Evidence map›Paper›PMID 32937131›Full record

ArticleCell reports2020

Extensive SUMO Modification of Repressive Chromatin Factors Distinguishes Pluripotent from Somatic Cells.

Ilan Theurillat, Ivo A Hendriks, Jack-Christophe Cossec, Alexandra Andrieux, Michael L Nielsen, Anne Dejean

Erratum issuedAbstract read
In one paragraph

Article in Cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
–field-weighted citation impact
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

30 citing papers in PubMed.

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  12. RNF212B E3 ligase is essential for crossover designation and maturation during male and female meiosis in the mouse.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  19. Signalling mechanisms and cellular functions of SUMO.Nature reviews. Molecular cell biology · 2022
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors.

Ilan TheurillatNuclear Organization and Oncogenesis Unit, Institut Pasteur, Équipe Labellisée Ligue Nationale Contre le Cancer, 75015 Paris, France; INSERM, U993, 75015 Paris, France; Sorbonne Université, Collège Doctoral, 75005 Paris, France.
Ivo A HendriksProteomics Program, Novo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, 2200 Copenhagen, Denmark.
Jack-Christophe CossecNuclear Organization and Oncogenesis Unit, Institut Pasteur, Équipe Labellisée Ligue Nationale Contre le Cancer, 75015 Paris, France; INSERM, U993, 75015 Paris, France.
Alexandra AndrieuxNuclear Organization and Oncogenesis Unit, Institut Pasteur, Équipe Labellisée Ligue Nationale Contre le Cancer, 75015 Paris, France; INSERM, U993, 75015 Paris, France.
Michael L NielsenProteomics Program, Novo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, 2200 Copenhagen, Denmark.
Anne DejeanNuclear Organization and Oncogenesis Unit, Institut Pasteur, Équipe Labellisée Ligue Nationale Contre le Cancer, 75015 Paris, France; INSERM, U993, 75015 Paris, France. Electronic address: anne.dejean@pasteur.fr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Post-translational modification by SUMO is a key regulator of cell identity. In mouse embryonic fibroblasts (MEFs), SUMO impedes reprogramming to pluripotency, while in embryonic stem cells (ESCs), it represses the emergence of totipotent-like cells, suggesting that SUMO targets distinct substrates to preserve somatic and pluripotent states. Using MS-based proteomics, we show that the composition of endogenous SUMOylomes differs dramatically between MEFs and ESCs. In MEFs, SUMO2/3 targets proteins associated with canonical SUMO functions, such as splicing, and transcriptional regulators driving somatic enhancer selection. In contrast, in ESCs, SUMO2/3 primarily modifies highly interconnected repressive chromatin complexes, thereby preventing chromatin opening and transitioning to totipotent-like states. We also characterize several SUMO-modified pluripotency factors and show that SUMOylation of Dppa2 and Dppa4 impedes the conversion to 2-cell-embryo-like states. Altogether, we propose that rewiring the repertoire of SUMO target networks is a major driver of cell fate decision during embryonic development.

Indexed as

SumoylationAnimalsCell DifferentiationChromatinEmbryo, MammalianEmbryonic Stem CellsFibroblastsHeLa CellsHumansMice, Inbred C57BLNuclear ProteinsPluripotent Stem CellsRNA, MessengerSmall Ubiquitin-Related Modifier ProteinsSubstrate SpecificityTranscription FactorsChromatinDppa2 protein, mouseDppa4 protein, mouseNuclear ProteinsRNA, MessengerSmall Ubiquitin-Related Modifier ProteinsTranscription Factors2C-like cellscell differentiationDppa2/4embryonic stem cellsheterochromatinpluripotencyproteomicssomatic cellsSUMOtotipotency

Identifiers

PMID32937131
PMCPMC7495044

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.