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关于锰致突变的酶学基础。

On the enzymatic basis for mutagenesis by manganese.

作者信息

Goodman M F, Keener S, Guidotti S, Branscomb E W

出版信息

J Biol Chem. 1983 Mar 25;258(6):3469-75.

PMID:6833210
Abstract

The effects of manganese on DNA synthesis fidelity are measured using T4 DNA polymerase. When the nucleotide analogue 2-aminopurine deoxyribonucleoside triphosphate competes against dATP at thymine sites on template DNA, the aminopurine misincorporation frequency increases from 6.3% in the presence of Mg2+ to 29.2% in the presence of Mn2+. The major cause of the increased error rate is an approximate 4-fold increase in the frequency of aminopurine misinsertions. Exonucleolytic proofreading of aminopurine is similar in the presence of Mn2+ and Mg2+. However, the excision frequency of the correct nucleotide, dAMP, is increased 2-fold with Mn2+. In experiments in which insertion and incorporation velocities of aminopurine and adenine are measured independently of each other, a 5- to 10-fold decrease in the Michaelis constant for aminopurine is observed in the presence of Mn2+ compared to a 2-fold decrease in the Km for adenine. In contrast to the marked differential reduction in the ratio of aminopurine to adenine Km values, the maximum insertion velocities of both nucleotides are reduced by similar amounts (40-fold). We suggest that the mutagenic action of Mn2+ can be attributed primarily to a significant differential increase in binding of mispaired relative to correctly paired nucleotides to the polymerase-template complex. The resulting increase in the ratio of residence times for mispaired compared with correctly paired nucleotides on the complex results in their increased frequency of misinsertion. A smaller contributing factor to Mn2+-induced mutagenesis is a loss of proofreading specificity. We propose that the losses in both the specificities of nucleotide insertion and excision (proofreading) share a common molecular origin in which nucleotides are bound in the presence of Mn2+ in distorted configurations at the polymerase insertion and excision active sites resulting in increased nonspecific enzyme-substrate binding forces at the expense of template-substrate base pair specific hydrogen bonds.

摘要

利用T4 DNA聚合酶来测定锰对DNA合成保真度的影响。当核苷酸类似物2-氨基嘌呤脱氧核糖核苷三磷酸在模板DNA的胸腺嘧啶位点上与dATP竞争时,氨基嘌呤错掺入频率从存在Mg2+时的6.3%增加到存在Mn2+时的29.2%。错误率增加的主要原因是氨基嘌呤错插入频率大约增加了4倍。在存在Mn2+和Mg2+的情况下,氨基嘌呤的核酸外切校正相似。然而,正确核苷酸dAMP的切除频率在Mn2+存在时增加了2倍。在分别测量氨基嘌呤和腺嘌呤的插入及掺入速度的实验中,与腺嘌呤的Km降低2倍相比,在Mn2+存在时观察到氨基嘌呤的米氏常数降低了5至10倍。与氨基嘌呤和腺嘌呤Km值比率的显著差异降低相反,两种核苷酸的最大插入速度降低的幅度相似(40倍)。我们认为,Mn2+的诱变作用主要可归因于错配核苷酸相对于正确配对核苷酸与聚合酶-模板复合物结合的显著差异增加。复合物上错配核苷酸与正确配对核苷酸停留时间比率的增加导致它们错插入频率的增加。Mn2+诱导诱变的一个较小的促成因素是校对特异性的丧失。我们提出,核苷酸插入和切除(校对)特异性的丧失有一个共同的分子根源,即在Mn2+存在下,核苷酸以扭曲的构型结合在聚合酶插入和切除活性位点,导致非特异性酶-底物结合力增加,而以模板-底物碱基对特异性氢键为代价。

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