Human transcription release factor 2 dissociates RNA polymerases I and II stalled at a cyclobutane thymine dimer

RNA polymerase II stalled at a lesion in the transcribed strand is thought to constitute a signal for transcription-coupled repair. Transcription fact ors that act on RNA polymerase in elongation mode potentially influence thi s mode of repair. Previously, it was shown that transcription elongation fa ctors TFIIS and Cockayne's syndrome complementation group B protein did not disrupt the ternary complex of RNA polymerase II stalled at a thymine cycl obutane dimer, nor did they enable RNA polymerase II to bypass the dimer, H ere we investigated the effect of the transcription factor 2 on RNA polymer ase II and RNA polymerase I stalled at thymine dimers. Transcription factor 2 is known to release transcripts from RNA polymerase II early elongation complex generated by pulse-transcription. We found that factor 2 (which is also called release factor) disrupts the ternary complex of RNA polymerase II at a thymine dimer and surprisingly exerts the same effect on RNA polyme rase I. These findings show that in mammalian cells a RNA polymerase I or R NA polymerase II transcript truncated by a lesion in the template strand ma y be discarded unless repair is accomplished rapidly by a mechanism that do es not displace stalled RNA polymerases.