CODING PROPERTIES OF POLY(DEOXYCYTIDYLIC ACID) TEMPLATES CONTAINING URACIL OR APYRIMIDINIC SITES - INVITRO MODULATION OF MUTAGENESIS BY DEOXYRIBONUCLEIC-ACID REPAIR ENZYMES
CODING PROPERTIES OF POLY(DEOXYCYTIDYLIC ACID) TEMPLATES CONTAINING URACIL OR APYRIMIDINIC SITES - INVITRO MODULATION OF MUTAGENESIS BY DEOXYRIBONUCLEIC-ACID REPAIR ENZYMES
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DOI：
10.1021/bi00269a020
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发表时间：
1982-01-01
期刊：
影响因子：
2.9
通讯作者：
LAVAL, J
中科院分区：
文献类型：
--
作者：
BOITEUX, S;LAVAL, J
聚脱氧胞苷酸[poly（dC）]的热处理诱导dUMP残基的形成，当通过大肠杆菌DNA聚合酶I和III复制时，dUMP残基编码dAMP（EC 2.7.7.7）。dUMP编码特性的特异性由dAMP掺入和dUMP残基在热处理的聚（dC）中的频率之间的定量关系表示。通过将含尿嘧啶的聚（dC）与尿嘧啶-DNA糖基化酶预孵育来防止dAMP掺入。尿嘧啶-DNA糖基化酶切除尿嘧啶导致无嘧啶位点（AP位点）的形成，其是大麦在生理条件下体外复制的。然而，E. Mn ~（2+）对大肠杆菌DNA聚合酶Ⅰ复制的保真度有很大的促进作用。与dTMP相比，在AP位点的对面有dAMP的优先掺入。通过将含有AP位点的poly（dC）与藤黄微球菌AP核酸内切酶B预孵育来防止dAMP掺入。结果表明，通过碱基切除进行的DNA修复与体外致突变过程的预防之间存在密切联系。由于DNA聚合酶保真度的改变允许非编码DNA损伤（AP位点）的一些复制，这可能意味着在SOS诱导的体内诱变中的作用。
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 (EC 2.7.7.7). 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 barley 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. 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.