Friedman S O, Hemphill H E
J Virol. 1976 Jun;18(3):839-47. doi: 10.1128/JVI.18.3.839-847.1976.
Wild-type bacteriophage phie and IS (interference-sensitive) mutants of the related phage SP82G did not productively infect strains of Bacillus subtilis that were lysogenic for temperate phage SPO2. In these abortive infections, the sensitive phages adsorbed to and penetrated the nonpermissive host, phage-directed macromolecular syntheses were initiated, but both viral and bacterial nucleic acid production abruptly stopped about 15 min after addition of the phages. The cessation of RNA and DNA synthesis was preceded or coincident with a reduction in oxygen utilization by the infected cultures. Genetic studies of both phie and SP82G suggest sensitivity to SPO2-mediated abortive infection was controlled by a single gene. A mutant of SPO2, SPO2ehp4-, lysogens of which no longer interfere with the development of SP82GIs, was also isolated. The discovery of this ehp- variant suggests the normal SPO2 prophage synthesized a substance that alters cell physiology in some manner detrimental to SP82GIs development. Since SPO2ehp4- grew on and lysogenized bacteria sensitive to wild-type SPO2, the product of the eph gene was apparently not an essential function of this temperate phage.Overall, these observations exhibit remarkable similarities to the inhibition of T4rII mutants by the product of the rex gene of phage lambda.
野生型噬菌体phie以及相关噬菌体SP82G的IS(干扰敏感型)突变体不能有效感染因温和噬菌体SPO2而溶源化的枯草芽孢杆菌菌株。在这些流产感染中,敏感噬菌体吸附并穿透了非允许宿主,启动了噬菌体指导的大分子合成,但在加入噬菌体约15分钟后,病毒和细菌核酸的产生突然停止。RNA和DNA合成的停止先于或与受感染培养物中氧气利用的减少同时发生。对phie和SP82G的遗传学研究表明,对SPO2介导的流产感染的敏感性由单个基因控制。还分离出了SPO2的一个突变体SPO2ehp4-,其溶源菌不再干扰SP82GIs的发育。这种ehp-变体的发现表明,正常的SPO2原噬菌体合成了一种物质,该物质以某种对SP82GIs发育有害的方式改变细胞生理学。由于SPO2ehp4-能在对野生型SPO2敏感的细菌上生长并使其溶源化,eph基因的产物显然不是这种温和噬菌体的必需功能。总体而言,这些观察结果与噬菌体λ的rex基因产物对T4rII突变体的抑制作用有显著相似之处。