApR, lac) vector [Casadaban, M.J. & Cohen, S.N. (1979) Proc. Natl. Acad. Sci. USA 76, 4530-4533] to insert the lactose structural genes randomly into the bacterial chromosome. Induction of beta-galactosidase in these strains, which carried fusions of lac to these din (damage-inducible) loci, was (i) triggered by UV light as well as by mitomycin C and (ii) abolished by either a recA- or a lexA- mutation. Similar characteristics of induction were observed when the lactose genes were fused to a prophage lambda promoter by using Mud(ApR, lac). These results indicate that E. coli contains a set of genes that, like prophage lambda genes, are expressed in response to DNA-damaging agents and regulated by the recA and lexA gene products. These din genes map at five bacterial loci. One din::Mud(ApR, lac) insertion results in a UV-sensitive phenotype and may be within the uvrA transcriptional unit.
在大肠杆菌中获得了操纵子融合体，这些融合体在受到DNA损伤剂丝裂霉素C处理时，β-半乳糖苷酶表达增加。这些融合体是通过使用Mud（ApR，lac）载体[卡萨达班，M.J.和科恩，S.N.（1979年）《美国国家科学院院刊》76，4530 - 4533]将乳糖结构基因随机插入细菌染色体而产生的。在这些携带lac与这些din（损伤诱导型）位点融合的菌株中，β-半乳糖苷酶的诱导（i）由紫外线以及丝裂霉素C触发，并且（ii）被recA或lexA突变消除。当使用Mud（ApR，lac）将乳糖基因与原噬菌体λ启动子融合时，观察到了类似的诱导特征。这些结果表明，大肠杆菌含有一组基因，这些基因与原噬菌体λ基因一样，在受到DNA损伤剂作用时表达，并受recA和lexA基因产物调控。这些din基因定位于五个细菌位点。一个din::Mud（ApR，lac）插入导致对紫外线敏感的表型，并且可能位于uvrA转录单位内。
