Intody Z, Perkins B D, Wilson J H, Wensel T G
Verna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, 1 Baylor Plaza, Houston, TX 77030, USA.
Nucleic Acids Res. 2000 Nov 1;28(21):4283-90. doi: 10.1093/nar/28.21.4283.
To explore the ability of triplex-forming oligodeoxyribonucleotides (TFOs) to inhibit genes responsible for dominant genetic disorders, we used two TFOs to block expression of the human rhodopsin gene, which encodes a G protein-coupled receptor involved in the blinding disorder autosomal dominant retinitis pigmentosa. Psoralen-modified TFOs and UVA irradiation were used to form photoadducts at two target sites in a plasmid expressing a rhodopsin-EGFP fusion, which was then transfected into HT1080 cells. Each TFO reduced rhodopsin-GFP expression by 70-80%, whereas treatment with both reduced expression by 90%. Expression levels of control genes on either the same plasmid or one co-transfected were not affected by the treatment. Mutations at one TFO target eliminated its effect on transcription, without diminishing inhibition by the other TFO. Northern blots indicated that TFO-directed psoralen photoadducts blocked progression of RNA polymerase, resulting in truncated transcripts. Inhibition of gene expression was not relieved over a 72 h period, suggesting that TFO-induced psoralen lesions are not repaired on this time scale. Irradiation of cells after transfection with plasmid and psoralen-TFOs produced photoadducts inside the cells and also inhibited expression of rhodopsin-EGFP. We conclude that directing DNA damage with psoralen-TFOs is an efficient and specific means for blocking transcription from the human rhodopsin gene.
为了探索三链形成寡脱氧核糖核苷酸(TFOs)抑制导致显性遗传病的基因的能力,我们使用了两种TFOs来阻断人类视紫红质基因的表达,该基因编码一种参与致盲疾病常染色体显性视网膜色素变性的G蛋白偶联受体。补骨脂素修饰的TFOs和紫外线A照射用于在表达视紫红质-增强绿色荧光蛋白(rhodopsin-EGFP)融合蛋白的质粒中的两个靶位点形成光加合物,然后将其转染到HT1080细胞中。每种TFO将视紫红质-绿色荧光蛋白的表达降低了70%-80%,而两种TFO共同处理则将表达降低了90%。同一质粒上或共转染的一个对照基因的表达水平不受该处理的影响。一个TFO靶位点的突变消除了其对转录的影响,但并未削弱另一个TFO的抑制作用。Northern印迹表明,TFO引导的补骨脂素光加合物阻断了RNA聚合酶的进程,导致转录本截短。在72小时内基因表达的抑制并未解除,这表明在这个时间尺度上TFO诱导的补骨脂素损伤未得到修复。用质粒和补骨脂素-TFOs转染细胞后进行照射,在细胞内产生了光加合物,同时也抑制了视紫红质-EGFP的表达。我们得出结论,用补骨脂素-TFOs引导DNA损伤是阻断人类视紫红质基因转录的一种有效且特异的方法。