Blocking transcription of the human rhodopsin gene by triplex-mediated DNA photocrosslinking

Nucleic Acids Res. 2000 Nov 1;28(21):4283-90. doi: 10.1093/nar/28.21.4283.

Abstract

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.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Base Sequence
  • Binding Sites
  • Cross-Linking Reagents / metabolism
  • Cross-Linking Reagents / pharmacology*
  • Cross-Linking Reagents / therapeutic use
  • DNA / genetics
  • DNA / metabolism
  • DNA / pharmacology*
  • DNA / therapeutic use
  • DNA Damage / genetics
  • Down-Regulation / drug effects
  • Down-Regulation / radiation effects
  • Ficusin / metabolism
  • Ficusin / pharmacology
  • Flow Cytometry
  • Fluorescence
  • Genes, Reporter / genetics
  • Genetic Therapy / methods
  • Humans
  • Mutation / genetics
  • Oligodeoxyribonucleotides / genetics
  • Oligodeoxyribonucleotides / metabolism
  • Oligodeoxyribonucleotides / pharmacology
  • Oligodeoxyribonucleotides / therapeutic use
  • Photosensitizing Agents / metabolism
  • Photosensitizing Agents / pharmacology*
  • Photosensitizing Agents / radiation effects
  • Photosensitizing Agents / therapeutic use
  • Plasmids / genetics
  • RNA, Messenger / analysis
  • RNA, Messenger / biosynthesis
  • RNA, Messenger / genetics
  • Retinitis Pigmentosa / genetics
  • Retinitis Pigmentosa / therapy
  • Rhodopsin / genetics*
  • Substrate Specificity
  • Thermodynamics
  • Time Factors
  • Transcription, Genetic / drug effects*
  • Transcription, Genetic / genetics
  • Transcription, Genetic / radiation effects*
  • Transfection
  • Tumor Cells, Cultured
  • Ultraviolet Rays

Substances

  • Cross-Linking Reagents
  • Oligodeoxyribonucleotides
  • Photosensitizing Agents
  • RNA, Messenger
  • triplex DNA
  • DNA
  • Rhodopsin
  • Ficusin