Tokuno S I, Gough M
J Virol. 1975 Nov;16(5):1184-90. doi: 10.1128/JVI.16.5.1184-1190.1975.
A Polymyxin B-sensitive mutant of Salmonella typhimurium (Pox-1) channels all infecting wild-type P22 toward lysogenization. The efficiency of this channeling is sufficiently high that P22c+ (wild type) cannot form plaques on Pox-1; phage mutants defective in repressor synthesis (P22c1, c2, c3) or refractory toward repressor (P22vir B) can form plaques. The lytic growth of all phages which have a functional c1 gene is retarded in Pox-1; this retardation is seen even in phages which cannot make repressor. We present experiments which are consistent with the explanation that the retardation is an exaggeration of a normal regulatory event. In a wild-type host, P22 genes c1 and c3 products, host RNA polymerase, and other host factors (?) interact at a promotor site (c27) IN THE PHAGE DNA. This interaction promotes repressor synthesis and represses transcription of lytic genes. In the mutant Pox-1, a host product involved in viral DNA synthesis and transcription is altered. The altered host product results in stronger retardation of lytic gene transcription. The importance of this interaction in the decision between lysis and lysogeny is discussed. The mutant Pox-1 alters the expression or activity of another phage gene. Gene c3 product is absolutely required for lysogenization in this host, although it is not so required in wild-type S. typhimurium.
鼠伤寒沙门氏菌的多粘菌素B敏感突变体（Pox-1）能使所有感染的野生型P22噬菌体都趋向于溶原化。这种导向作用的效率足够高，以至于P22c+（野生型）无法在Pox-1上形成噬菌斑；在阻遏物合成方面有缺陷的噬菌体突变体（P22c1、c2、c3）或对阻遏物有抗性的噬菌体（P22vir B）能够形成噬菌斑。所有具有功能性c1基因的噬菌体在Pox-1中的裂解生长都会受到抑制；即使在那些无法产生阻遏物的噬菌体中也能观察到这种抑制现象。我们进行的实验与以下解释一致，即这种抑制是正常调节事件的一种夸张表现。在野生型宿主中，P22基因c1和c3的产物、宿主RNA聚合酶以及其他宿主因子（？）在噬菌体DNA中的一个启动子位点（c27）相互作用。这种相互作用促进阻遏物的合成并抑制裂解基因的转录。在突变体Pox-1中，一种参与病毒DNA合成和转录的宿主产物发生了改变。这种改变后的宿主产物导致裂解基因转录受到更强的抑制。讨论了这种相互作用在裂解和溶原化决策中的重要性。突变体Pox-1改变了另一个噬菌体基因的表达或活性。在这个宿主中，溶原化绝对需要基因c3的产物，尽管在野生型鼠伤寒沙门氏菌中并非如此。
