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首页> 外文期刊>Journal of Virology >Bacteriophage-induced Inhibition of Host Functions II. Evidence for Multiple, Sequential Bacteriophage-induced Deoxyribonucleases Responsible for Degradation of Cellular Deoxyribonucleic Acid
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Bacteriophage-induced Inhibition of Host Functions II. Evidence for Multiple, Sequential Bacteriophage-induced Deoxyribonucleases Responsible for Degradation of Cellular Deoxyribonucleic Acid

机译：噬菌体诱导的宿主功能抑制II。多种序贯的噬菌体诱导的脱氧氧核酸酶负责细胞脱氧核糖核酸降解的证据

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摘要

Degradation of bacterial deoxyribonucleic acid (DNA) after infection with T4 bacteriophage was studied in an endonuclease I-deficient host. The kinetics of degradation were similar to those seen in other hosts with a normal level of this enzyme. Irradiation of extracellular phage with ultraviolet (UV) destroyed the capacity of the infecting virus to induce extensive breakdown of host DNA, which was, however, converted to high-molecular-weight material. Addition of chloramphenicol to T4-infected cells provided data which can be interpreted to indicate the involvement of at least two endodeoxyribonucleases and one exodeoxyribonuclease having a high degree of specificity. A model is proposed showing the sequential action of two endodeoxyribonucleases followed by an exodeoxyribonuclease in the degradation of host DNA. The appearance of these hydrolytic enzymes requires protein synthesis. Infections leading to partial degradation only (UV-irradiated phages, gene 46 mutants) effectively inhibited the synthesis of bacterial messenger ribonucleic acid and of β-galactosidase.
机译：在核酸酶I缺陷型宿主中研究了用T4噬菌体感染后细菌脱氧核糖核酸（DNA）的降解。降解的动力学与在其他酶的正常水平中看到的那些。用紫外线（UV）的细胞外噬菌体的照射破坏了感染病毒诱导宿主DNA广泛突破的能力，然而，转化为高分子量材料。向T4感染细胞添加氯霉素提供了可以解释的数据，以指示至少两个掺脱氧基菌素酶和具有高特异性的过脱氧基核酸酶的累积。提出了一种模型，显示了两种掺脱氧罗布脲酶的顺序作用，然后在宿主DNA的降解中进行过脱氧基核酸酶。这些水解酶的外观需要蛋白质合成。仅导致部分降解的感染（UV辐照噬菌体，基因46突变体）有效地抑制了细菌信使核糖核酸和β-半乳糖苷酶的合成。

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