Goze A, Devoret R
Mutat Res. 1979 Jul;61(2):163-79. doi: 10.1016/0027-5107(79)90123-4.
In E. coli K12 bacteria carrying plasmid pKM101, prophage lambda was induced at UV doses higher than in plasmid-less parental bacteria. UV-induced reactivation per se was less effective. Bacteria with pKM101 showed no alteration in their division cycle. Plasmid pKM101 coded for a constitutive error-prone repair different from the inducible error-prone repair called SOS repair. Plasmid pKM101 protected E. coli bacteria from UV damage but slightly sensitized them to X-ray lesions. Protection against UV damage was effective in mutant bacteria deficient in DNA excision-repair provided that the recA, lexA and uvrE genes were functional. Survival of phages lambda and S13 after UV irradiation was enhanced in bacteria carrying plasmid pKM101; phage lambda mutagenesis was also increased. Plasmid pKM101 repaired potentially lethal DNA lesions, although wild-type DNA sequences may not necessarily be restored; hence the mutations observed are the traces of the original DNA lesions.
在携带质粒pKM101的大肠杆菌K12细菌中，与无质粒的亲代细菌相比，λ原噬菌体在更高的紫外线剂量下被诱导。紫外线诱导的复活本身效果较差。带有pKM101的细菌其分裂周期没有改变。质粒pKM101编码一种组成型易错修复，不同于被称为SOS修复的诱导型易错修复。质粒pKM101保护大肠杆菌免受紫外线损伤，但使其对X射线损伤稍有敏感。只要recA、lexA和uvrE基因功能正常，对紫外线损伤的保护在缺乏DNA切除修复的突变细菌中有效。携带质粒pKM101的细菌在紫外线照射后，λ噬菌体和S13噬菌体的存活率提高；λ噬菌体的诱变率也增加。质粒pKM101修复潜在的致死性DNA损伤，尽管不一定恢复野生型DNA序列；因此观察到的突变是原始DNA损伤的痕迹。
