Goodson M, Rowbury R J
J Gen Virol. 1987 Jul;68 ( Pt 7):1785-9. doi: 10.1099/0022-1317-68-7-1785.
Phages P1vir and P1cmclrf100 failed to form plaques on or multiply in Escherichia coli strains carrying the ColV,I-K94 plasmid; with P1cmclr100, the effect occurred both with phage from the lytic cycle and with that induced from a lysogen. The effect was on attachment, these P1 phages attaching poorly to ColV,I-K94+ strains. This receptor defect appeared to result mainly from the presence of ColV-encoded transfer and colicin components in the cells carrying ColV,I-K94 and it was specific to this plasmid. Phage Mu (which uses an attachment mechanism similar to that of phage P1) in the G(+) form attached to both Col- and ColV,I-K94+ strains but the G(-) form attached to neither type.
噬菌体P1vir和P1cmclrf100无法在携带ColV,I-K94质粒的大肠杆菌菌株上形成噬菌斑或在其中增殖;对于P1cmclr100,无论是来自裂解周期的噬菌体还是从溶原菌诱导产生的噬菌体,都会出现这种效应。这种效应发生在吸附阶段,这些P1噬菌体很难吸附到ColV,I-K94+菌株上。这种受体缺陷似乎主要是由于携带ColV,I-K94的细胞中存在ColV编码的转移和大肠杆菌素成分,并且这种缺陷是该质粒特有的。G(+)形式的噬菌体Mu(其使用与噬菌体P1类似的吸附机制)能吸附到Col-和ColV,I-K94+菌株上,但G(-)形式的噬菌体Mu对这两种类型的菌株均无吸附作用。