ArticleCommunications biology2025
Histone H2B monoubiquitylation regulates elongation-to-termination transition in RNA polymerase II transcription.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Spt5's central KOW domains and the Pol II stalk collaborate to regulate chromatin and 3'-end processing in Saccharomyces cerevisiae.G3 (Bethesda, Md.) · 2026Article
- Epigenetic regulation of cardiac physiology and pathophysiology: biological sex matters.The journal of cardiovascular aging · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
RNA Polymerase II (Pol II) transcription is tightly regulated across initiation, elongation, and termination, with key transitions at initiation-to-elongation and elongation-to-termination. While elongation and termination are well-studied, their transition remains unclear. Using chromatin immunoprecipitation (ChIP) and sequencing, we show in Schizosaccharomyces pombe that Cdk9, with its cyclin partner Pch1, disengages from the elongation complex as Pol II nears the cleavage and polyadenylation signal (CPS), while Dis2 (PP1 ortholog) binding increases beyond the CPS, showing an inverse relationship with Cdk9. ChIP-seq analysis reveals histone H2B monoubiquitylation (H2Bub1) regulates Cdk9 occupancy, promoting its recruitment during elongation and dissociation at the CPS, mirroring pSpt5 distribution. Dis2, a pSpt5 phosphatase, exhibits an inverse pattern, decreasing with H2Bub1 loss (htb1-K119R) and increasing with persistent H2Bub1 (ubp8Δ). H2Bub1 perturbations inversely affect Pol II CTD Tyr1/Ser2 phosphorylation, Ser2 kinase Lsk1, mRNA 3'-end processing factors (Pfs2, Pla1), and termination factors (Rhn1, Pcf11)-H2Bub1 loss reduces recruitment, while its persistence enhances occupancy. These findings align with a model in which H2Bub1 loss disrupts termination, whereas its sustained presence reinforces it. Collectively, our findings suggest that H2Bub1-mediated Cdk9 eviction at the CPS facilitates Dis2 binding, pSpt5 dephosphorylation, Pol II slowing, and efficient termination, revealing a yet unknown regulatory paradigm in transcription.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.