Nisioka T, Ozeki H
J Virol. 1968 Nov;2(11):1249-54. doi: 10.1128/JVI.2.11.1249-1254.1968.
Growth of phage BF23 was restricted in Escherichia coli K-12 strains carrying a colicin I factor (ColIb); most infected cells lysed early without producing progeny phages. Either addition of chloramphenicol before phage infection or ultraviolet irradiation of phage prevented early abortive lysis, an indication that certain phage functions are required for this phenomenon. Very little or no phage-induced lysozyme was synthesized in the infected ColI(+) cells. This result suggests that early abortive lysis was not due to the lysozyme action. A small fraction (0.05) of BF23-infected ColI(+) cells showed normal phage growth. This "escaped growth" may reflect the physiological state of the host bacteria rather than the heterogeneity of the infecting phage. Host-controlled modification was not observed. A phage mutant, BF23hI, able to grow on ColI(+) cells, was isolated and was characterized to be recessive to the wild-type BF23 in its ability to undergo early abortive lysis. Among the T series phages, T5 induced early abortive lysis, and growth of T5 was restricted upon infection to ColI(+) cells. These results and the other observations, including the occurrence of phenotypic mixing between BF23 and T5, suggest that these two phages are related to each other even though the receptor sites for BF23 and T5 are apparently different.
噬菌体BF23在携带大肠杆菌素I因子(ColIb)的大肠杆菌K - 12菌株中的生长受到限制;大多数被感染的细胞早期裂解,不产生子代噬菌体。在噬菌体感染前添加氯霉素或对噬菌体进行紫外线照射可防止早期流产性裂解,这表明该现象需要某些噬菌体功能。在被感染的ColI(+)细胞中,很少或几乎不合成噬菌体诱导的溶菌酶。这一结果表明早期流产性裂解不是由于溶菌酶的作用。一小部分(0.05)被BF23感染的ColI(+)细胞显示出正常的噬菌体生长。这种“逃逸生长”可能反映了宿主细菌的生理状态,而不是感染噬菌体的异质性。未观察到宿主控制的修饰。分离出一种能够在ColI(+)细胞上生长的噬菌体突变体BF23hI,其在经历早期流产性裂解的能力方面对野生型BF23呈隐性。在T系列噬菌体中,T5诱导早期流产性裂解,并且T5感染ColI(+)细胞时生长受到限制。这些结果以及包括BF23和T5之间发生表型混合在内的其他观察结果表明,尽管BF23和T5的受体位点明显不同,但这两种噬菌体彼此相关。