Chao J, Leach M, Karam J
J Virol. 1977 Nov;24(2):557-63. doi: 10.1128/JVI.24.2.557-563.1977.
Some mutations in the structural gene for T4 DNA polymerase (gene 43) behave as suppressors of a deficiency in T4 dCMP-hydroxymethylase (gene 42). The suppression appears to involve a functional interaction between the two enzymes at the level of DNA replication. The hydroxymethylase deficiency caused DNA structural abnormalities in replication, and DNA polymerase lesions appeared to partially reverse these abnormalities. The results do not necessarily imply protein-protein interactions between the two enzymes, although both enzymes appear to play roles in controlling the fidelity of phage DNA replication.
T4 DNA聚合酶(基因43)结构基因中的一些突变表现为T4 dCMP-羟甲基化酶(基因42)缺陷的抑制因子。这种抑制作用似乎涉及这两种酶在DNA复制水平上的功能相互作用。羟甲基化酶缺陷在复制过程中导致DNA结构异常,而DNA聚合酶损伤似乎部分逆转了这些异常。尽管这两种酶似乎都在控制噬菌体DNA复制的保真度中发挥作用,但这些结果并不一定意味着两种酶之间存在蛋白质-蛋白质相互作用。