DNA中的3-甲基腺嘌呤残基可诱导大肠杆菌中的SOS功能sfiA。
3-Methyladenine residues in DNA induce the SOS function sfiA in Escherichia coli.
作者信息
Boiteux S, Huisman O, Laval J
出版信息
EMBO J. 1984 Nov;3(11):2569-73. doi: 10.1002/j.1460-2075.1984.tb02175.x.
Abstract
The induction by methylating agents of the SOS function sfiA was measured by means of a sfiA::lac operon fusion in Escherichia coli mutants defective in alkylation repair. The sfiA operon was turned on at a 10-fold lower concentration of methylmethane sulfonate or dimethyl sulfate in tagA strains, lacking specific 3-methyladenine-DNA glycosylase, than in wild-type strains. In contrast, the induction of sfiA by u.v. light was not affected by a tagA mutation. We confirm that tagA strains specifically accumulate 3-methyladenine in their DNA. We conclude that the persistence of 3-methyladenine in E. coli DNA most likely induces the SOS functions. Results on in vitro DNA synthesis further suggest that this induction is due to an unscheduled arrest of DNA synthesis at this lesion.
摘要
通过在大肠杆菌中采用sfiA::lac操纵子融合的方法，在缺乏烷基化修复功能的突变体中测量甲基化试剂对SOS功能sfiA的诱导作用。在缺乏特异性3-甲基腺嘌呤-DNA糖基化酶的tagA菌株中，与野生型菌株相比，在甲基磺酸甲酯或硫酸二甲酯浓度低10倍时，sfiA操纵子就会被激活。相反，紫外线对sfiA的诱导不受tagA突变的影响。我们证实tagA菌株的DNA中会特异性积累3-甲基腺嘌呤。我们得出结论，大肠杆菌DNA中3-甲基腺嘌呤的持续存在很可能诱导了SOS功能。体外DNA合成的结果进一步表明，这种诱导是由于DNA合成在该损伤处意外停滞所致。
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