Uncoupling of late transcription from DNA replication in bacteriophage T4 development.
Uncoupling of late transcription from DNA replication in bacteriophage T4 development.
复制标题
噬菌体 T4 发育中晚期转录与 DNA 复制的解偶联。
DOI：
10.1016/0022-2836(70)90448-1
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发表时间：
1970
影响因子：
5.6
通讯作者：
E. Geiduschek
中科院分区：
文献类型：
--
作者：
S. Riva;A. Cascino;E. Geiduschek
已经探索了将T4晚期转录与并行复制解偶联的条件。当病毒DNA未被糖基化时，复制-晚期转录偶联被保留。偶联也保留在已经用噬菌体T3预感染的细菌中。已知后者诱导水解S-腺苷甲硫氨酸的酶的合成，S-腺苷甲硫氨酸是DNA甲基化中的甲基供体。然而，为了证明连接对复制-晚期转录偶联的这种作用，有必要防止未连接的DNA的溶核降解。这是通过引入基因46突变来实现的。Thustsgene 43（DNA聚合酶）-tsoramgene 30（DNA连接酶）-amgene 46突变体已被发现在缺乏连续DNA合成的情况下产生晚期信使、尾纤维蛋白和溶菌酶。这些DNA的亲本未复制DNA也可以作为晚期转录的模板，并伴随着单链断裂。在此基础上，提出了一个晚转录的DNA“能力”模型。(1)感受态DNA含有中断（断裂或缺口），这对于T4晚期RNA转录的结合起始步骤是必不可少的。(2)缺口是由核酸内切酶作用或作为不连续复制的直接结果产生的。(3)DNA连接酶封闭这些中断并负性地控制晚期转录。
The conditions for uncoupling T4 late transcription from concurrent replication have been explored. Replication-late transcription coupling is retained when viral DNA is not glucosylated. Coupling is also retained in bacteria that have been pre-infected with phage T3. The latter are known to induce the synthesis of an enzyme that hydrolysesS-adenosylmethionine, the methyl group donor in DNA methylation. However, in order to demonstrate this effect of ligation on replication-late transcription coupling it is necessary to prevent nucleolytic degradation of unligated DNA. This has been done by introducing a gene 46 mutation. Thustsgene 43 (DNA polymerase)-tsoramgene 30 (DNA ligase)-amgene 46 mutants have been found to make late messenger, tail fiber protein and lysozyme in the absence of continuing DNA synthesis. The parental, unreplicated DNA of these phages can also serve as a template for late transcription and concomitantly undergoes single-strand scissions. A model of DNA “competence” for late transcription is proposed on the basis of these observations. (1) Competent DNA contains interruptions (breaks or gaps) that are essential for the binding-initiation steps of T4 late RNA transcription. (2) Gaps are created by endonuclease action or as the direct consequence of discontinuous replication. (3) DNA ligase seals these interruptions and controls late transcription negatively.