Levine M, Chakravorty M, Bronson M J
J Virol. 1970 Oct;6(4):400-5. doi: 10.1128/JVI.6.4.400-405.1970.
A replication complex for the vegetative synthesis of the deoxyribonucleic acid (DNA) of the temperate phage P22 previously has been described. This complex is an association of parental phage DNA, most of the newly synthesized phage DNA made during pulses with (3)H-thymidine, and other cell constituents, and has a sedimentation rate in neutral sucrose gradients of at least 1,000S. The complex is one of the intermediates, intermediate I, in the synthesis and maturation of phage P22 DNA after infection or induction. Evidence supporting the replicative nature of intermediate I is presented. Phage replication is repressed in lysogenic bacteria. On superinfection of P22 lysogens with nonvirulent phage, little association of the input phage DNA with a rapidly sedimenting fraction is demonstrable. However, after induction with ultraviolet light, the superinfecting parental phage DNA quickly acquires the rapid sedimentation rate characteristic of intermediate I; phage DNA synthesis follows; and progeny phages are produced. Infection with a virulent mutant of P22 produces progeny phages in lysogens. Its DNA associates with intermediate I. In mixed infection with the virulent phage, replication of nonvirulent phage P22 is still repressed, even though the virulent replicates normally. The nonvirulent input DNA does not associate with intermediate I. The repressor of the lysogenic cell prevents replication by interfering with the physical association of template material with intermediate I. A phage function is required for association of phage template with the replication machinery.
先前已描述了用于温和噬菌体P22的脱氧核糖核酸(DNA)营养合成的复制复合体。该复合体是亲本噬菌体DNA、脉冲期间用(3)H-胸苷合成的大部分新合成噬菌体DNA以及其他细胞成分的结合体,在中性蔗糖梯度中的沉降速率至少为1000S。该复合体是感染或诱导后噬菌体P22 DNA合成和成熟过程中的中间体之一,即中间体I。文中提供了支持中间体I具有复制性质的证据。噬菌体复制在溶原性细菌中受到抑制。用无毒噬菌体对P22溶原菌进行超感染时,几乎无法证明输入的噬菌体DNA与快速沉降组分有结合。然而,用紫外线诱导后,超感染的亲本噬菌体DNA迅速获得中间体I特有的快速沉降速率;随后进行噬菌体DNA合成;并产生子代噬菌体。用P22的毒性突变体感染溶原菌会产生子代噬菌体。其DNA与中间体I结合。在与毒性噬菌体的混合感染中,无毒噬菌体P22的复制仍然受到抑制,尽管毒性噬菌体正常复制。无毒的输入DNA不与中间体I结合。溶原性细胞的阻遏物通过干扰模板物质与中间体I的物理结合来阻止复制。噬菌体模板与复制机制的结合需要一种噬菌体功能。