Rudé J M, Doudney C O
J Bacteriol. 1974 Jul;119(1):123-8. doi: 10.1128/jb.119.1.123-128.1974.
The ultraviolet resistance of a streptolydigin-susceptible strain of Escherichia coli B/r hcr(-) increased during preirradiation treatment with streptolydigin (an inhibitor of deoxyribonucleic acid-dependent ribonucleic acid polymerase) for 20 min and then remained constant. During preirradiation treatment with chloramphenicol (an inhibitor of protein synthesis), resistance to ultraviolet light increased for 1 to 2 h, and reached a maximal level significantly above that attained in streptolydigin-containing medium. These results suggest that there are two mechanisms that function in Hcr(-) cells during chloramphenicol treatment which contribute to the concomitant ultraviolet resistance enhancement. One is ribonucleic acid dependent and is inhibited by streptolydigin. This ribonucleic acid-dependent mechanism appears to be absent in wild-type and RecA E. coli B/r strains.
对链霉溶菌素敏感的大肠杆菌B/r hcr(-)菌株在接受链霉溶菌素（一种依赖脱氧核糖核酸的核糖核酸聚合酶抑制剂）预辐照处理20分钟期间，其抗紫外线能力增强，之后保持恒定。在用氯霉素（一种蛋白质合成抑制剂）进行预辐照处理期间，对紫外线的抗性增强1至2小时，并达到显著高于含链霉溶菌素培养基中所达到的最高水平。这些结果表明，在氯霉素处理期间，Hcr(-)细胞中有两种机制发挥作用，有助于同时增强抗紫外线能力。一种是依赖核糖核酸的，且受链霉溶菌素抑制。这种依赖核糖核酸的机制在野生型和RecA大肠杆菌B/r菌株中似乎不存在。
