Finch P W, Brough C L, Emmerson P T
Gene. 1986;44(1):47-53. doi: 10.1016/0378-1119(86)90041-7.
A recombinant plasmid, pPF5, has been constructed which contains a 5.5-kb fragment of Methylophilus methylotrophus DNA inserted into pAT153, and which confers resistance to UV and mitomycin C (MC) upon Escherichia coli recA mutants. Hybridisation analysis indicates that sequence homology exists between the cloned DNA and a fragment of E. coli chromosomal DNA that contains the recA gene. Tn1000 insertions have been isolated within pPF5 that inactivate its ability to complement recA mutations, and the site of each insertion has been determined by restriction mapping. A 36-kDa protein is synthesised by pPF5 but not by any of the Tn1000 derivatives, indicating that this protein is the product of the gene responsible for the complementation. Comparison of the size of truncated polypeptides produced by selected pPF5::Tn1000 derivatives with the position of the insertion sites of the transposon, gave the direction of transcription of the M. methylotrophus recA+ gene. SOS proteins are induced in E. coli recA mutants harbouring pPF5 following MC treatment.
构建了一种重组质粒pPF5,它含有一段插入到pAT153中的甲基营养型嗜甲基菌DNA的5.5 kb片段,能赋予大肠杆菌recA突变体对紫外线和丝裂霉素C(MC)的抗性。杂交分析表明,克隆的DNA与大肠杆菌染色体DNA中包含recA基因的片段之间存在序列同源性。已在pPF5内分离出Tn1000插入片段,这些插入片段使其互补recA突变的能力失活,并且每个插入位点已通过限制性图谱分析确定。pPF5能合成一种36 kDa的蛋白质,但任何Tn1000衍生物都不能合成,这表明该蛋白质是负责互补作用的基因的产物。通过比较选定的pPF5::Tn1000衍生物产生的截短多肽的大小与转座子插入位点的位置,得出了甲基营养型嗜甲基菌recA⁺基因的转录方向。在用MC处理后,携带pPF5的大肠杆菌recA突变体中会诱导SOS蛋白。