Evidence map›Paper›PMID 32496538›Full record

ArticleNucleic acids research2020

Cdk9 and H2Bub1 signal to Clr6-CII/Rpd3S to suppress aberrant antisense transcription.

Miriam Sansó, Pabitra K Parua, Daniel Pinto, J Peter Svensson, Viviane Pagé, Danny A Bitton, Sarah MacKinnon, Patricia Garcia, Elena Hidalgo, Jürg Bähler and 2 more

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.7field-weighted citation impact, top 16% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 29 citations in OpenAlex.

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  17. Decoding histone ubiquitylation.Frontiers in cell and developmental biology · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 6 institutions in 5 countries.

Miriam SansóDepartment of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Pabitra K ParuaDepartment of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Daniel PintoDepartment of Pharmacology and Therapeutics, McGill University, Montreal, Canada.
J Peter SvenssonDepartment of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden.
Viviane PagéDepartment of Pharmacology and Therapeutics, McGill University, Montreal, Canada.
Danny A BittonResearch Department of Genetics, Evolution & Environment, University College, London, UK.
Sarah MacKinnonDepartment of Pharmacology and Therapeutics, McGill University, Montreal, Canada.
Patricia GarciaDepartament de Ciènces Experimentals i de la Salut, Universitat Pompeu Fabra, Barcelona, Spain.
Elena HidalgoDepartament de Ciènces Experimentals i de la Salut, Universitat Pompeu Fabra, Barcelona, Spain.
Jürg BählerResearch Department of Genetics, Evolution & Environment, University College, London, UK.
Jason C TannyDepartment of Pharmacology and Therapeutics, McGill University, Montreal, Canada.
Robert P FisherDepartment of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
McGill University · CAIcahn School of Medicine at Mount Sinai · USUniversitat Pompeu Fabra · ESUniversity College London · GBKarolinska Institutet · SEVall d'Hebron Institute of Oncology · ES

Funding

Cyclin-dependent kinase control of cell-division and transcription cyclesR35GM127289 · NIGMS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI ROBERT P FISHER · 2018 to 2026
$4.4M
CIHR MOP-130362NIGMS NIH HHS R35 GM127289Wellcome Trust 095598/Z/11/Z
6 · The paper itself

Abstract

Mono-ubiquitylation of histone H2B (H2Bub1) and phosphorylation of elongation factor Spt5 by cyclin-dependent kinase 9 (Cdk9) occur during transcription by RNA polymerase II (RNAPII), and are mutually dependent in fission yeast. It remained unclear whether Cdk9 and H2Bub1 cooperate to regulate the expression of individual genes. Here, we show that Cdk9 inhibition or H2Bub1 loss induces intragenic antisense transcription of ∼10% of fission yeast genes, with each perturbation affecting largely distinct subsets; ablation of both pathways de-represses antisense transcription of over half the genome. H2Bub1 and phospho-Spt5 have similar genome-wide distributions; both modifications are enriched, and directly proportional to each other, in coding regions, and decrease abruptly around the cleavage and polyadenylation signal (CPS). Cdk9-dependence of antisense suppression at specific genes correlates with high H2Bub1 occupancy, and with promoter-proximal RNAPII pausing. Genetic interactions link Cdk9, H2Bub1 and the histone deacetylase Clr6-CII, while combined Cdk9 inhibition and H2Bub1 loss impair Clr6-CII recruitment to chromatin and lead to decreased occupancy and increased acetylation of histones within gene coding regions. These results uncover novel interactions between co-transcriptional histone modification pathways, which link regulation of RNAPII transcription elongation to suppression of aberrant initiation.

Indexed as

Transcription Elongation, GeneticCell Cycle ProteinsCyclin-Dependent Kinase 9HistonesPhosphorylationRNA Polymerase IISchizosaccharomycesSchizosaccharomyces pombe ProteinsTranscriptional Elongation FactorsUbiquitinationCell Cycle ProteinsClr6 protein, S pombeCyclin-Dependent Kinase 9HistonesRNA Polymerase IISchizosaccharomyces pombe ProteinsTranscriptional Elongation Factors

Identifiers

PMID32496538
PMCPMC7367204
OpenAlexW3032385310

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.