Evidence map›Paper›PMID 35621159›Full record

ArticleeLife2022

Oct4 differentially regulates chromatin opening and enhancer transcription in pluripotent stem cells.

Le Xiong, Erik A Tolen, Jinmi Choi, Sergiy Velychko, Livia Caizzi, Taras Velychko, Kenjiro Adachi, Caitlin M MacCarthy, Michael Lidschreiber, Patrick Cramer and 1 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.0field-weighted citation impact, top 7% 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

22 citing papers in PubMed, 36 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

11 authors at 2 institutions in 1 country.

Le Xiong *Max Planck Institute for Multidisciplinary Sciences, Department of Molecular Biology, Göttingen, Germany.ORCID 0000-0001-8180-768X
Erik A Tolen *Max Planck Institute for Molecular Biomedicine, Department of Cell and Developmental Biology, Münster, Germany.ORCID 0000-0002-7147-7506
Jinmi ChoiMax Planck Institute for Multidisciplinary Sciences, Department of Molecular Biology, Göttingen, Germany.
Sergiy VelychkoMax Planck Institute for Molecular Biomedicine, Department of Cell and Developmental Biology, Münster, Germany.ORCID 0000-0002-6227-3966
Livia CaizziMax Planck Institute for Multidisciplinary Sciences, Department of Molecular Biology, Göttingen, Germany.ORCID 0000-0001-9723-6893
Taras VelychkoMax Planck Institute for Multidisciplinary Sciences, Department of Molecular Biology, Göttingen, Germany.
Kenjiro AdachiMax Planck Institute for Molecular Biomedicine, Department of Cell and Developmental Biology, Münster, Germany.
Caitlin M MacCarthyMax Planck Institute for Molecular Biomedicine, Department of Cell and Developmental Biology, Münster, Germany.ORCID 0000-0001-8434-5441
Michael LidschreiberMax Planck Institute for Multidisciplinary Sciences, Department of Molecular Biology, Göttingen, Germany.ORCID 0000-0002-6740-2755
Patrick CramerMax Planck Institute for Multidisciplinary Sciences, Department of Molecular Biology, Göttingen, Germany.ORCID 0000-0001-5454-7755
Hans R SchölerMax Planck Institute for Molecular Biomedicine, Department of Cell and Developmental Biology, Münster, Germany.ORCID 0000-0002-7422-8847
Max Planck Institute for Multidisciplinary SciencesMax Planck Institute for Molecular Biomedicine · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transcription factor Oct4 is essential for the maintenance and induction of stem cell pluripotency, but its functional roles are not fully understood. Here, we investigate the functions of Oct4 by depleting and subsequently recovering it in mouse embryonic stem cells (ESCs) and conducting a time-resolved multiomics analysis. Oct4 depletion leads to an immediate loss of its binding to enhancers, accompanied by a decrease in mRNA synthesis from its target genes that are part of the transcriptional network that maintains pluripotency. Gradual decrease of Oct4 binding to enhancers does not immediately change the chromatin accessibility but reduces transcription of enhancers. Conversely, partial recovery of Oct4 expression results in a rapid increase in chromatin accessibility, whereas enhancer transcription does not fully recover. These results indicate different concentration-dependent activities of Oct4. Whereas normal ESC levels of Oct4 are required for transcription of pluripotency enhancers, low levels of Oct4 are sufficient to retain chromatin accessibility, likely together with other factors such as Sox2.

Indexed as

ChromatinPluripotent Stem CellsAnimalsGene Regulatory NetworksMiceMouse Embryonic Stem CellsTranscription, GeneticChromatinchromatin accessibilitychromosomesenhancereRNAgene expressiongene regulationgeneticsgenomicsmouseOct4pluripotency

Identifiers

PMID35621159
PMCPMC9142147
OpenAlexW4282034433

What OpenQuestion holds

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LicenceCC BY
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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.