Moyer R W, Fu A S, Szabo C
J Virol. 1972 May;9(5):804-12. doi: 10.1128/JVI.9.5.804-812.1972.
The I-type colicinogenic factor ColIb transforms Escherichia coli from a permissive to a nonpermissive host for bacteriophage T5 reproduction by preventing complete expression of the phage genome. T5-infected ColIb(+) cells synthesize only class I (early) phage protein and ribonucleic acid (RNA). Neither phage-specific class II proteins [associated with viral deoxyribonucleic acid (DNA) replication] nor class III proteins (phage structural components) are formed due to the failure of the infected ColIb(+) cells to synthesize class II or class III phage-specific messenger RNA. Comparable studies with T5-infected cells colicinogenic for the related ColIa factor revealed no decrease in the yield of progeny phage although the presence of the ColIa factor leads to a significant reduction in the amount of phage-directed class III protein synthesis.
I型产大肠杆菌素因子ColIb通过阻止噬菌体基因组的完全表达，将大肠杆菌从噬菌体T5繁殖的允许宿主转变为非允许宿主。被T5感染的ColIb(+)细胞仅合成I类（早期）噬菌体蛋白和核糖核酸（RNA）。由于被感染的ColIb(+)细胞无法合成II类或III类噬菌体特异性信使RNA，因此既不形成与病毒脱氧核糖核酸（DNA）复制相关的噬菌体特异性II类蛋白，也不形成III类蛋白（噬菌体结构成分）。对携带相关ColIa因子产大肠杆菌素的、被T5感染的细胞进行的类似研究表明，尽管ColIa因子的存在导致噬菌体导向的III类蛋白合成量显著减少，但子代噬菌体的产量并未降低。
