Dobson P P, Walker G C
Mutat Res. 1980 Jun;71(1):25-41. doi: 10.1016/0027-5107(80)90004-4.
In Escherichia coli K12 the reactivation of UV-irradiated phage in UV-irradiated cells (Weigle reactivation) is inhibited if the protein synthesis inhibitor chloramphenicol is present during the post-irradiation incubation. In contrast, in E. coli K12 or Salmonella typhimurium LT2 containing the plasmid pKM101 the kinetics of the W-reactivation response were not affected by chloramphenicol. Under the conditions used, protein synthesis was greater than 99% inhibited and no preferential synthesis of plasmid-coded proteins was apparent in the residual protein synthesis. This increased capacity to reactivate irradiated phage decayed over 2 h if the cells were allowed to grow but was relatively stable if they were incubated in 10 mM MgSO4. Whereas the capacity of UV-irradiated bacteria with or without pKM101 to carry out W-reactivation had largely decayed by the end of a 2 h post-irradiation incubation in minimal-glucose with chloramphenicol, the capacity to synthesize high levels of the recA protein had not. Post-irradiation treatment with chloramphenicol did not abolish the UV-protective effect of pKM101 or R46. pKM101-mediated W-reactivation is recA+-dependent in S. typhimurium and recA+ lexA+-dependent in E. coli K-12. The inefficiency of S. typhimurium LT2 relative to E. coli in carrying out W-reactivation is not due to the presence of the cryptic plasmid in the LT2 strains. Two possible models are discussed.
在大肠杆菌K12中，如果在辐射后培养期间存在蛋白质合成抑制剂氯霉素，那么在紫外线照射的细胞中紫外线照射的噬菌体的再活化（韦格勒再活化）会受到抑制。相比之下，在含有质粒pKM101的大肠杆菌K12或鼠伤寒沙门氏菌LT2中，W再活化反应的动力学不受氯霉素影响。在所使用的条件下，蛋白质合成受到超过99%的抑制，并且在残留的蛋白质合成中没有明显的质粒编码蛋白质的优先合成。如果让细胞生长，这种增加的再活化受辐射噬菌体的能力在2小时内衰减，但如果将它们在10 mM硫酸镁中培养则相对稳定。在含有或不含有pKM101的紫外线照射细菌进行W再活化的能力在含有氯霉素的最低限度葡萄糖培养基中辐射后2小时培养结束时已基本衰减，但合成高水平recA蛋白的能力并未衰减。辐射后用氯霉素处理并没有消除pKM101或R46的紫外线保护作用。在鼠伤寒沙门氏菌中，pKM101介导的W再活化依赖于recA +，在大肠杆菌K - 12中依赖于recA + lexA +。鼠伤寒沙门氏菌LT2相对于大肠杆菌在进行W再活化方面效率较低并不是由于LT2菌株中存在隐蔽质粒。讨论了两种可能的模型。
