Goodman M F, Hopkins R, Gore W C
Proc Natl Acad Sci U S A. 1977 Nov;74(11):4806-10. doi: 10.1073/pnas.74.11.4806.
We measured the in vivo incorporation of 2-aminopurine into DNA of T4 bacteriophage allelic for gene 43 (DNA polymerase), mutator (L56), 43+, and antimutator (L141). The magnitude of incorporation (mol/mol of Thy) was 1/1500 in L56, 1/1600 in 43+, and 1/8900 in L141. The incorporation ratio L56:43+:L141 in vivo was equal to that mediated by the purified DNA polymerases of these allelic phages in vitro. A model for 2-aminopurine-induced A-T in equilibrium G-C transitions is discussed. The model is used to predict the magnitudes of replication errors (C mispairing with a template 2-aminopurine) and incorporation errors (2-aminopurine mispairing with a template C) per round of replication and to investigate the asymmetry in 2-aminopurine-induced transitions favoring the A-T leads to G-C pathway over G-C leads to A-T. We suggest that the fidelity of L56 and L141 DNA polymerases exemplifies one-step and two-step editing, respectively.
我们测定了2-氨基嘌呤在T4噬菌体基因43(DNA聚合酶)、诱变型(L56)、野生型(43+)和抗诱变型(L141)等位基因的DNA中的体内掺入情况。掺入量(每摩尔胸腺嘧啶的摩尔数)在L56中为1/1500,在43+中为1/1600,在L141中为1/8900。2-氨基嘌呤在体内的掺入比例L56:43+:L141与这些等位基因噬菌体的纯化DNA聚合酶在体外介导的比例相同。讨论了2-氨基嘌呤诱导的A-T与G-C平衡转换的模型。该模型用于预测每轮复制中复制错误(胞嘧啶与模板2-氨基嘌呤错配)和掺入错误(2-氨基嘌呤与模板胞嘧啶错配)的大小,并研究2-氨基嘌呤诱导的转换中有利于A-T到G-C途径而非G-C到A-T途径的不对称性。我们认为,L56和L141 DNA聚合酶的保真度分别体现了一步编辑和两步编辑。