Journal
MOLECULAR CELL
Volume 72, Issue 6, Pages 942-+Publisher
CELL PRESS
DOI: 10.1016/j.molcel.2018.10.018
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Funding
- Francis Crick Institute [FC001203]
- Cancer Research UK [FC001203]
- UK Medical Research Council [FC001203]
- Wellcome Trust [FC001203]
- Agency for Science, Technology and Research (A*STAR) of Singapore
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Many active eukaryotic gene promoters exhibit divergent noncoding transcription, but the mechanisms restricting expression of these transcripts are not well understood. Here, we demonstrate how a sequence-specific transcription factor represses divergent noncoding transcription at highly expressed genes in yeast. We find that depletion of the transcription factor Rap1 induces noncoding transcription in a large fraction of Rap1-regulated gene promoters. Specifically, Rap1 prevents transcription initiation at cryptic promoters near its binding sites, which is uncoupled from transcription regulation in the protein-coding direction. We further provide evidence that Rap1 acts independently of previously described chromatin-based mechanisms to repress cryptic or divergent transcription. Finally, we show that divergent transcription in the absence of Rap1 is elicited by the RSC chromatin remodeler. We propose that a sequence-specific transcription factor limits access of basal transcription machinery to regulatory elements and adjacent sequences that act as divergent cryptic promoters, thereby providing directionality toward productive transcription.
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