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通过M13基因组上携带的丙烷脱氧鸟苷加合物进行位点特异性诱变。

Site-specific mutagenesis by a propanodeoxyguanosine adduct carried on an M13 genome.

作者信息

Burcham P C, Marnett L J

机构信息

A. B. Hancock, Jr. Memorial Laboratory for Cancer Research, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-0146.

出版信息

J Biol Chem. 1994 Nov 18;269(46):28844-50.

PMID:7961843
Abstract

The spectrum of mutations induced upon in vivo replication of an M13 genome containing a site-specifically located propanodeoxyguanosine (PdG) adduct was determined. PdG was used as a model for the major deoxyguanosine adduct produced on reaction of DNA with the endogenous genotoxin malondialdehyde. PdG was introduced at position 6256 of M13MB102 by ligating the oligodeoxynucleotide 5'-GGT(PdG)TCCG-3' into an 8-base gap in the (-)-strand of duplex M13MB102. Replication of the adducted strand was maximized by incorporation of uracil into the unadducted (+)-strand. Following replication of dG-containing and PdG-containing M13MB102 genomes in Escherichia coli JM105, frameshift mutations were detected as phenotypic changes in the lacZ alpha marker gene. Base pair substitutions were detected by differential hybridization using 32P-labeled 13-mers bearing different bases opposite position 6256. Neither frameshift nor base pair substitution mutations were detected following replication of PdG-adducted genomes in non-SOS-induced JM105. However, PdG-->T transversions and PdG-->A transitions were detected following transformation of PdG-adducted M13MB102 into SOS-induced JM105. Both types of mutations were detected at comparable frequencies, and the total mutation frequency was approximately 2%. The results indicate that PdG is an efficient premutagenic lesion in E. coli strains in which the SOS response is induced.

摘要

确定了含有位点特异性定位的丙烷脱氧鸟苷(PdG)加合物的M13基因组在体内复制时诱导产生的突变谱。PdG被用作DNA与内源性基因毒素丙二醛反应产生的主要脱氧鸟苷加合物的模型。通过将寡脱氧核苷酸5'-GGT(PdG)TCCG-3'连接到双链M13MB102(-)链中的一个8碱基缺口,将PdG引入M13MB102的6256位。通过将尿嘧啶掺入未加合的(+)链中,使加合链的复制最大化。在大肠杆菌JM105中对含dG和含PdG的M13MB102基因组进行复制后,移码突变被检测为lacZα标记基因中的表型变化。使用在6256位对面带有不同碱基的32P标记的13聚体通过差异杂交检测碱基对替换。在未诱导SOS的JM105中对PdG加合基因组进行复制后,未检测到移码突变和碱基对替换突变。然而,在将PdG加合的M13MB102转化到诱导SOS的JM105后,检测到PdG→T颠换和PdG→A转换。两种类型的突变以相当的频率被检测到,总突变频率约为2%。结果表明,在诱导SOS反应的大肠杆菌菌株中,PdG是一种有效的前诱变损伤。

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