Evidence map›Paper›PMID 32483291›Full record

ArticleNature genetics2020

Selective Mediator dependence of cell-type-specifying transcription.

Martin G Jaeger, Björn Schwalb, Sebastian D Mackowiak, Taras Velychko, Alexander Hanzl, Hana Imrichova, Matthias Brand, Benedikt Agerer, Someth Chorn, Behnam Nabet and 9 more

Open access · greenAbstract read
In one paragraph

Article in Nature genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
7.1field-weighted citation impact, top 2% 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

81 citing papers in PubMed, 137 citations in OpenAlex.

  1. Review
  2. Loss ofGenes & diseases · 2026
    Article
  3. The molecular basis of transcription initiation by RNA polymerase II.Nature reviews. Molecular cell biology · 2026
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21 more citing papers are in PubMed but not listed here.

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

19 authors at 5 institutions in 3 countries.

Martin G JaegerCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.ORCID http://orcid.org/0000-0002-7985-9744
Björn SchwalbDepartment of Molecular Biology, Max Planck Institute for Biophysical Chemistry, Göttingen, Germany.ORCID http://orcid.org/0000-0003-2987-2622
Sebastian D MackowiakDepartment of Genome Regulation, Max Planck Institute for Molecular Genetics, Berlin, Germany.
Taras VelychkoDepartment of Molecular Biology, Max Planck Institute for Biophysical Chemistry, Göttingen, Germany.ORCID http://orcid.org/0000-0003-4087-3730
Alexander HanzlCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.
Hana ImrichovaCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.ORCID http://orcid.org/0000-0003-0385-1823
Matthias BrandCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.
Benedikt AgererCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.ORCID http://orcid.org/0000-0002-0044-8396
Someth ChornCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.
Behnam NabetDepartment of Cancer Biology, Dana--Farber Cancer Institute, Boston, MA, USA.ORCID http://orcid.org/0000-0002-6738-4200
Fleur M FergusonDepartment of Cancer Biology, Dana--Farber Cancer Institute, Boston, MA, USA.ORCID http://orcid.org/0000-0003-4091-7617
André C MüllerCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.
Andreas BergthalerCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.ORCID http://orcid.org/0000-0003-0597-1976
Nathanael S GrayDepartment of Cancer Biology, Dana--Farber Cancer Institute, Boston, MA, USA.ORCID http://orcid.org/0000-0001-5354-7403
James E BradnerNovartis Institutes for BioMedical Research, Cambridge, MA, USA.ORCID http://orcid.org/0000-0002-2718-4415
Christoph BockCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.ORCID http://orcid.org/0000-0001-6091-3088
Denes HniszDepartment of Genome Regulation, Max Planck Institute for Molecular Genetics, Berlin, Germany.ORCID http://orcid.org/0000-0002-6256-1693
Patrick CramerDepartment of Molecular Biology, Max Planck Institute for Biophysical Chemistry, Göttingen, Germany. patrick.cramer@mpibpc.mpg.de.ORCID http://orcid.org/0000-0001-5454-7755
Georg E WinterCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria. gwinter@cemm.oeaw.ac.at.ORCID http://orcid.org/0000-0001-6606-1437
Austrian Academy of Sciences · ATHarvard University · USMax Planck Institute for Biophysical Chemistry · DEMax Planck Institute for Molecular Genetics · DENovartis (United States) · US

Funding

Austrian Science Fund FWF P 31690European Research Council 679146
6 · The paper itself

Abstract

The Mediator complex directs signals from DNA-binding transcription factors to RNA polymerase II (Pol II). Despite this pivotal position, mechanistic understanding of Mediator in human cells remains incomplete. Here we quantified Mediator-controlled Pol II kinetics by coupling rapid subunit degradation with orthogonal experimental readouts. In agreement with a model of condensate-driven transcription initiation, large clusters of hypophosphorylated Pol II rapidly disassembled upon Mediator degradation. This was accompanied by a selective and pronounced disruption of cell-type-specifying transcriptional circuits, whose constituent genes featured exceptionally high rates of Pol II turnover. Notably, the transcriptional output of most other genes was largely unaffected by acute Mediator ablation. Maintenance of transcriptional activity at these genes was linked to an unexpected CDK9-dependent compensatory feedback loop that elevated Pol II pause release rates across the genome. Collectively, our work positions human Mediator as a globally acting coactivator that selectively safeguards the functionality of cell-type-specifying transcriptional networks.

Indexed as

Gene Expression RegulationTranscription, GeneticAnimalsCell Line, TumorChromatinDrosophilaGene Expression ProfilingGene Knock-In TechniquesHumansMediator ComplexPositive Transcriptional Elongation Factor BRNA Polymerase IIChromatinMED14 protein, humanMediator ComplexPositive Transcriptional Elongation Factor BRNA Polymerase II

Identifiers

PMID32483291
PMCPMC7610447
OpenAlexW3030331522

What OpenQuestion holds

Textmetadata
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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.