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脱嘌呤作用会在SOS诱导的细胞中引发突变。

Depurination causes mutations in SOS-induced cells.

作者信息

Schaaper R M, Loeb L A

出版信息

Proc Natl Acad Sci U S A. 1981 Mar;78(3):1773-7. doi: 10.1073/pnas.78.3.1773.

Abstract

Introduction of apurinic sites into phi X174 am3 DNA leads to loss of biological activity when measured in a transfection assay. For single-stranded DNA, approximately one apurinic site constitutes a lethal hit; for double-stranded (RFI) DNA, approximately 3.5 hits per strand are lethal. When the reversion frequency of am3 DNA is measured, no increase due to depurination is observed above the background level. However, a large increase in reversion frequency is observed when the same DNA is assayed by using spheroplasts derived from bacteria previously exposed to UV light. The results suggest that apurinic sites are impediments to a replicating DNA polymerase; however, nucleotides can be incorporated opposite these sites under SOS-induced conditions. We estimate the frequency of mutagenesis per apurinic site to be less than 1 in 1400 in normal spheroplasts and 1 in 100 in SOS-induced spheroplasts.

摘要

在转染试验中检测时,将无嘌呤位点引入噬菌体φX174 am3 DNA会导致生物活性丧失。对于单链DNA,大约一个无嘌呤位点就构成一个致死性损伤;对于双链(RFI)DNA,每条链大约3.5个损伤是致死性的。当测量am3 DNA的回复突变频率时,在背景水平之上未观察到由于脱嘌呤导致的增加。然而,当使用先前暴露于紫外线的细菌来源的原生质球检测相同DNA时,观察到回复突变频率大幅增加。结果表明,无嘌呤位点是复制性DNA聚合酶的障碍;然而,在SOS诱导的条件下,核苷酸可以掺入这些位点相对的位置。我们估计,在正常原生质球中,每个无嘌呤位点的诱变频率小于1/1400,在SOS诱导的原生质球中为1/100。

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