The study demonstrates that DRB differentially inhibits adenovirus RNA polymerase II transcription, blocking elongation from the major late promoter while allowing synthesis of the unspliced polypeptide IX mRNA.
DRB-resistant polypeptide IX transcription suggests promoter-specific control; leaves open extension to mammalian gene regulation.
5,6-Dichloro-beta-D ribofuranosyl benzimidazole (DRB) inhibits transcription from the major late adenovirus promoter, located on the r-strand at map position 16.3 on the viral genome. 100-500 nucleotides long RNA chains with capped 5'-termini are transcribed from this promoter in the presence of 70 muM DRB. Synthesis of the mRNA for polypeptide IX which is unspliced and maps on the r-strand between positions 9.7 and 10.9 appears, however, to be DRB-resistant although it is transcribed by polymerase II and capped. Translatable mRNA for polypeptide IX is synthesized in the presence of DRB while the mRNAs for the other viral structural proteins are not synthesized. This differential DRB-inhibition of polymerase II transcription suggests either that short mRNAs may escape inhibition or that unspliced mRNAs are insensitive to the drug.
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Vennström et al. (1979) studied this question.
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