Bruner R, Souther A, Suggs S
J Virol. 1972 Jul;10(1):88-92. doi: 10.1128/JVI.10.1.88-92.1972.
When T-even phage infect Escherichia coli, synthesis of host deoxyribonucleic acid (DNA) rapidly ceases. If the phage carry a mutation in a gene essential for phage DNA synthesis, then the infected bacteria should make no DNA, either host DNA or phage DNA. However, we have found that infection with certain T4 gene 56 (deoxycytidine triphosphatase)-rII double mutants leads to substantial DNA synthesis. Only rII deletion mutations which extend into the middle third of the adjacent, nonessential D region lead to the anomalous DNA synthesis, when combined with a gene 56 mutation; the requirement probably is that the deletion extend into the D2a transcriptional unit identified by Sederoff et al. Genetic evidence indicates that the observed anomalous DNA synthesis is synthesis of phage DNA. We suggest that the D2a region controls, directly or indirectly, a nuclease involved in the breakdown of cytosine-containing DNA. In the absence of the D2a product, the cytosine-containing phage DNA made by the gene 56 mutant is stabilized.
当T偶数噬菌体感染大肠杆菌时,宿主脱氧核糖核酸(DNA)的合成会迅速停止。如果噬菌体在噬菌体DNA合成所必需的基因中发生突变,那么受感染的细菌就不会合成DNA,无论是宿主DNA还是噬菌体DNA。然而,我们发现,用某些T4基因56(脱氧胞苷三磷酸酶)-rII双突变体进行感染会导致大量的DNA合成。只有当与基因56突变结合时,延伸到相邻非必需D区域中间三分之一的rII缺失突变才会导致异常的DNA合成;可能的要求是缺失延伸到由塞德罗夫等人确定的D2a转录单位。遗传学证据表明,观察到的异常DNA合成是噬菌体DNA的合成。我们认为,D2a区域直接或间接控制一种参与含胞嘧啶DNA分解的核酸酶。在没有D2a产物的情况下,由基因56突变体产生的含胞嘧啶噬菌体DNA会得到稳定。