Shames R B, Lorkiewicz Z K, Kozinski A W
J Virol. 1973 Jul;12(1):1-8. doi: 10.1128/JVI.12.1.1-8.1973.
When UV-irradiated T4 bacteriophage (v(+)) infects in the presence of chloramphenicol, the phage DNA rapidly acquires single-stranded breaks proportional to the dose of UV. In contrast, when UV-irradiated T4 v(1) (radiation sensitive mutant) infects under identical conditions, the phage DNA remains integral. A series of coinfections with v(+) and v(1) phage (UV-v(1) + majority non-UV-v(+) and UV-v(+) and majority non-UV-v(1)) show that the enzyme responsible for breakage is injected by the phage. It is also demonstrated that the v(1) phage injects an inactive enzyme that delays breakage by the v(+) enzyme and interferes with subsequent repair. The cross of v(+) and v(1) phage produces mixed progeny that contain both active and inactive enzyme in a single capsid. The possible function of this breaking enzyme, necessitating injection of multiple copies, is considered.
当紫外线照射的T4噬菌体(v(+))在氯霉素存在的情况下进行感染时,噬菌体DNA会迅速出现与紫外线剂量成比例的单链断裂。相比之下,当紫外线照射的T4 v(1)(辐射敏感突变体)在相同条件下进行感染时,噬菌体DNA保持完整。一系列用v(+)和v(1)噬菌体进行的共感染实验(紫外线处理的v(1) + 大部分未紫外线处理的v(+)以及紫外线处理的v(+)和大部分未紫外线处理的v(1))表明,负责断裂的酶是由噬菌体注入的。还证明v(1)噬菌体注入一种无活性的酶,该酶会延迟v(+)酶引起的断裂,并干扰后续的修复过程。v(+)和v(1)噬菌体杂交产生的混合后代在单个衣壳中同时含有活性酶和无活性酶。本文考虑了这种断裂酶需要注入多个拷贝的可能功能。