MacPhee D G, Liaskou D
Department of Microbiology, La Trobe University, Bundoora, Vic., Australia.
Mutat Res. 1989 Dec;227(4):251-5. doi: 10.1016/0165-7992(89)90106-1.
The antitumour drug nitracrine [1-nitro-9-(dimethylaminopropylamino)acridine], known to be a potent frameshift mutagen in strains of Salmonella typhimurium, also strongly reverts the lacZ19124 frameshift marker in Escherichia coli. The results in E. coli indicate that nitracrine causes DNA damage which can be excised by the UvrA,B,C excinuclease, can generate mutations by a recA-dependent mechanism, and gives enhanced yields of mutants when plasmid pKM101 is present. Despite these observations, mutagenesis by nitracrine appears to be independent of the UmuC gene product, and hence nitracrine differs from most (but not all) other chemicals which generate mutations via the SOS response. Given that umuC mutants are about as mutable by nitracine as the wild-type parent strain, it is somewhat surprising that plasmid pKM101 causes an enhancement of nitracrine mutagenesis. Nevertheless, we have found that the observed enhancement of mutagenesis by pKM101 is a function of the mucB gene, normally assumed to be essentially homologous to the umuC gene.
抗肿瘤药物硝吖啶[1-硝基-9-(二甲基氨基丙基氨基)吖啶]，已知在鼠伤寒沙门氏菌菌株中是一种强效的移码诱变剂，它也能强烈回复大肠杆菌中的lacZ19124移码标记。在大肠杆菌中的结果表明，硝吖啶会导致DNA损伤，这种损伤可被UvrA、B、C核酸外切酶切除，能通过recA依赖的机制产生突变，并且当存在质粒pKM101时会提高突变体的产量。尽管有这些观察结果，但硝吖啶的诱变作用似乎与UmuC基因产物无关，因此硝吖啶与大多数（但不是全部）通过SOS反应产生突变的其他化学物质不同。鉴于umuC突变体被硝吖啶诱变的程度与野生型亲本菌株相当，质粒pKM101会增强硝吖啶的诱变作用这一点有点令人惊讶。然而，我们发现观察到的pKM101对诱变作用的增强是mucB基因的作用，通常认为该基因与umuC基因基本同源。
