Radany E H, Nguyen H T, Minton K W
Department of Pathology, F.E. Hebert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD 20814-4799.
Mol Gen Genet. 1987 Aug;209(1):83-9. doi: 10.1007/BF00329840.
The in vivo excision repair functions of Escherichia coli exonuclease III and 3-methyladenine DNA glycosylase I, and bacteriophage T4 pyrimidine dimer-DNA glycosylase were investigated. Following exposure of bacteriophage T4 or lambda to methyl methanesulfonate or ultraviolet irradiation, survival was determined by plating on E. coli have various genetic backgrounds. Although exonuclease III was shown to participate in base excision repair initiated by 3-methyladenine DNA glycosylase I, it had no detectable role in base excision repair initiated by the T4 pyrimidine dimer-DNA glycosylase. Despite its 3' apurinic/apyrimidinic endonuclease activity in vitro, T4 pyrimidine dimer-DNA glycosylase, even in large quantities, did not complement mutants defective in exonuclease III in the repair of apurinic sites generated by 3-methyladenine DNA glycosylase I in vivo.
对大肠杆菌核酸外切酶III、3-甲基腺嘌呤DNA糖基化酶I以及噬菌体T4嘧啶二聚体-DNA糖基化酶的体内切除修复功能进行了研究。在噬菌体T4或λ暴露于甲磺酸甲酯或紫外线照射后,通过在具有不同遗传背景的大肠杆菌平板上接种来确定存活率。虽然核酸外切酶III被证明参与由3-甲基腺嘌呤DNA糖基化酶I启动的碱基切除修复,但它在由T4嘧啶二聚体-DNA糖基化酶启动的碱基切除修复中没有可检测到的作用。尽管T4嘧啶二聚体-DNA糖基化酶在体外具有3'无嘌呤/无嘧啶内切酶活性,但即使大量存在,它也不能在体内修复由3-甲基腺嘌呤DNA糖基化酶I产生的无嘌呤位点时,补充核酸外切酶III缺陷的突变体。