Hoechst 33258 selectively inhibits group I intron self-splicing by affecting RNA folding

Chembiochem. 2004 Dec 3;5(12):1647-52. doi: 10.1002/cbic.200400159.

Abstract

Fungal pathogens are increasing in prevalence due to an increase in resistant strains and the number of immunocompromised humans. Candida albicans is one of these pathogens, and approximately 40% of strains contain a group I self-splicing intron, which is a potential RNA drug target, in their large subunit rRNA precursor. Here, we report that Hoechst 33258 and derivatives thereof are selective inhibitors of C. albicans group I intron self-splicing with an IC50 of 17 microM in 2 mM Mg2+. Chemical probing of the intron in the presence of Hoechst 33258 reveals that the folding of several nucleotides in the P4/P6 region of the intron is affected. A nucleotide near the J4/5 region is protected from chemical modification in the presence of Hoechst 33258 and several nearby are more reactive; this suggests that this region is the molecule's binding site. These results expand the available information on small-molecule targeting of RNA and suggest that the RNA-targeting scaffold provided by Hoechst may prove valuable in designing compounds that inhibit the functions of RNA.

Publication types

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

MeSH terms

  • Base Sequence
  • Bisbenzimidazole / pharmacology*
  • Candida albicans / genetics*
  • Catalytic Domain / genetics
  • Inhibitory Concentration 50
  • Introns / genetics*
  • Molecular Sequence Data
  • Nucleic Acid Conformation
  • RNA Splicing / drug effects*
  • RNA Splicing / genetics
  • RNA, Ribosomal, Self-Splicing / antagonists & inhibitors*
  • RNA, Ribosomal, Self-Splicing / genetics

Substances

  • RNA, Ribosomal, Self-Splicing
  • Bisbenzimidazole