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大肠杆菌alkB突变体对DNA中无碱基位点和3-甲基腺嘌呤残基的修复

Repair in Escherichia coli alkB mutants of abasic sites and 3-methyladenine residues in DNA.

作者信息

Dinglay S, Gold B, Sedgwick B

机构信息

Imperial Cancer Research Fund, Clare Hall Laboratories, Herts, UK.

出版信息

Mutat Res. 1998 Mar;407(2):109-16. doi: 10.1016/s0921-8777(97)00065-7.

DOI:10.1016/s0921-8777(97)00065-7
PMID:9637239
Abstract

Escherichia coli alkB mutants are sensitive to methyl methanesulfonate and dimethylsulphate, and are defective in the processing of methylated DNA. The function of the AlkB protein has not been determined. Here, we show that alkB mutants are not defective in repairing several different types of potentially toxic DNA lesions that are known to be generated by MMS, including apyrimidinic and apurinic sites, and secondary lesions that could arise at these sites (DNA-protein cross-links and DNA interstrand cross-links). Also, alkB mutants were not sensitive to MeOSO2-(CH2)2-Lex, a compound that alkylates the minor groove of DNA generating primarily 3-methyladenine.

摘要

大肠杆菌alkB突变体对甲磺酸甲酯和硫酸二甲酯敏感,并且在甲基化DNA的处理过程中存在缺陷。AlkB蛋白的功能尚未确定。在此,我们表明alkB突变体在修复几种已知由甲磺酸甲酯产生的潜在毒性DNA损伤方面没有缺陷,这些损伤包括无嘧啶和无嘌呤位点,以及可能在这些位点出现的继发性损伤(DNA-蛋白质交联和DNA链间交联)。此外,alkB突变体对MeOSO2-(CH2)2-Lex不敏感,MeOSO2-(CH2)2-Lex是一种使DNA小沟烷基化主要产生3-甲基腺嘌呤的化合物。

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