Bridges B A, Sekiguchi M, Tajiri T
MRC Cell Mutation Unit, University of Sussex, Falmer, Brighton, UK.
Mol Gen Genet. 1996 Jun 12;251(3):352-7. doi: 10.1007/BF02172526.
MutY specifies a DNA glycosylase that removes adenines unnaturally paired with various bases including oxidized derivatives of guanine, such as 7,8-dihydro-8-oxoguanine (8-oxoG). The rate of mutation in starved Escherichia coli cells is markedly raised in mutY mutants defective in this glycosylase. As predicted, the mutations produced include G to T transversions. Bacteria carrying mutM or fpg-1 mutations (defective in Fapy glycosylase, which removes oxidized guanine residues such as 8-oxoG) show little or no enhancement of mutation under starvation conditions. When present together with mutY, however, mutM clearly further enhances the rate of mutation in starved cells. Plasmids resulting in overproduction of MutY or Fapy glycosylases reduce the rate of mutation in starved cells. We conclude that, in non-growing bacteria, oxidized guanine residues, including 8-oxoG, constitute an important component of spontaneous mutation. Addition of catalase to the plates did not reduce the mutant yield, indicating that extracellular hydrogen peroxide is not involved in the production of the premutational damage. Singlet oxygen, known to give rise to 8-oxoG, may be the ultimate oxidative species.
MutY 基因编码一种 DNA 糖基化酶,该酶可去除与包括鸟嘌呤氧化衍生物(如 7,8 - 二氢 - 8 - 氧代鸟嘌呤,8 - oxoG)在内的各种碱基非自然配对的腺嘌呤。在缺乏这种糖基化酶的 mutY 突变体中,饥饿的大肠杆菌细胞的突变率显著提高。正如所预测的那样,产生的突变包括 G 到 T 的颠换。携带 mutM 或 fpg - 1 突变(Fapy 糖基化酶缺陷,该酶可去除诸如 8 - oxoG 等氧化鸟嘌呤残基)的细菌在饥饿条件下几乎没有或根本没有显示出突变增强。然而,当与 mutY 同时存在时,mutM 明显进一步提高了饥饿细胞中的突变率。导致 MutY 或 Fapy 糖基化酶过量产生的质粒降低了饥饿细胞中的突变率。我们得出结论,在不生长的细菌中,包括 8 - oxoG 在内的氧化鸟嘌呤残基是自发突变的重要组成部分。在平板中添加过氧化氢酶并没有降低突变体产量,这表明细胞外过氧化氢不参与诱变前损伤的产生。已知能产生 8 - oxoG 的单线态氧可能是最终的氧化物种。