Farrell L D, Reiter H
Can J Microbiol. 1976 May;22(5):645-53. doi: 10.1139/m76-095.
Phleomycin-stimulated solubilization of Escherichia coli DNA is inhibited by infecting the cells with mutants of bacteriophage T4 before treatment with the antibiotic, inhibition requiring phage-specified protein synthesis. Two different modes of inhibition can be differentiated by infecting with mutants which are defective in an early state (gene den A-; endonuclease II-independent inhibition) or a late stage (gene 46-; endonuclease II-dependent inhibition) of phage-directed degradation of host DNA. Endonuclease II-independent inhibition results from interference with phleomycin-induced release of host DNA from the cytoplasmic membrane. In the presence of endonuclease II, the host DNA is converted to fragments, with average molecular weights of 10(6) daltons, the further degradation of which is not promoted by continuous exposure of the cells to phleomycin.
在用抗生素处理之前,用噬菌体T4的突变体感染大肠杆菌细胞,可抑制博来霉素刺激的大肠杆菌DNA溶解,这种抑制作用需要噬菌体指定的蛋白质合成。通过用在噬菌体指导的宿主DNA降解的早期状态(基因den A-;不依赖于核酸内切酶II的抑制)或晚期状态(基因46-;依赖于核酸内切酶II的抑制)有缺陷的突变体进行感染,可以区分两种不同的抑制模式。不依赖于核酸内切酶II的抑制是由于干扰了博来霉素诱导的宿主DNA从细胞质膜的释放。在核酸内切酶II存在的情况下,宿主DNA被转化为平均分子量为10^6道尔顿的片段,细胞持续暴露于博来霉素不会促进这些片段的进一步降解。