Frameshift lesions induced by oxazolopyridocarbazoles are recognized by the mismatch repair system in Escherichia coli

Brigitte René, Christian Auclair, Claude Paoletti
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引用次数: 5

Abstract

The simple reversible intercalating agent isopropyl-OPC (iPr-OPC) induces frameshift-1 mutations in Salmonella typhimurium and Escherichia coli. The mutagenic responses of S. typhimurium and E. coli wild-type strains are not proportional to the amount of drug intercalated into double-stranded nucleic acids in living bacteria; it occurs only above a minimum level of binding. The fact that mismatch-repair-deficient (mutS) as well as adenine-methylation-deficient (dam) E. coli mutants are hypermutable at low concentrations of iPr-OPC suggests that the majority of mutants induced by this intercalating drug occur as mismatch-repairable mutations (or lesions) in the newly synthesized DNA strand close to the replication fork.

由恶唑吡啶咔唑引起的移码损伤被大肠杆菌错配修复系统识别
简单可逆插层剂异丙基opc (iPr-OPC)可诱导鼠伤寒沙门菌和大肠杆菌发生帧移-1突变。鼠伤寒沙门氏菌和大肠杆菌野生型菌株的致突变反应与活菌双链核酸中嵌入药物的量不成正比;它只发生在最低绑定级别之上。错配修复缺陷(mutS)和腺嘌呤甲基化缺陷(dam)大肠杆菌突变体在低浓度的iPr-OPC下是超可变的,这一事实表明,这种插入药物诱导的大多数突变发生在靠近复制叉的新合成DNA链上,是可错配修复的突变(或病变)。
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