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噬菌体诱导的宿主功能抑制。II. 多种连续的噬菌体诱导的脱氧核糖核酸酶导致细胞脱氧核糖核酸降解的证据。

Bacteriophage-induced inhibition of host functions. II. Evidence for multiple, sequential bacteriophage-induced deoxyribonucleases responsible for degradation of cellular deoxyribonucleic acid.

作者信息

Bose S K, Warren R J

出版信息

J Virol. 1969 Jun;3(6):549-56. doi: 10.1128/JVI.3.6.549-556.1969.

Abstract

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 beta-galactosidase.

摘要

在一个缺乏核酸内切酶I的宿主中研究了T4噬菌体感染后细菌脱氧核糖核酸(DNA)的降解情况。降解动力学与在该酶水平正常的其他宿主中观察到的相似。用紫外线(UV)照射细胞外噬菌体破坏了感染病毒诱导宿主DNA广泛降解的能力,不过,宿主DNA被转化为高分子量物质。向感染T4的细胞中添加氯霉素提供的数据可以解释为表明至少有两种内切脱氧核糖核酸酶和一种具有高度特异性的外切脱氧核糖核酸酶参与其中。提出了一个模型,显示在宿主DNA降解过程中两种内切脱氧核糖核酸酶随后是一种外切脱氧核糖核酸酶的顺序作用。这些水解酶的出现需要蛋白质合成。仅导致部分降解的感染(紫外线照射的噬菌体、基因46突变体)有效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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