Childs J D
J Virol. 1973 Jan;11(1):1-8. doi: 10.1128/JVI.11.1.1-8.1973.
The genetic basis of superinfection exclusion by bacteriophage T4 was investigated by using incomplete genomes derived from the gene 66 mutant E920g. Incomplete genomes, which included a region of T4 between genes 42 and 44, were able to exclude superinfecting phage with an efficiency similar to that of complete genomes. Those genomes which did not include this region were unable to exclude superinfecting phage. A mutant with reduced ability to exclude super-infecting phage was isolated after mutagenesis with hydroxylamine. The mutation maps midway between amN122 in gene 42 and amB22 in gene 43. The efficiency of exclusion of superinfecting phage (as measured by the percentage of superinfected cells which failed to release any phage carrying selected markers of the superinfecting phage) by this mutant was 50 to 60%, whereas for wild type it was 85 to 95%. Uptake of (3)H-leucine by cells infected with the mutant was inhibited by superinfection with ghosts and it has therefore been designated imm1, for lack of immunity to superinfecting phage and ghosts. The formation of infective centers by cells infected with imm1 or another imm(-) mutant (imm2) was not inhibited by superinfection with ghosts.
利用源自基因66突变体E920g的不完整基因组,研究了噬菌体T4进行超感染排除的遗传基础。包含T4基因42和44之间区域的不完整基因组能够以与完整基因组相似的效率排除超感染噬菌体。那些不包含该区域的基因组则无法排除超感染噬菌体。在用羟胺诱变后,分离出了一个排除超感染噬菌体能力降低的突变体。该突变位于基因42中的amN122和基因43中的amB22之间的中间位置。该突变体排除超感染噬菌体的效率(通过未能释放携带超感染噬菌体选定标记的任何噬菌体的超感染细胞百分比来衡量)为50%至60%,而野生型的效率为85%至95%。被突变体感染的细胞对³H-亮氨酸的摄取受到空斑超感染的抑制,因此它被命名为imm1,意思是对超感染噬菌体和空斑缺乏免疫力。被imm1或另一个imm(-)突变体(imm2)感染的细胞形成感染中心不受空斑超感染的抑制。