Wallace S S, Melamede R J
J Virol. 1972 Dec;10(6):1159-69. doi: 10.1128/JVI.10.6.1159-1169.1972.
T4+ exhibits increased ultraviolet sensitivity on derivatives of Escherichia coli K12 or B lacking deoxyribonucleic acid (DNA) polymerase I. However, the sensitivity of T4v is not affected by the absence of host DNA polymerase. T4x and T4y also show increased sensitivity on DNA polymerase-deficient strains, but to a lesser extent than observed with wild-type T4. When T4x or T4y, but not T4+, are plated on a double mutant lacking both DNA polymerase and the uvrA gene product, a partial suppression of the polymerase effect is observed. Host ligase appears to be able to suppress to some extent the T4y phenotype but has no effect on wild-type T4 or other T4 mutants. T4xv incubated in E. coli B or B(s-1) in the presence of chloramphenicol (50 mug/ml) shows increased resistance over directly plated irradiated phage. Increased survival under the same conditions was not observed with T4+ or other T4 mutants. The repair of X-ray-damaged T4 was investigated by examining survival curves of T4+, T4x, T4y, T4ts43, and T4ts30. The repair processes were further defined by observing the effects of plating irradiated phage on various hosts including strains lacking DNA polymerase I or polynucleotide ligase. Two classes of effects were observed. Firstly, the x and y gene products seem to be involved in a repair system utilizing host ligase. Secondly, in the absence of host DNA polymerase, phage sensitivity is increased in an unknown manner which is enhanced by the presence of host uvrA gene product.
T4+在缺乏脱氧核糖核酸（DNA）聚合酶I的大肠杆菌K12或B的衍生物上表现出对紫外线的敏感性增加。然而，T4v的敏感性不受宿主DNA聚合酶缺失的影响。T4x和T4y在DNA聚合酶缺陷型菌株上也表现出敏感性增加，但程度低于野生型T4。当将T4x或T4y（而非T4+）接种在同时缺乏DNA聚合酶和uvrA基因产物的双突变体上时，可观察到对聚合酶效应的部分抑制。宿主连接酶似乎能够在一定程度上抑制T4y的表型，但对野生型T4或其他T4突变体没有影响。在氯霉素（50微克/毫升）存在的情况下，在大肠杆菌B或B(s - 1)中培养的T4xv对直接接种的经辐照噬菌体表现出更高的抗性。在相同条件下，T4+或其他T4突变体未观察到存活率增加。通过检查T4+、T4x、T4y、T4ts43和T4ts30的存活曲线来研究X射线损伤的T4的修复。通过观察将经辐照的噬菌体接种在各种宿主上的效果，包括缺乏DNA聚合酶I或多核苷酸连接酶的菌株，进一步确定了修复过程。观察到两类效应。首先，x和y基因产物似乎参与了利用宿主连接酶的修复系统。其次，在没有宿主DNA聚合酶的情况下，噬菌体敏感性以未知方式增加，并且宿主uvrA基因产物的存在会增强这种增加。
