Evidence map›Paper›PMID 28209164›Full record

ArticleGenome biology2017

RNF40 regulates gene expression in an epigenetic context-dependent manner.

Wanhua Xie, Sankari Nagarajan, Simon J Baumgart, Robyn Laura Kosinsky, Zeynab Najafova, Vijayalakshmi Kari, Magali Hennion, Daniela Indenbirken, Stefan Bonn, Adam Grundhoff and 3 more

Open access · goldAbstract read
In one paragraph

Article in Genome biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

43 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
  2. Article
  3. Decoding RNF20: an epigenetic modifier and beyond.Frontiers in cell and developmental biology · 2026
    Review
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  12. RNF20 contributes to epigenetic immunosuppression through CDK9-dependent LSD1 stabilization.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
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  16. Review
  17. Review
  18. Monoubiquitination in Homeostasis and Cancer.International journal of molecular sciences · 2022
    Review
  19. Article
  20. Article
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

13 authors at 5 institutions in 1 country.

Wanhua XieDepartment of General, Visceral and Pediatric Surgery, Göttingen Center for Molecular Biosciences, University Medical Center Göttingen, Justus-von-Liebig-Weg 11, 37077, Göttingen, Germany.
Sankari NagarajanDepartment of General, Visceral and Pediatric Surgery, Göttingen Center for Molecular Biosciences, University Medical Center Göttingen, Justus-von-Liebig-Weg 11, 37077, Göttingen, Germany.
Simon J BaumgartDepartment of General, Visceral and Pediatric Surgery, Göttingen Center for Molecular Biosciences, University Medical Center Göttingen, Justus-von-Liebig-Weg 11, 37077, Göttingen, Germany.
Robyn Laura KosinskyDepartment of General, Visceral and Pediatric Surgery, Göttingen Center for Molecular Biosciences, University Medical Center Göttingen, Justus-von-Liebig-Weg 11, 37077, Göttingen, Germany.
Zeynab NajafovaDepartment of General, Visceral and Pediatric Surgery, Göttingen Center for Molecular Biosciences, University Medical Center Göttingen, Justus-von-Liebig-Weg 11, 37077, Göttingen, Germany.
Vijayalakshmi KariDepartment of General, Visceral and Pediatric Surgery, Göttingen Center for Molecular Biosciences, University Medical Center Göttingen, Justus-von-Liebig-Weg 11, 37077, Göttingen, Germany.
Magali HennionResearch Group for Computational Systems Biology, German Center for Neurodegenerative Diseases (DZNE), Griesebachstraße 5, 37077, Göttingen, Germany.
Daniela IndenbirkenHeinrich Pette Institute, Leibniz Institute for Experimental Virology, 20251, Hamburg, Germany.
Stefan BonnResearch Group for Computational Systems Biology, German Center for Neurodegenerative Diseases (DZNE), Griesebachstraße 5, 37077, Göttingen, Germany.
Adam GrundhoffHeinrich Pette Institute, Leibniz Institute for Experimental Virology, 20251, Hamburg, Germany.
Florian WegwitzDepartment of General, Visceral and Pediatric Surgery, Göttingen Center for Molecular Biosciences, University Medical Center Göttingen, Justus-von-Liebig-Weg 11, 37077, Göttingen, Germany.
Ahmed MansouriDepartment of Molecular Cell Biology, Max-Planck Institute for Biophysical Chemistry, Am Fassberg, 37077, Göttingen, Germany.
Steven A JohnsenDepartment of General, Visceral and Pediatric Surgery, Göttingen Center for Molecular Biosciences, University Medical Center Göttingen, Justus-von-Liebig-Weg 11, 37077, Göttingen, Germany. steven.johnsen@med.uni-goettingen.de.
Universitätsmedizin Göttingen · DEUniversity of Göttingen · DEGerman Center for Neurodegenerative Diseases · DELeibniz Institute of Virology (LIV) · DEMax Planck Institute for Biophysical Chemistry · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMonoubiquitination of H2B (H2Bub1) is a largely enigmatic histone modification that has been linked to transcriptional elongation. Because of this association, it has been commonly assumed that H2Bub1 is an exclusively positively acting histone modification and that increased H2Bub1 occupancy correlates with increased gene expression. In contrast, depletion of the H2B ubiquitin ligases RNF20 or RNF40 alters the expression of only a subset of genes.

resultsUsing conditional Rnf40 knockout mouse embryo fibroblasts, we show that genes occupied by low to moderate amounts of H2Bub1 are selectively regulated in response to Rnf40 deletion, whereas genes marked by high levels of H2Bub1 are mostly unaffected by Rnf40 loss. Furthermore, we find that decreased expression of RNF40-dependent genes is highly associated with widespread narrowing of H3K4me3 peaks. H2Bub1 promotes the broadening of H3K4me3 to increase transcriptional elongation, which together lead to increased tissue-specific gene transcription. Notably, genes upregulated following Rnf40 deletion, including Foxl2, are enriched for H3K27me3, which is decreased following Rnf40 deletion due to decreased expression of the Ezh2 gene. As a consequence, increased expression of some RNF40-"suppressed" genes is associated with enhancer activation via FOXL2.

conclusionTogether these findings reveal the complexity and context-dependency whereby one histone modification can have divergent effects on gene transcription. Furthermore, we show that these effects are dependent upon the activity of other epigenetic regulatory proteins and histone modifications.

Indexed as

Epigenesis, GeneticGene Expression RegulationAnimalsCyclin-Dependent Kinase 9Enhancer Elements, GeneticEnhancer of Zeste Homolog 2 ProteinFibroblastsGenes, HomeoboxHistonesMiceMice, KnockoutOrgan SpecificityProtein BindingTranscriptional ActivationTranscription Elongation, GeneticTranscription, GeneticCyclin-Dependent Kinase 9Enhancer of Zeste Homolog 2 ProteinEzh2 protein, mouseHistonesRNF20 protein, mouseUbiquitin-Protein LigasesBroad H3K4me3EnhancerEpigeneticsEzh2FOXL2H2Bub1RNF40

Identifiers

PMID28209164
PMCPMC5314486
OpenAlexW2588155275

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.