Havre P A, Glazer P M
Department of Therapeutic Radiology, Yale University School of Medicine, New Haven, Connecticut 06510.
J Virol. 1993 Dec;67(12):7324-31. doi: 10.1128/JVI.67.12.7324-7331.1993.
Triple-helical DNA can be formed by oligonucleotides that bind as third strands of DNA in a sequence-specific manner in the major groove in homopurine/homopyrimidine stretches in duplex DNA. Such triple helix-forming oligonucleotides have been used to inhibit gene expression by blocking transcription factor access to promoter sites in transient expression assays. In an alternative approach to genetic manipulation using triplex DNA, we show that triplex-forming oligonucleotides can be used to produce site-specific, targeted mutations in a viral genome in order to achieve a permanent, heritable effect on gene function and expression. We use a triplex-forming oligonucleotide linked to a psoralen derivative at its 5' end to achieve targeted mutagenesis in a simian virus 40 (SV40) vector genome. Site-specific triplex formation delivers the psoralen to the targeted site in the SV40 DNA. Photoactivation of the psoralen yields adducts and thereby mutations at that site. Mutations were produced in the target gene in over 6% of the viral genomes. DNA sequence analysis of the mutations in the target gene showed that all were in the targeted region, and 55% were found to be the same T:A-to-A:T transversion precisely at the targeted base pair. In control experiments, no mutagenesis above the background frequency in the assay was produced by a non-triplex-forming, psoralen-linked oligonucleotide unless a vast excess of this oligonucleotide was used, demonstrating the specificity of the targeted mutagenesis. This frequency of targeted mutagenesis of SV40 in monkey cells represents a 30-fold increase relative to similar experiments using lambda phage in bacteria, suggesting that fixation of the triplex-directed lesion into a mutation occurs more efficiently in mammalian cells. If the ability to reproducibly and predictably target mutations to sites in viral DNA in vitro by using modified oligonucleotides can be extended to DNA in vivo, this approach may prove useful as a technique for gene therapy, as a strategy for antiviral therapeutics, and as a tool for genetic engineering.
三链螺旋DNA可由寡核苷酸形成,这些寡核苷酸在双链DNA的同型嘌呤/同型嘧啶区段的大沟中以序列特异性方式作为第三条DNA链结合。此类三链螺旋形成寡核苷酸已被用于在瞬时表达试验中通过阻断转录因子进入启动子位点来抑制基因表达。在使用三链体DNA进行基因操作的另一种方法中,我们表明三链体形成寡核苷酸可用于在病毒基因组中产生位点特异性的靶向突变,以便对基因功能和表达实现永久性、可遗传的影响。我们使用在其5'端连接了补骨脂素衍生物的三链体形成寡核苷酸,在猴病毒40(SV40)载体基因组中实现靶向诱变。位点特异性三链体的形成将补骨脂素递送至SV40 DNA中的靶向位点。补骨脂素的光活化产生加合物,从而在该位点产生突变。超过6%的病毒基因组中靶基因发生了突变。对靶基因中突变的DNA序列分析表明,所有突变均位于靶向区域,并且发现55%的突变恰好是在靶向碱基对处发生相同的T:A到A:T颠换。在对照实验中,除非使用大量过量的非三链体形成、补骨脂素连接的寡核苷酸,否则该寡核苷酸不会产生高于试验背景频率的诱变,这证明了靶向诱变的特异性。猴细胞中SV40的这种靶向诱变频率相对于在细菌中使用λ噬菌体进行的类似实验提高了30倍,表明三链体导向的损伤在哺乳动物细胞中更有效地固定为突变。如果通过使用修饰的寡核苷酸在体外将病毒DNA中的位点可重复且可预测地靶向突变的能力扩展到体内DNA,那么这种方法可能被证明是一种有用的基因治疗技术、抗病毒治疗策略和基因工程工具。