Evidence map›Paper›PMID 27183194›Full record

ArticleNature structural & molecular biology2016

Functional interplay between MSL1 and CDK7 controls RNA polymerase II Ser5 phosphorylation.

Sarantis Chlamydas, Herbert Holz, Maria Samata, Tomasz Chelmicki, Plamen Georgiev, Vicent Pelechano, Friederike Dündar, Pouria Dasmeh, Gerhard Mittler, Filipe Tavares Cadete and 8 more

Abstract read
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In one paragraph

Article in Nature structural & molecular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

16 citing papers in PubMed, 27 citations in OpenAlex.

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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

18 authors at 7 institutions in 4 countries.

Sarantis ChlamydasMax Planck Institute of Immunobiology and Epigenetics, Freiburg im Breisgau, Germany.
Herbert HolzMax Planck Institute of Immunobiology and Epigenetics, Freiburg im Breisgau, Germany.
Maria SamataMax Planck Institute of Immunobiology and Epigenetics, Freiburg im Breisgau, Germany.
Tomasz ChelmickiMax Planck Institute of Immunobiology and Epigenetics, Freiburg im Breisgau, Germany.
Plamen GeorgievMax Planck Institute of Immunobiology and Epigenetics, Freiburg im Breisgau, Germany.
Vicent PelechanoGenome Biology Unit, European Molecular Biology Laboratory (EMBL), Heidelberg, Germany.
Friederike DündarMax Planck Institute of Immunobiology and Epigenetics, Freiburg im Breisgau, Germany.
Pouria DasmehMax Planck Institute of Immunobiology and Epigenetics, Freiburg im Breisgau, Germany.
Gerhard MittlerMax Planck Institute of Immunobiology and Epigenetics, Freiburg im Breisgau, Germany.
Filipe Tavares CadeteThe Francis Crick Institute, London, UK.
Fidel RamírezMax Planck Institute of Immunobiology and Epigenetics, Freiburg im Breisgau, Germany.
Thomas ConradMax Planck Institute of Immunobiology and Epigenetics, Freiburg im Breisgau, Germany.
Wu WeiGenome Biology Unit, European Molecular Biology Laboratory (EMBL), Heidelberg, Germany.
Sunil RajaMax Planck Institute of Immunobiology and Epigenetics, Freiburg im Breisgau, Germany.
Thomas MankeMax Planck Institute of Immunobiology and Epigenetics, Freiburg im Breisgau, Germany.
Nicholas M LuscombeThe Francis Crick Institute, London, UK.
Lars M SteinmetzGenome Biology Unit, European Molecular Biology Laboratory (EMBL), Heidelberg, Germany.
Asifa AkhtarMax Planck Institute of Immunobiology and Epigenetics, Freiburg im Breisgau, Germany.
Max Planck Institute of Immunobiology and Epigenetics · DEEuropean Molecular Biology Laboratory · DEScience for Life Laboratory · SEStanford University · USThe Francis Crick Institute · GBUniversity College London · GBUniversity of Freiburg · DE

Funding

Cancer Research UK 16358
6 · The paper itself

Abstract

Proper gene expression requires coordinated interplay among transcriptional coactivators, transcription factors and the general transcription machinery. We report here that MSL1, a central component of the dosage compensation complex in Drosophila melanogaster and Drosophila virilis, displays evolutionarily conserved sex-independent binding to promoters. Genetic and biochemical analyses reveal a functional interaction of MSL1 with CDK7, a subunit of the Cdk-activating kinase (CAK) complex of the general transcription factor TFIIH. Importantly, MSL1 depletion leads to decreased phosphorylation of Ser5 of RNA polymerase II. In addition, we demonstrate that MSL1 is a phosphoprotein, and transgenic flies expressing MSL1 phosphomutants show mislocalization of the histone acetyltransferase MOF and histone H4 K16 acetylation, thus ultimately causing male lethality due to a failure of dosage compensation. We propose that, by virtue of its interaction with components of the general transcription machinery, MSL1 exists in different phosphorylation states, thereby modulating transcription in flies.

Indexed as

AnimalsAnimals, Genetically ModifiedChromatinCyclin-Dependent Kinase-Activating KinaseCyclin-Dependent KinasesDosage Compensation, GeneticDrosophila melanogasterDrosophila ProteinsFemaleGene DeletionMaleMutationNuclear ProteinsPhosphorylationPromoter Regions, GeneticProtein BindingCdk7 protein, DrosophilaChromatinCyclin-Dependent Kinase-Activating KinaseCyclin-Dependent KinasesDrosophila Proteinsmsl-1 protein, DrosophilaNuclear ProteinsRNA Polymerase IISerineTranscription Factors

Identifiers

PMID27183194
OpenAlexW2394820684

What OpenQuestion holds

Textmetadata
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.