ArticleJournal of molecular biology2020
The CTD Is Not Essential for the Post-Initiation Control of RNA Polymerase II Activity.
Article in Journal of molecular biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed.
- A tunable CTD grammar governs the spatial programming of the transcription cycle.Nature communications · 2026Article
- Spatial Chromatin Organization Across the Cell Cycle: Insights from Auxin-Inducible Protein Depletion.Cells · 2025Review
- Article
- Domain acquisition enabled functional expansion of the TFIIS transcription factor family.Cell & bioscience · 2025Review
- Defining gene ends: RNA polymerase II CTD threonine 4 phosphorylation marks transcription termination regions genome-wide.Nucleic acids research · 2025Article
- RNA polymerase II CTD is dispensable for transcription and required for termination in human cells.EMBO reports · 2023Article
- Aclarubicin stimulates RNA polymerase II elongation at closely spaced divergent promoters.Science advances · 2023Article
- Cross-regulome profiling of RNA polymerases highlights the regulatory role of polymerase III on mRNA transcription by maintaining local chromatin architecture.Genome biology · 2022Article
- Regulation of Promoter Proximal Pausing of RNA Polymerase II in Metazoans.Journal of molecular biology · 2021Review
- Transcription activation depends on the length of the RNA polymerase II C-terminal domain.The EMBO journal · 2021Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Interest in the C-terminal domain (CTD) of the RPB1 subunit of the RNA polymerase II (Pol II) has been revived in recent years, owing to its numerous posttranslational modifications and its "phase-separation" properties. A large number of studies have shown that the status of CTD modifications is associated with the activity of Pol II during the transcription cycle. However, because this domain is essential in living cells, the functional requirement of the full CTD for the control of Pol II activity at endogenous mammalian genes has never been addressed directly in living cells. Using an inducible Pol II-degradation system that we previously established, we investigated here the roles of the CTD in the post-initiation control of Pol II. The selective ablation of the RPB1 CTD, post-initiation, at promoter-proximal pause-sites revealed that this domain, and by extension the CTD heptads and their modifications, is functionally neither absolutely required to maintain pausing in the absence of CDK9 activity nor essential for the release of Pol II into productive elongation.
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Registered trials
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