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Updated: Feb 11, 2026
Analysis of Termination of Transcription Using BrUTP-strand-specific Transcription Run-on TRO Approach
Published on: March 12, 2017
Cell-Cycle Modulation of Transcription Termination Factor Sen1
Hannah E Mischo1, Yujin Chun2, Kevin M Harlen3
1Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA; Sir William Dunn School of Pathology, Oxford University, South Parks Road, Oxford OX1 3RE, UK; Mechanisms of Transcription Laboratory, Clare Hall Laboratories, Cancer Research UK London Research Institute, South Mimms EN6 3LD, UK.
Sen1 helicase levels rise during the cell cycle, enhancing non-coding RNA (ncRNA) termination. Tightly regulated Sen1 prevents toxicity and ensures proper gene expression.
Area of Science:
- Molecular Biology
- Cell Biology
- Genetics
Background:
- Non-coding RNA (ncRNA) termination in S. cerevisiae relies on the Nrd1-Nab3-Sen1 complex.
- Low Sen1 helicase levels present a paradox for efficient ncRNA processing.
Purpose of the Study:
- Investigate the role of Sen1 helicase levels in ncRNA termination.
- Determine the impact of Sen1 abundance regulation on cell fitness and transcription.
Main Methods:
- Cell cycle analysis to track Sen1 levels.
- NET-seq (Nascent End-capture sequencing) to analyze termination events.
- Genetic manipulation (overexpression, mutations) to assess Sen1 function and toxicity.
Main Results:
- Sen1 levels increase during S and G2 phases, boosting NNS termination activity.
- Sen1 overexpression or impaired degradation reduces cell fitness and ncRNA production.
- Altered mRNA termination observed upon Sen1 overexpression.
- Sen1 toxicity is mitigated by mutations in other termination factors.
Conclusions:
- Sen1 levels are tightly regulated via ubiquitin-proteasome system to prevent aberrant termination.
- Sen1 modulates ncRNA levels and coding gene transcription termination for cell cycle-specific functions.
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