Dowden S B, Glazebrook J A, Strike P
Mol Gen Genet. 1984;193(2):316-21. doi: 10.1007/BF00330687.
The UV protection and mutation properties of the I group plasmid TP110 have been investigated. It is demonstrated that the genes responsible for these effects are able to complement the deficiency in umuC36 mutants of E. coli, as are the similar genes carried by the B group plasmid R16. Mu-lac inserts into TP110 have been isolated which abolish the UV protection and mutation functions. Restriction mapping of these inserts locates them within a single region of the genome. A comparison of the restriction sites of this region with the muc region of pKM101 reveals very little similarity. Expression of beta-galactosidase in those Mu-lac inserts in which the lacZ gene is fused to the promoter for the protection and mutation functions is inducible by DNA damaging agents, and induction in mutant strains suggests that these genes are under the direct control of the lexA repressor.
对I组质粒TP110的紫外线防护和诱变特性进行了研究。结果表明，负责这些效应的基因能够弥补大肠杆菌umuC36突变体中的缺陷，B组质粒R16携带的类似基因也能如此。已分离出插入TP110的Mu - lac，其消除了紫外线防护和诱变功能。这些插入片段的限制性图谱将它们定位在基因组的单个区域内。该区域的限制性位点与pKM101的muc区域的比较显示出很少的相似性。在那些lacZ基因与防护和诱变功能的启动子融合的Mu - lac插入片段中，β - 半乳糖苷酶的表达可被DNA损伤剂诱导，并且在突变菌株中的诱导表明这些基因受lexA阻遏物的直接控制。
