UvrA and UvrB enhance mutations induced by oxidized deoxyribonucleotides
UvrA and UvrB enhance mutations induced by oxidized deoxyribonucleotides
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DOI：
10.1016/j.dnarep.2007.06.013
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发表时间：
2007-12-01
期刊：
影响因子：
3.8
通讯作者：
Kamiya, Hiroyuki
中科院分区：
文献类型：
--
作者：
Hori, Mika;Ishiguro, Chieko;Kamiya, Hiroyuki
氧化损伤的DNA前体（脱氧核糖核苷酸）由活性氧形成。当受损的DNA前体被整合到DNA中后，它们可能会被DNA修复酶去除。在这项研究中，为了检测核苷酸切除修复酶，大肠杆菌UvrABC是否可以抑制体内氧化脱氧核糖核苷酸诱导的突变，将氧化的DNA前体，8-羟基-2 '-脱氧鸟苷5'-三磷酸和2-羟基-2 '-脱氧腺苷5'-三磷酸引入uvrA、uvrB和uvrC E。大肠杆菌菌株，和染色体rpoB基因的突变进行了分析。出乎意料的是，这些氧化的DNA前体在uvrA和uvrB菌株中仅轻微诱导突变。相反，未观察到uvrC缺乏的影响。接下来，mutT、mutT/uvrA和mutT/uvrB E。用H_2O_2处理大肠杆菌菌株，计算rpoB突变频率。H2 O2诱导的突变的频率增加，在所有的测试菌株，但是，增加是三至四倍低mutT/uvrA和mutT/uvrB菌株比mutT菌株。因此，UvrA和UvrB参与增强，但不参与抑制，由这些氧化的脱氧核糖核苷酸诱导的突变。这些结果表明UvrA和UvrB在氧化损伤过程中的新作用。(C)2007 Elsevier B. V.保留所有权利。
Oxidatively damaged DNA precursors (deoxyribonucleotides) are formed by reactive oxygen species. After the damaged DNA precursors are incorporated into DNA, they might be removed by DNA repair enzymes. in this study, to examine whether a nucleotide excision repair enzyme, Escherichia coli UvrABC, could suppress the mutations induced by oxidized deoxyribonucleotides in vivo, oxidized DNA precursors, 8-hydroxy-2'-deoxyguanosine 5'-triphosphate and 2-hydroxy-2'-deoxyadenosine 5'-triphosphate, were introduced into uvrA, uvrB, and uvrC E. coli strains, and mutations in the chromosomal rpoB gene were analyzed. Unexpectedly, these oxidized DNA precursors induced mutations only slightly in the uvrA and uvrB strains. In contrast, effect of the uvrC-deficiency was not observed. Next, mutT, mutT/uvrA, and mutT/uvrB E. coli strains were treated with H2O2, and the rpoB mutant frequencies were calculated. The frequency of the H2O2-induced mutations was increased in all of the strains tested; however, the increase was three- to four-fold lower in the mutT/uvrA and mutT/uvrB strains than in the mutT strain. Thus, UvrA and UvrB are involved in the enhancement, but not in the suppression, of the mutations induced by these oxidized deoxyribonucleotides. These results suggest a novel role for UvrA and UvrB in the processing of oxidative damage. (C) 2007 Elsevier B.V. All rights reserved.