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Ribosomal RNA, transcribed by RNA polymerase (Pol) I, accounts for most cellular RNA. Since Pol I transcribes rDNA repeats with high processivity and polymerase density, transcription termination is a critical process. Early in vitro studies proposed polymerase pausing by Reb1 and transcript release at the T-rich element T1 determined transcription termination. However recent in vivo studies revealed a 'torpedo' mechanism for Pol I termination: co-transcriptional RNA cleavage by Rnt1 provides an entry site for the 5'-3' exonuclease Rat1 that degrades Pol I-associated transcripts destabilizing the transcription complex. Significantly Rnt1 inactivation in vivo reveals a second co-transcriptional RNA cleavage event at T1 which provides Pol I with an alternative termination pathway. An intact Reb1-binding site is also required for Rnt1-independent termination. Consequently our results reconcile the original Reb1-mediated termination pathway as part of a failsafe mechanism for this essential transcription process.

Original publication




Journal article


Nucleic Acids Res

Publication Date





1439 - 1448


DNA Helicases, DNA, Ribosomal, DNA-Binding Proteins, Exoribonucleases, Gene Deletion, Mutagenesis, RNA Helicases, RNA Polymerase I, RNA, Ribosomal, Ribonuclease III, Saccharomyces cerevisiae, Saccharomyces cerevisiae Proteins, Terminator Regions, Genetic, Thymine, Transcription Factors, Transcription, Genetic