Halpern M, Mattson T, Kozinski A W
J Virol. 1982 May;42(2):422-31. doi: 10.1128/JVI.42.2.422-431.1982.
Through the use of the technique of hybridization to cloned genes, the site specificity of the reinitiation of T4 DNA replication was examined at late times after infection, when a large amount of DNA had accumulated in the infected cell. Replication was examined under two conditions; (i) when there was recombination but the repair of the recombinants was inhibited, and (ii) when recombination was followed by covalent joining. When no covalent repair of recombinant was allowed, reinitiation occurred in the areas known to be also involved in the initiation of replication of the parental molecule: thus late reinitiation, if covalent joining is prevented, is site specific. When there was covalent joining, reinitiation displayed no apparent site specificity. The results are discussed in light of the possibility that at late times after infection recombinant intersections act as primers. The similarity of the model proposed to the "break-and-copy" model for lambda phage and the fitness of the proposed model to the genetic phenomena described by others are emphasized.
通过运用与克隆基因杂交的技术，在感染后的较晚时期，即当大量DNA已在受感染细胞中积累时，对T4 DNA复制重新起始的位点特异性进行了检测。在两种条件下检测复制情况：（i）存在重组但重组体的修复受到抑制时；（ii）重组后进行共价连接时。当不允许对重组体进行共价修复时，重新起始发生在已知也参与亲代分子复制起始的区域：因此，如果阻止共价连接，后期重新起始具有位点特异性。当存在共价连接时，重新起始没有表现出明显的位点特异性。根据感染后较晚时期重组交叉点充当引物的可能性对结果进行了讨论。强调了所提出的模型与λ噬菌体的“断裂并复制”模型的相似性以及所提出的模型与其他人描述的遗传现象的契合度。
