作者: Brian A. Donahue , Robert P. P. Fuchs , Daniel Reines , Philip C. Hanawalt
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摘要: Abstract A prominent model for the mechanism of transcription-coupled DNA repair proposes that an arrested RNA polymerase directs nucleotide excision complex to transcription-blocking lesion. The specific role II in this can be examined by comparing extent arrest with a Previously we reported cyclobutane pyrimidine dimer is repaired preferentially transcribed genes strong block transcript elongation pol (Donahue, B. A., Yin, S., Taylor, J.-S., Reines, D., and Hanawalt, P. C.(1994) Proc. Natl. Acad. Sci. U. S. A. 91, 8502-8506). Here report C-8 guanine adduct formed N-2-aminofluorene, lesion does not appear repaired. Templates vitro transcription assay were constructed either N-2-aminofluorene or helix-distorting N-2-acetylaminofluorene situated at site downstream from major late promoter adenovirus. Consistent repair, aminofluorene located on strand was weak pause II. An acetylaminofluorene absolute transcriptional elongation. Either nontranscribed enhanced nearby sequence-specific site.