Kinetic Competition between RNA Polymerase II and Sen1-Dependent Transcription Termination

SummaryThe essential helicase-like protein Sen1 mediates termination of RNA Polymerase II (Pol II) transcription at snoRNAs and other noncoding RNAs in yeast. A mutation in the Pol II subunit Rpb1 that increases the elongation rate increases read-through transcription at Sen1-mediated terminators. Termination and growth defects in sen1 mutant cells are partially suppressed by a slowly transcribing Pol II mutant and are exacerbated by a faster-transcribing Pol II mutant. Deletion of the nuclear exosome subunit Rrp6 allows visualization of noncoding RNA intermediates that are terminated but not yet processed. Sen1 mutants or faster-transcribing Pol II increase the average lengths of preprocessed snoRNA, CUT, and SUT transcripts, while slowed Pol II transcription produces shorter transcripts. These connections between transcription rate and Sen1 activity support a model whereby kinetic competition between elongating Pol II and Sen1 helicase establishes the temporal and spatial window for early Pol II termination.

Graphical AbstractFigure optionsDownload high-quality image (265 K)Download as PowerPoint slideHighlights
► Fast Pol II elongation rate leads to Sen1-dependent termination defects
► Deletion of Rrp6 reveals a noncoding RNA termination window sensitive to Pol II rate
► Slow Pol II rate promotes earlier Sen1 termination events, rescues sen1 defects
► Fast Pol II rate promotes later Sen1 termination events, worsens sen1 defects