Schmitt C K, Kemp P, Molineux I J
Department of Microbiology, University of Texas, Austin 78712-1095.
J Bacteriol. 1991 Oct;173(20):6507-14. doi: 10.1128/jb.173.20.6507-6514.1991.
Infections of F plasmid-containing strains of Escherichia coli by bacteriophage T7 result in membrane damage that allows nucleotides to exude from the infected cell into the culture medium. Only pifA of the F pif operon is necessary for "leakiness" of the T7-infected cell. Expression of either T7 gene 1.2 or gene 10 is sufficient to cause leakiness, since infections by phage containing null mutations in both of these genes do not result in permeability changes of the F-containing cell. Even in the absence of phage infection, expression from plasmids of either gene 1.2 or 10 can cause permeability changes, particularly of F plasmid-containing cells. In contrast, gene 1.2 of the related bacteriophage T3 prevents leakiness of the infected cell. In the absence of T3 gene 1.2 function, expression of gene 10 causes membrane damage that allows nucleotides to leak from the cell. Genes 1.2 and 10 of both T3 and T7 are the two genes involved in determining resistance or sensitivity to F exclusion; F exclusion and leakiness of the phage-infected cell are therefore closely related phenomena. However, since leakiness of the infected cell does not necessarily result in phage exclusion, it cannot be used as a predictor of an abortive infection.
噬菌体T7感染含F质粒的大肠杆菌菌株会导致膜损伤，使核苷酸从受感染细胞渗出到培养基中。F pif操纵子中只有pifA对于T7感染细胞的“渗漏”是必需的。T7基因1.2或基因10的表达足以导致渗漏，因为感染含有这两个基因无效突变的噬菌体不会导致含F细胞的通透性改变。即使在没有噬菌体感染的情况下，基因1.2或10从质粒表达也会导致通透性改变，特别是含F质粒的细胞。相比之下，相关噬菌体T3的基因1.2可防止受感染细胞渗漏。在没有T3基因1.2功能的情况下，基因10的表达会导致膜损伤，使核苷酸从细胞中泄漏。T3和T7的基因1.2和10是参与决定对F排除的抗性或敏感性的两个基因；因此，噬菌体感染细胞的F排除和渗漏是密切相关的现象。然而，由于受感染细胞的渗漏不一定导致噬菌体排除，它不能用作流产感染的预测指标。
