Boiteux S, Laval J
Biochemistry. 1982 Dec 21;21(26):6746-51. doi: 10.1021/bi00269a020.
Heat treatment of poly(deoxycytidylic acid)-[poly(dC)] induces the formation of dUMP residues, which code for dAMP when replicated by Escherichia coli DNA polymerases I and III. The specificity of dUMP coding properties is indicated by the quantitative relation between the dAMP incorporated and the frequency of dUMP residues in the heat-treated poly(dC). The dAMP incorporation is prevented by preincubation of uracil containing poly(dC) with uracil-DNA glycosylase. The excision of uracil by uracil-DNA glycosylase leads to the formation of apyrimidinic sites (AP sites), which are barely replicated in vitro under physiological conditions. However, the alteration of E. coli DNA polymerase I fidelity of replication by Mn2+ greatly stimulates the replication of AP sites. There is a preferential incorporation of dAMP, as compared to dTMP, opposite the AP sites. The dAMP incorporation is prevented by preincubation of poly(dC) containing AP sites with Micrococcus luteus AP endonuclease B. The results show a close association between DNA repair by base excision and the prevention of mutagenic processes in vitro. Furthermore, since the alteration of DNA polymerase fidelity allows some replication of the noncoding DNA lesion (AP site), this could imply a role in SOS-induced mutagenesis in vivo.
聚（脱氧胞苷酸）-[聚（dC）]的热处理会诱导dUMP残基的形成，当由大肠杆菌DNA聚合酶I和III复制时，这些残基编码dAMP。掺入的dAMP与热处理后的聚（dC）中dUMP残基频率之间的定量关系表明了dUMP编码特性的特异性。含有尿嘧啶的聚（dC）与尿嘧啶-DNA糖基化酶预孵育可阻止dAMP的掺入。尿嘧啶-DNA糖基化酶切除尿嘧啶会导致无嘧啶位点（AP位点）的形成，在生理条件下，这些位点在体外几乎不被复制。然而，Mn2+改变大肠杆菌DNA聚合酶I的复制保真度会极大地刺激AP位点的复制。与dTMP相比，AP位点对面优先掺入dAMP。含有AP位点的聚（dC）与藤黄微球菌AP内切核酸酶B预孵育可阻止dAMP的掺入。结果表明，碱基切除修复与体外诱变过程的预防之间存在密切关联。此外，由于DNA聚合酶保真度的改变允许一些非编码DNA损伤（AP位点）进行复制，这可能意味着其在体内SOS诱导的诱变中起作用。
